Beruflich Dokumente
Kultur Dokumente
A Symptom-based Approach
in Internal Medicine
Diagnosis
A Symptom-based Approach
in Internal Medicine
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Diagnosis: A Symptom-based Approach in Internal Medicine
© 2011, Jaypee Brothers Medical Publishers
All rights reserved. No part of this publication should be reproduced, stored in a retrieval system, or transmitted
in any form or by any means: electronic, mechanical, photocopying, recording, or otherwise, without the
prior written permission of the author and the publisher.
This book has been published in good faith that the material provided by author is original. Every effort
is made to ensure accuracy of material, but the publisher, printer and author will not be held responsible
for any inadvertent error (s). In case of any dispute, all legal matters are to be settled under Delhi
jurisdiction only.
The best physician is the one who is able to differentiate the possible and the impossible.
Herophilus of Alexandria
Diagnosis: A Symptom-based Approach in Internal Medicine was conceived during my practice in
general internal medicine. I wrote this book because I wished it had been written for me. Although
there are many textbooks and excellent manuals devoted to symptom-oriented diagnosis, I
personally felt the need for a book that provides the essential information necessary in a concise
and practical method, and thus relieve one from time and labor in searching through voluminous
medical textbooks on the diagnostic process of symptoms presented by patients in today’s arduous
ambulatory health care delivery system.
A symptom is commonly defined as,”Any affection which accompanies disease; a perceptible
change in the body or its functions, which indicates disease, or the kind or phases of disease”.
The importance of symptoms, therefore, cannot be overemphasized because symptoms are why
patients visit physicians; and based on their analysis, a physician attempts to make as accurate a
clinical diagnosis as possible.
Many symptoms encountered in everyday practice may suggest undifferentiated problems
and many may suggest problems that are self-limited, while many symptoms are characteristic
of early disease. New or serious symptoms often drive patients to overcrowded office or emergency
departments. However, physicians need medical resource that can deliver timely and effective
diagnostic information which, besides providing diagnosis on an established or common disease,
does not ignore other possibilities. Besides, relevant diagnostic investigations and clinical aspects
of related disorders are essential to support the diagnosis of any disease and treatment accordingly.
Thus, in a busy ambulatory care, diagnosis has to be made without it being unrecognized until
advance disease is present, treatment options are limited, and prognosis may be unfavorable.
It is in this context, I have made an attempt to first project common symptoms encountered in
internal medicine, especially as applicable to the epidemiological incidence to the adult patient
population, and then create a framework in which a physician can arrive at a tentative diagnosis.
The main features which remain constant for each symptom are:
• Synopsis: A symptom introduction in brief;
• Differential diagnosis of the symptom: Classified in three main groups, namely—common, occasional
and rare;
• Investigations: In two sections, namely—general and specific;
• Clinical notes: In short paragraphs, helpful in the diagnosis of most of the diseases;
• Red flags: Key points highlighted to alert serious disorders not to be missed;
• Tables: To simplify and comprehensively illustrate text, wherever needed;
• Selective glossary: Brief summary of assorted, common and uncommon diseases, denoted by the
sign “vide infra ↓↓”; and
• References: From various journals, textbooks, etc. where applicable.
viii
Thus, the contents of this book are focused on commonly encountered symptoms, with their
differential diagnosis in a concise form, which will lead to a working diagnosis and investigations.
The emphasis is on the axiom, ‘common diseases present commonly, and its converse, uncommon
diseases present uncommonly’. However, pointers to ‘red flags’, i.e. uncommon manifestations of
common diseases should alert the physician of serious diseases not to be missed. No attempt has
been made to discuss etiology or pathology of illness, or the complexities of practice management.
The frequency with which a disease is encountered by physician will depend upon its
prevalence in the region from which their patients are drawn and also their specialty; therefore,
regional variations in the incidence of diseases or methodology, or guidelines for investigations
and diagnosis are not discussed, which can be accessed from other relevant sources.
The book assumes much basic knowledge and the information it contains must be supplemented
by further reading. However, my endeavor has been to cover a spectrum of symptoms, with
emphasis on practical features of diagnosis, based on recent evidence-based guidelines. The contents
of the book are intended for medical students, internists, and house-officers during their daily
office or hospital practice, and also to physicians to boost their diagnostic skills during busy
practice day, and preparation for ‘rounds’ and clinical teaching. I also anticipate that physicians
of other specialties will also value this book as an easy-to-use ready-reference guide beyond their
everyday experience and in various practice settings.
There is no substitute for knowledge, and this book, I believe, will make symptom-based
diagnostic process more accessible to many physicians, and if it prompts others to delve further
and achieve sophistication in this clinical expertise, then this book has accomplished its purpose.
Finally, I would welcome feedback, which can be posted to me via my website: www.drcsm.com,
or email: vidya_csm@yahoo.com, or to the publishers.
CS Madgaonkar
ACKNOWLEDGMENTS
My work in writing this book has been shared among many individuals.
First of all, I would like to appreciate the comments and advice of the following eminent
specialists who reviewed appropriate chapters of this book:
• Dr Vidya C Madgaonkar MD DA, Professor of Anesthesiology, Bangalore Medical College and
Research Institute, Bengaluru, Karnataka, India.
• Dr AS Guruprasad MS, Fellow Sankara Nethralaya, Head of Vitreoretinal Services, MM Joshi
Eye Institute, Hubli, Karnataka, India.
• Dr Shailesh E Gokavi MD , Infertility Consultant and Gynecological Endoscopic Surgeon, Hubli,
Karnataka, India.
• Dr Neminath R Patil MS DLO, Consulting ENT Surgeon, Shravan ENT Neuro-Otology Clinic,
Hearing Aid Center, Hubli, Karnataka, India.
I have received most generous assistance from the former Dean Dr YS Rai FRCS (Ed), SDM
College of Medical Sciences and Hospital, Manjushree Nagar, Sattur, Dharwad, Karnataka for
extending Central Library facilities, and also to the library staff, who took immense care and
pains to provide innumerable references in the compilation of this book.
I would also like to sincerely thank the library staff of my alma mater, Kasturba Medical
College, Manipal, Karnataka, India who have been a consistent resource.
My sincere thanks are extended to Shri Jitendar P Vij (Chairman and Managing Director), and
Mr Tarun Duneja, (Director-Publishing), M/s Jaypee Brothers Medical Publishers (P) Ltd, New
Delhi, India who have helped me throughout and displayed patience, understanding and
professionalism in publishing this book. I would also like to record my appreciation from Mr Venu
Gopal V, (Bengaluru branch) for extending his cooperation at every step.
I owe a debt of gratitude to my dear mother, Smt Sumitra S Madgaonkar, for her unstinted
support, encouragement, and forbearance. Thanks, as ever, also goes to my other family members
and friends, for their constant support, guidance and encouragement. The true kudos, however,
belong to my wife, Dr Vidya, and my son, Varun, for their eternal patience and incredible support
throughout, which ultimately made this book a realty.
CONTENTS
Plasmoprotein Electrophoresis 38; Bence Jones Protein 38; CXR 38; US Abdomen 38; CT
Spine 39; HRCT Abdomen 39; MRI Spine 39; Bone Scans (Technetium) 39; Upper GI
Endoscopy 39; CSF Analysis 39; Electrodiagnosis 39; Histocompatibility Antigen Test
(HLA-B 27) 39; Myelography, Discography, Diagnostic Selective Nerve Blockade 39; Bone
Marrow Biopsy/Aspiration 39
7. Breast Lump ...................................................................................................................................42
Common 42; Occasional 43; Rare 43; CBC 43; ESR 43; LFTs 43; Serum Calcium 43; CXR 43;
Mammography 43; Digital Mammography 43; FNAC or FNA Biopsy (FNAB)†† 44;
US Breast 44; US Abdomen 44; MRI 44; Core-needle Biopsy 44; Excision Biopsy 44;
Triple Diagnosis Test 44; Genetic Testing for Breast Cancer 44
8. Chest Pain ....................................................................................................................................... 48
Common 49; Occasional 49; Rare 49; CBC 50; Blood Glucose/Lipid Profile 50; ECG 50; CXR 50;
Cardiac Enzymes 50; Exercise ECG 51; Echocardiography – 2-D and Doppler 51; HRCT/
MRI 51; Ventilation-perfusion (V/Q) Scans 51; Myocardial Perfusion Imaging 51; Coronary
Angiography 51; Intravascular Ultrasound (IVUS) 51; Multislice Computed Tomography
(MSCT)/ 64-Slice Spiral Computed Tomography 52; GI Studies 52; PFTs 52; TFTs 52
9. Constipation .................................................................................................................................. 57
Common 58; Occasional 58; Rare 58; CBC 58; ESR 58; FOBT 58; Proctoscopy (Anoscopy) 58;
Urea, Creatinine, Electrolytes 58; Endocrine Panel 58; Serum Calcium 59; AXR 59; US
Abdomen 59; Colonoscopy 59; Sigmoidoscopy/Barium Enema 59; MRI—Brain, Spine 59;
Expanded Physiological Studies 59; Rectal Biopsy 59
10. Convulsions ...................................................................................................................................63
Common 64; Occasional 64; Rare 64; CBC 64; Blood Glucose 65; Serum Electrolytes 65; ECG 65;
Neuroimaging 65; Biochemistry Panel 65; CSF 65; EEG 65; Ambulatory EEG (aEEG) 65;
Video-EEG Monitoring2, 3 65; Toxicology (Serum and Urine) Screen 65
11. Cough .............................................................................................................................................. 68
Common 69; Occasional 69; Rare 69; CBC 69; Sputum 69; CXR 70; Peak Expiratory Flow
Rate (PEFR) 70; PFTs 70; Pulse Oximetry 70; pH Studies 70; CT Chest /MRI 70; CT Sinus 70;
Esophagogastroduodenoscopy (EGD) 71; Bronchoscopy 71; Purified Protein Derivative (PPD)
Skin Test 71; HIV Serology 71; Culture of Nasopharyngeal Secretions/PCR 71; Sputum
Cytology 71
12. Dementia ........................................................................................................................................73
Common 74; Occasional 75; Rare 75; CBC 75; ESR 75; Urea, Creatinine, LFTs 75; Electrolytes—
Sodium, Potassium, Calcium, Glucose 75; TFTs 75; Neuroimaging—CT/MRI 76; Infection
Screen 76; Vitamin B12 Assay 76; VDRL/Fluorescein Treponema Antibody (FTA-ABS) 76; HIV
Serology 76; ANA, Anti-ds DNA 76; CSF 76; CXR/ECG 76; EEG 76; SPECT/PET 76; MR
Angiography (MRA) 77; Brain and Meningeal Biopsy 77; Genetic Test 77;
Neuropsychologic evaluation 77
13. Diarrhea .......................................................................................................................................... 83
Common 84; Occasional 84; Rare 84; CBC 84; ESR 84; Blood Glucose 84; Metabolic Panel 84;
HIV 84; Fecal Leukocytes 84; Rectal Swab for c/s 85; FOBT 85; Stool for Protozoa 85; Stools for
Contents xiii
Clostridium Difficile Titer 85; Stool pH 85; Stool for ZN Stain (Modified) 85; Stool Chemical
Analysis 85; Stool Fat (Sudan Stain) 85; TFTs 85; LFTs 85; Sigmoidoscopy with Biopsy and
Culture 85; Colonoscopy or Barium Enema 85; US or CT Abdomen 85; Upper GI Barium
Series 86; Laxative Abuse Detection 86; Urine 24-hr Collection for 5-HIAA Excretion 86;
Serum Gastrin 86; Serum Calcitonin 86
14. Dyspepsia ....................................................................................................................................... 90
Common 90; Occasional 91; Rare 91; CBC 91; ESR 91; FOBT and Parasites 91; ECG 91;
Metabolic Panel 91; TFTs 91; LFTs, Amylase, Lipase 91; EGD with or without Biopsy for H.
pylori (HP) 92; Tests for HP 92; US Abdomen or CT 92; Esophagography and upper GI
Barium Meal Series 92; Esophageal Manometry 92; 24-hour esophageal pH Manometry 93;
Fasting Serum Gastrin 93
15. Dysphagia ......................................................................................................................................97
Oropharyngeal Causes 98; Esophageal Causes 99; CBC, ESR 99; CXR 99; X-ray
Neck—lateral view 99; Barium Swallow (Barium Esophagography, or Modified Barium Swallow
(MBS) 99; EGD 100; Esophageal Manometry (Stationary and Ambulatory) 100; Esophageal
24-hours pH Reflux Study 100; Videofluoroscopic Swallowing Function Study (VSFS) 101;
Radionucleotide Study (Tc-99m Sulfur Colloid Bolus) 101; CT Scan/MRI 101; Muscle
Enzymes 101; TFTs 101; RF, ANA 101; Antiacetylcholine Antibodies 101; Genetic Analysis 101;
Common 108
16. Dyspnea—Acute ........................................................................................................................ 108
Occasional 109; Rare 109; CBC 109; Blood Glucose, Electrolytes, Urinalysis 109; Peak
Expiratory Flow Rate (PEFR) 109; ECG 109; CXR 109; X-ray Neck—Lateral View 109;
Pulse Oximetry 109; Sr Cardiac Markers 110; Sputum and Blood Culture 110; Pulmonary
Function Tests 110; Arterial Blood Gases (ABG) 110; Bronchoscopy 110; D-dimer 110; HRCT
of Thorax 110; V/Q scan 110; BNP (Brain or B-type Natriuretic Peptide) 110;
Echocardiography 110; Drug Screen 110
17. Dyspnea—Chronic .................................................................................................................... 114
Common 114; Occasional 115; Rare 115; CBC 115; Sputum 115; CXR 115; Pulse Oximetry 115;
ECG 115; Metabolic Panel 115; Blood Chemistry 116; PFT/Spirometry 116; Methacholine
Challenge Test 116; Echocardiography 116; B-type Natriuretic Peptide (BNP) 116; HRCT 116;
HRCT Angiography 117; V/Q Scan 117; 24-hour Esophageal pH Monitoring 117; EMG and
NCS 117; Noninvasive Cardiovascular Testing 117; Cardiopulmonary Exercise (CPEx)
Testing 117; Bronchoscopy / Lung Biopsy 117
18. Facial Asymmetry and Weakness ........................................................................................... 120
Common 121; Occasional 121; Rare 121; CBC 121; Blood Glucose 121; VDRL 121; CXR 121;
CT Skull 121; MRI with Gadolinium 121; CSF 121; EMG/NCS 122; Lyme titer 122;
Serum Calcium and Angiotensin-converting Enzyme Levels 122
19. Facial Swelling ........................................................................................................................... 127
Common 127; Occasional 127; Rare 128; CBC 128; ESR 128; Urinalysis 128; Plasma
Protein 128; Urea, Creatinine 128; Blood Glucose 128; CXR 128; X-ray PNS 128; TFTs 128;
ANA 128; Parotid Sialography 128; CT/MRI Brain 128; CT/MRI Lungs, Abdomen 128;
CT/MRI PNS 128; Plasma/urinary Cortisol 129; Muscle Biopsy (Bx) 129
xiv Diagnosis: A Symptom-based Approach in Internal Medicine
Echocardiography 278; Holter Monitor 278; Carotid Doppler US 278; CT/MRI brain 278;
Head-up Tilt-Testing 278; Electrophysiology study (EPS) 278; Implantable Loop Recorder
(ILR) 278; Electroencephalography (EEG) 278; Psychiatric Evaluation 279
41. Tingling and Numbness .......................................................................................................... 284
Common 285; Occasional 285; Rare 285; Transient 286; Upper Limbs 286; Lower Limbs 286;
CBC 286; ESR 286; Blood Glucose, Urea, Creatinine, Electrolytes 286; CXR 287; X-ray 287;
TSH 287; Rheumatology Screen 287; Angiotensin-Converting Enzyme Level 287; Urine for
Porphobilinogen 287; Nerve Conduction Study (NCS) 287; CT/MRI 287; Nerve Biopsy 287;
Lyme Titer 287; HIV 287; Serum B12 and Folate Levels 287; CSF Analysis 287; Serum Protein
Electrophoresis and Immuno-fixation 287; Toxic Screen 287; Genetic Test 287
42. Tinnitus ........................................................................................................................................ 291
Common 292; Otologic 292; Nonotologic 292; Physiological 292; Occasional 292; Rare 292;
CBC, ESR 292; FBG, PPBG 293; Audiogram 293; Tympanogram 293; Biochemistry 293;
TFTs 293; CT Scan 293; MRI Scan 293; MRI Cerebral Angiography 293; X-ray 293; CSF 293;
Brainstem Evoked Potentials 293
43. Tiredness ..................................................................................................................................... 296
Common 296; Occasional 297; Rare 297; CBC 297; ESR 297; Blood Glucose 297; LFTs 297;
Urea, Electrolytes and Creatinine 297; TFTs 297; Pregnancy Test 297; CXR 297; Chronic
Infection Screening 297; HIV and VDRL Serology 298; RF and ANA 298; Plasma Cortisol
(8 AM-10 AM specimen) 298; Muscle Enzymes CK, CK-MB 298; Tensilon (edrophonium)
Test 298; EMG 298; Muscle / Tissue Biopsy 298; Bone Marrow Biopsy/Aspirate 298; MRI
Brain 298; Polysomnography (Sleep Study) 298; Cancer Screening 298
44. Urinary Frequency ..................................................................................................................... 302
Common 303; Occasional 303; Rare 303; Urinalysis 304; Quantitative Culture for
Bacteriuria 304; Suprapubic Aspiration/ Catheterization 304; CBC 304; Blood Glucose 304;
Urea, Creatinine 304; Electrolytes 304; Pregnancy Test 304; Urine Culture 304; US of Kidneys,
Ureter, and Bladder (KUB) 304; CT scan of KUB 304; Intravenous pyelography (IVP) or
Intravenous Urography (IVU) 305; MRI Brain/Spine 305; Cystoscopy 305
45. Urticaria and Angioedema ....................................................................................................... 308
Occasional 309; Rare 309; CBC 309; ESR 309; Urinalysis 309; Stools 309; Challenge Testing
for Physical Urticaria 310; Throat and Urine Culture 310; Multichemistry Screening Panel 310;
TFTs 310; Serology 310; Skin Prick Test or Patch Test 310; Serum Immunoglobulin Analysis 310;
Autologous Serum Skin Test (ASST) 310; Serum Complement 310; Cold Agglutinins and
Cryoproteins 311; ANA 311; Skin Biopsy 311
46. Vaginal Bleeding—Abnormal ................................................................................................ 315
Common 316; Occasional 316; Rare 316; Pregnancy Test 316; CBC 316; Coagulation
Profile 317; Blood Sugar 317; Pap Smear 317; Cervical Culture 317; Thyroid Function
Test 317; Pelvic US 317; Transvaginal Ultrasound (TVUS) 317; Saline Infusion Sonography (SIS):
Conventional and 3D-SIS 317; Hysteroscopy 318; Coagulation Profile 318; Serum
Progesterone 318; LH, FSH 318; Prolactin (PRL) 318; Serum Testosterone, Free
Testosterone, 17-Hydroxyprogesterone 318; Urinary Gonadotropins 318; Abdominal CT
xviii Diagnosis: A Symptom-based Approach in Internal Medicine
Scan 318; MRI of Pituitary 318; Endometrial Biopsy (EMB) 318; Pelvic Examination 321;
Digital Rectal Examination (DRE) and Proctoscopy 321
47. Vertigo .......................................................................................................................................... 323
Common 324; Occasional 324; Rare 325; CBC 325; ESR 325; Audiometry 325; CT Head 325;
MRI and Angiography 325; Brainstem Evoked Response (BSER) 325; Carotid Doppler
Ultrasound 325; ECG/Holter Monitor 325; EEG 325; X-ray Cervical Spine 325
48. Vision Loss—Gradual ............................................................................................................... 330
Common 331; Occasional 331; Rare 331; CBC 331; ESR 331; Blood Glucose/HbA1C 331;
Lipid Profile 331; Coagulation Screen 331; TFTs 331; IOP (Tonometry) 331; Visual Field
(Perimetry) 332; Fluorescein Angiography 332; US of Eye and Orbits 332; CT Scan Skull,
Orbits/MRI Brain 332; Carotid Doppler Scan 332; Echocardiogram 332; Visual evoked
response (VER) 332; Temporal Artery Biopsy 332
49. Vision Loss—Sudden ................................................................................................................ 335
Common 335; Occasional 336; Rare 336
50. Weakness in the Arms and Legs ................................................................................................. 339
Occasional 340; Rare 340; CBC 340; ESR 340; Blood Glucose 340; Biochemistry and
Metabolic Panel 341; Thyroid Function Tests 341; CT Scan Brain 341; X-ray Skull, Cervical
and Lumbosacral Spine 341; CXR 341; Blood Culture 341; Creatine Kinase (total)—(CK) 341;
Serum Acetylcholine Receptor Antibody Titer 341; ANA 341; Tensilon (Edrophonium Chloride)
Test 341; Urine 341; CT—Thorax 341; MRI—Cervical and Lumbosacral Spine 341; Magnetic
Resonance Angiography (MRA) 342; US (Duplex Scanning) of Carotid and Vertebral Arteries
in the Neck 342; CSF Analysis 342; Nerve Conduction Study (NCS) 342; Electromyography
(EMG) 342; Muscle Biopsy 342
51. Weight Loss ................................................................................................................................. 346
Common 347; Occasional 347; Rare 347; CBC 347; ESR 347; Urinalysis 347; Blood
Glucose 347; HIV 347; Urea, Creatinine, Electrolytes 347; Tuberculin or PPD Test 347;
LFTs 348; TFTs 348; Serum Calcium 348; CXR 348; Stool 348; US Abdomen / Pelvis 348;
Endoscopy 348; CT / MRI abdomen 348; Fecal Fat 348; Antigliadin Antibodies 348; Other
Screening Procedures 348
1 Abdominal Distension
• Pregnancy Urinalysis
• Distended bladder
• Ascites • Albuminuria in renal disorders
• Intra-abdominal lump (organomegaly, • Urobilinogenuria may be present in hepatic
tumor, cyst, neoplasm). disorders, absent in complete biliary obs-
truction
OCCASIONAL • In women, hCG to rule out pregnancy.
motility and visceral hypersensitivity) that are systemic lupus erythematosus and enlarged
associated with symptom generation, the ovaries.
findings are not specific for diagnosis, and the
clinician has limited ability to evaluate them in Proctalgia Fugax
practice. In the absence of any objective marker,
Proctalgia fugax is a diagnosis of exclusion, and
the identification and classification of FGIDs are
defined as sudden, severe pain in the anorectal
based on symptoms, and consist of a wide
region lasting several seconds or minutes, and
spectrum of syndromes which cross over and in
then disappearing completely. It is common but
some cases overlap various anatomic areas of
largely underreported. The etiology is not well-
the luminal gut. Although IBS has traditionally
defined. Attacks are infrequent, left-sided, and
been the most studied and written about, FGIDs
short-lived. Patients are asymptomatic between
constitute a number of unique disorders,
episodes. The discomfort is usually triggered by
including functional esophageal disorders
stressful event; can occur during the day or
(noncardiac chest pain, functional dysphagia,
night; although it is not typically associated
and globus sensation); functional dyspepsia
with bowel movements, it may be relieved by
(pain, discomfort, nausea, and other symptoms
heat, anal dilatation, or relaxation techniques.
above the navel in persons who do not meet the
diagnostic criteria for IBS); functional abdominal
Rumination Syndrome
pain syndrome; functional abdominal bloating;
functional diarrhea; functional disorders of the Rumination means repeated regurgitation
biliary tract, including Oddi sphincter; functional (backflow of food from the stomach into the
disorders of the anorectal area, such as pelvic mouth) and rechewing of food, i.e. voluntary or
floor dyssynergia; and proctalgia fugax. The involuntary regurgitation and rechewing
diagnosis of FGIDs relies heavily on the clinical of partially digested food that is either re
history, a limited diagnostic evaluation and early swallowed or expelled. This regurgitation
symptomatic treatment that include symptom appears effortless, may be preceded by a
monitoring and reassessment. There is increasing belching sensation, and typically does not
evidence that psychopharmacologic and psycho- involve retching or nausea. In rumination, the
therapeutic management of FGIDs are highly regurgitant does not taste sour or bitter. The
effective and, in many instances, surpass the behavior must exist for at least 1 month, with
efficacy of standard medical treatment. evidence of normal functioning prior to onset.
Rumination occurs within a few minutes
Meigs Syndrome postprandial and may last 1-2 hours. Though
Meigs syndrome is defined as the triad of benign frequency may vary, rumination typically
ovarian tumor with ascites and pleural effusion occurs daily and may persist for many months
that resolves after resection of the tumor. The or years. Although the etiology of rumination is
ovarian tumor in Meigs syndrome is a fibroma. unknown, multiple theories have been advan-
Pseudo-Meigs syndrome consists of pleural ced to explain the disorder. These theories range
effusion, ascites, and benign tumors of the from psychosocial factors to organic origins.
ovary other than fibromas. Pseudo-pseudo Cultural, socioeconomic, organic, and psycho-
Meigs syndrome includes patients with dynamic factors have been implicated.
6
2 Abdominal Pain
movement of the diaphragm and subsequent Table 2.1: Embryogenic location of abdominal pain
aggravation of the peritoneum. When visceral Origin Organs Spinal Pain
pain is replaced by parietal pain, it is typically levels locations
an indication that the condition has progressed, Foregut Distal esophagus, T5-T6 to Between
stomach, proximal (first T8-T9 xiphoid
and is potentially worsening, e.g. the pain of
two parts) duodenum, and
acute appendicitis—felt initially around the liver, biliary tree, umbilicus, i.e.
umbilicus as visceral pain, and then becomes pancreas epigastrium
localized to the right iliac fossa as parietal or Midgut Duodenum (3rd T8-T11 to Periumb-
somatic pain when the peritoneum becomes and 4th parts) L1 -ilical
Small intestine,
involved. appendix, ascending
Referred pain is a type of visceral or organ pain colon, proximal 2/3
that is felt away from the actual affected organ of transverse colon
site, even though the patient is complaining of Hindgut Distal 1/3 of transverse T11- L1 Between
colon, descending umbilicus
discomfort or pain in that particular area.
colon, rectosigmoid and pubis,
Because of fewer nerve endings in the organs, the Reproductive organs i.e. supra-
brain may misinterpret (i.e. cortical misper- (ovaries, fallopian pubic
tubes, uterus, seminal
ception of either visceral or parietal afferent vesicles, prostate),
stimuli; viscerosomatic convergence) where the bladder
pain is coming from. For example, cholecystitis
pain is commonly referred to the right shoulder Table 2.2: Extraintestinal and extra-abdominal
area; renal pain is commonly felt in the testis on causes of acute abdominal pain: what not to miss
the same side; and appendicitis may also Diagnosis Investigations/remarks
manifest by pain in the right testis.
Cardiac: Acute MI; Usually elderly patient;
Patterns of referred pain are also based on especially inferior wall cardiac risk factors present;
embryologic sharing of dermatomes. (Table 2.1). obtain ECG/cardiac enzymes
A pair of sites may share development from the Vascular: Ruptured Request abdominal US;
abdominal aneurysm HRCT/MRI
same embryologic tissue, and may share
Mesenteric infarction Abdominal duplex US; MR
innervation to some extent. Therefore, pain at mesenteric angiography
one site may be referred to the other site, even Pulmonary: Pulmonary Subdiaphragmatic referred
though the pathologic site is not painful initially. embolism; lower pain; CXR; HRCT
pneumonia
For example, epigastric pain may be the initial
Metabolic: Diabetic Blood glucose; ketones;
symptom of appendicitis; acute cholecystitis ketoacidosis; electrolytes; ABG
may cause shoulder pain; acute inferior wall Hypercalcemia (hyperth- ‘Stones, bones, abdominal
myocardial infarction may cause abdominal yroidism or malignancy) moans, and psychic groans’;
serum calcium; PTH
pain. Just as abdominal conditions may cause
Hematological: Porphyr- Typical urine
referred pain outside of the abdominal cavity, ia-acute intermittent discoloration; urine
the same is true for some extraintestinal and Sickle-cell disease porphobilinogen
abdominal conditions (Table 2.2). Hemolytic anemia; sickled
erythrocytes; hemoglobin
Although each type of pain is thought to have electrophoresis
a different neuropathophysiology, the categories Gynecological: Ectopic Missed if pregnancy is not
are not entirely discrete because of variability in pregnancy-ruptured confirmed in women of
child-bearing age
innervation between patients, and due to the
complex dual visceral and parietal sensory Contd...
Abdominal Pain 9
indicated (time consuming and excess obstruction, perforation; acute biliary disease,
radiation exposure). However, where CT ectopic pregnancy, etc. particularly if there is
scan facility is lacking, a barium enema will preoperative diagnostic uncertainty. Biopsy
confirm the diagnosis of volvulus of sigmoid of the pathological organ may be performed.
colon (‘beaked’ appearance). IVP may be
needed occasionally when it is difficult to CLINICAL NOTES
differentiate right sided ureteric colic and
acute appendicitis. In such cases a single film • Perhaps in no other situation is the history
IVP is found to be useful. In ureteric colic and physical examination more important
there may not be secretion of dye on the in arriving at a rapid diagnosis than in the
affected side, or there may be hold up in the acute abdomen.$ Decisions have to be made
line of ureter. Intravenous cholangiography quickly with minimum investigations.
is now replaced by US and HIDA scans in Therapeutic efforts have to be instituted often
the diagnosis of jaundiced patients and those within minutes. A structured date sheet** is
suspected with cholangitis. now widely used in many health services as
aide-memoire to minimize diagnostic errors
FNAC and Biopsy
• Special points to note in the general examination
• Histopathological or exfoliative cytology of in a patient with an acute abdomen include:
superficial lesion, e.g. in patients suspected general appearance (well looking, or ill, thin,
with lymph node tuberculosis, or metastasis; emaciated); alertness or state of consciousness;
or ultrasound/CT guided biopsies of abdo- hydration; temperature-pulse-respiration; and
minal organs; or endoscopically obtained blood pressure. Life-threatening causes (Table
specimen in inflammatory or malignant 2.5) should always be ruled out before focussing
disease, e.g. abdominal TB, hepatocellular on less serious diagnosis. Periodic examination
carcinoma, metastatic liver disease, adeno- and critical assessment of the changes in the
carcinomas, lymphomas, and neoplastic condition of the patient, including vital signs
lesions of retroperitoneal organs like kidneys and appearance are clues to risk stratification
and adrenals.
and appropriate diagnosis
• A careful examination of hernial sites,
Paracentesis
scrotum, pelvis, and rectal examination is
• In patients with SBP, TB peritonitis, chylous mandatory in every patient with abdominal
ascites, and for peritoneal cytology. pain—especially in acute cases to rule out
intestinal obstruction.
Laparoscopy
• A less invasive procedure for the diagnosis $
Dr Zachary Cope in the classical text Cope’s Early Diagnosis
of extraluminal, intra-abdominal solid of the acute Abdomen, reminds us that, “the general rule can
lesions which cannot be visualized by be laid down that the majority of severe abdominal pains
endoscopic procedures. that ensue in patients who have been previously fairly
well, and that last for as long as six hours, are caused by
conditions of surgical import”.
Surgical Exploration **For a typical example refer to—Michael M Henry et al.
Clinical Surgery, 2nd International edn.; Publisher: WB
• May be required in a few complicated or Saunders Company; Chapter 22—Acute Abdominal
undiagnosed cases, e.g. intestinal adhesions, Conditions—p. 367.
14 Diagnosis: A Symptom-based Approach in Internal Medicine
Table 2.5: Physical findings in various acute • In a woman with abdominal pain a detailed
abdominal conditions gynecological history, including the timing of
Condition Helpful symptoms and signs LMP, pregnancy history, and vaginal discharge
Hemorrhage Increasing restlessness; air- or dysmenorrhea should be obtained
(Internal) hunger; pallor; shock; • Pregnant women with abdominal pain, in
increasing distension; pulsatile
(aneurysm) or tender (ectopic
addition to all other causes of abdominal
pregnancy) mass; rectal pain, may present with atypical locations of
bleeding (occasionally) abdominal conditions. 8,9 Also, prior to
Obstruction Patient anxious, restless; examination of the abdomen, the patient
(Intestinal) vomiting (in high obstruction);
constipation (in low
should empty the bladder
obstruction); Distension; • History of collapse or fainting in a patient
hyperperistalsis (early); visible with abdominal pain is suggestive of an acute
peristalsis (late); ‘silent vascular catastrophe such as internal
abdomen’ (late); diffuse pain
without rebound
hemorrhage, ruptured ectopic pregnancy,
tenderness acute pancreatitis, torsion, strangulation, or
Torsion (sigmoid Sudden, severe pain; rapid mesenteric vascular thrombosis or embolism
colon/ovary) distension; palpable
• Past history of abdominal surgery makes
sigmoid colon (like a pneumatic
tyre) in left lower abdomen; or intestinal obstruction from adhesions more likely
in a female palpable, freely • In elderly patients with history of CAD or
mobile, cystic swelling in the presence of cardiac risk factors with abdominal
lower abdomen
pain, especially upper abdominal pain of acute
Vascular (ischemia) Patient elderly; atherosclerosis
or valvular heart disease; post- onset, obtain an ECG to rule out MI
prandial acute pain but little • In elderly patients with abdominal pain
tenderness; not distended (till associated with skin xanthomas and
late); rectal bleeding
(occasionally) generalized atherosclerosis, the possibility of
Inflammation (mass Fever; Tender MI, AAA, and mesenteric ischemia must be
or abscess) mass (abdominal, Rectal, or excluded by obtaining ECG, US, or CT scan
pelvic); special signs (Murphy’s
psoss, Obturator)
• Drug history should include prescription and
Peritonitis Patient motionless; fever; illicit drug use as well as alcohol. NSAIDs,
tachycardia; cough and steroids and immunosuppressants facilitate
rebound tenderness; board-like
perforation or peritonitis. Anticoagulants
rigidity (late); absent bowel
sounds enhance bleeding and hematoma formation.
Perforation (viscus) Patient pale, anxious, lies still in Alcohol predisposes to pancreatitis. Purgatives
bed; vomiting; rising pulse; may ease perforation in a case of acute
hypotension; tenderness,
rigidity (early); increasing appendicitis. Sulpha, steroids, barbiturates,
distension; diffuse tenderness estrogen, beta-blockers are known to
(late); loss of liver dullness; precipitate porphyria. Megadoses of vitamin A
absent bowel sounds
and D, diuretics, lithium, oral calcium intake
Note: mnemonic “HOT—VIP (double) P” lead to hypercalcemia which may present with
acute abdominal pain
• Biliary diseases such as cholecystitis, • There are specific signs associated with
cholelithiasis occur commonly in a fatty, certain specific diagnosis (Table 2.6); these
flatulent, fertile, and female of forty should be elicited where applicable.
15
• Typically lasting minutes to a few hours, but Myofascial pain syndrome (MPS)— Myofascial
may extend as long as 24-48 hours pain is a chronic, painful condition that affects
• Usually sharp, cramping, distinctive pain. the fascia, i.e. the connective tissue that covers
• Severe (rare) the muscles-either a single muscle or a muscle
• May switch sides from month to month or group. Myofascial pain symptoms usually
from one episode to another involve muscle pain with specific “trigger” or
• Begins midway through the menstrual cycle. “tender” points. Trigger points can be identified
by pain that results when pressure is applied
Signs and tests: A pelvic examination shows no
to an area of the patient’s body. The pain can be
abnormalities. Other diagnostic procedures
(such as an US abdomen) may be performed to made worse with activity or stress. In addition
to the local or regional pain associated with MPS,
rule out other causes of ovarian pain if ovulatory
people with this disorder also can suffer from
pain is prolonged.
depression, fatigue, and behavioral distur-
Munchausen syndrome (pronunciation: Mun- bances. No specific lab tests confirm the
chau-zen) was named after the Baron Karl diagnosis of MPS, but lab tests can be helpful in
Friedrich Hieronymus Freiherr von Munchau- looking for predisposing conditions, such as
sen, who was a German cavalry officer and hypothyroidism, hypoglycemia, and vitamin
known as a tremendous liar. Patients with deficiencies. Chronic infections and sleep
Munchausen syndrome go from physician to deprivation have been cited as causative factors,
physician dramatically presenting very as have radiculopathy, visceral diseases, and
plausible symptoms and histories and receiving depression. The pathogenesis likely has a central
care, up to and including surgery. They fake mechanism with peripheral clinical mani-
physical signs of illness and abnormal festations.
laboratory findings. The person may:
• Claim that he or she has symptoms, when REFERENCES
none exist.
1. Dietrich CF, et al. Acute abdomen, gastroentero-
• Produce false test results, such as by sticking logists view. Praxis (Bern 1994), 2007; 96(16):645-
a thermometer in hot water to mimic a fever 59. [PMID: 17474291: Abstract].
2. Heikkinen M, et al. GPs’ ability to diagnose
or by putting bacteria or something else in
dyspepsia based only on physical examination
laboratory test samples. a n d p a t i e n t h i s t o r y. S c a n d J P r i m H e a l t h
• Self-inflict injuries, such as cutting the skin. C a r e 2 0 0 0;1 8 ( 2 ) : 9 9 - 1 0 4 . [ P M I D : 1 0 9 4 4 0 6 4 :
Abstract].
• Create symptoms, such as causing vomiting 3. Kalish GM, et al. Computed tomographic and
by taking medication. magnetic resonance features of gynecologic
• Say that symptoms are worse than they abnormalities in women presenting with acute or
chronic abdominal pain. Ultrasound Q. 2007;
really are, such as claiming to have severe 23(3):167-75. [PMID: 17805165: Abstract].
pain or bleeding when a milder condition is 4. Patel MD, et al. Reimaging the female pelvis with
actually present. ultrasound after CT: General principles.
Ultrasound Q. 2007;23(3):177-87. [PMID:
• Request surgical procedures. 17805166: Abstract].
Approximately 50% of those with Munchau- 5. Pfister SA, et al. Unenhanced helical computed
sen syndrome are subject to drug abuse, and tomography vs intravenous urography in patients
with acute flank pain: Accuracy and economic
many have borderline personality disorder. The impact in a randomized prospective trial. Eur
disorder generally starts during early adult- Radiol 2003;13(11):2513-20. Epub 2003 Jul 24.
hood, but may begin during childhood. [PMID: 12898174: Abstract].
Abdominal Pain 17
6. Yen HP, et al. Ultrasonography is superior to 8. Cappell MS, et al. Abdominal pain during pregnancy.
plain radiography in the diagnosis of Gastroenterol Clin North Am 2003;32(1):1-58.
pneumoperito-neum. British J of Sur 2002;89(3) [PMID: 12635413: Abstract].
:351-4. [Abstract].
9. Gray J, et al. Abdominal pain, abdominal pain in
7. Okkes Ibrahim Karahan, et al. New method for
the detection of intraperitoneal free air by sono- women, complications of pregnancy and labour.
graphy: Scissors maneuver. J of Clinical Ultra- Emerg Med J 2004;21(5):606-13. [PMID: 15333547:
sound 2004;32(8):381-5. [Abstract]. Free full text].
CHAPTER
3 Amenorrhea
and a few need detail investigations, especially • Systemic disorders (autoimmune disease,
if fertility is desired but impaired. adrenal tumor)
• Radiation, chemotherapy.
DIFFERENTIAL DIAGNOSIS
B—Secondary Amenorrhea (Table 3.1)
The causes for amenorrhea are grouped into Common
primary and secondary, but these are shared
• Physiological (pregnancy, lactation, menopause)
between the two categories
• Functional hypothalamic amenorrhea (due to
A—Primary Amenorrhea emotional, physical, social stress; depression)
Common • Drug-induced hyperprolactinemia (Table 3.2)
• Post-pill amenorrhea
• Constitutional (i.e. physiological: delayed
• Infection (mumps, tuberculosis of the genital
menarche and puberty)
tract)
• Severe psychogenic stress, depression
• Rapid weight loss (10-15%) or extreme obesity
• Chronic illness
• Anorexia nervosa, bulimia
• Weight loss / lean body weight2,3
• Surgery (hysterectomy)
• Anorexia nervosa
• Endometrial ablation
• Heavy exercise.
• Progestogen IUD
Occasional • Polycystic ovarian syndrome (PCOS)
• Imperforate hymen# • Female athlete triad (vide infra ↓↓).
• Vaginal septum
• Primary hypothyroidism, hyperthyroi-dism Occasional
• Diabetes mellitus (Type 1) • Premature ovarian failure (POF)
• Systemic disease (endometrial TB, malnutrition) • Prolactin secreting adenoma
• Drugs (hormones, antiemetics, antihy- • Primary hypothyroidism
pertensives, antipsychotics). • Surgery, chemotherapy, radiotherapy.
Rare
Rare
• Pregnancy before menarche4
• Disorders of cerebral cortex (trauma, tumor) • Disorders of pituitary (Sheehan’s syndrome)
• Disorders of hypothalamus (Kallmann’s • Disorders of ovary (virilizing ovarian
syndrome) tumors, resistant ovarian syndrome)
• Disorders of anterior pituitary (prolacti- • Disorders of genital outflow tract (Asherman’s
noma, Cushing’s disease, Fröhlich syndrome, syndrome, Rokitansky-Küster-Hauser
Laurence-Moon-Biedl syndrome, empty syndrome)
sella syndrome) • Systemic disorders (autoimmune disease,
• Disorders of ovary (Turner ’s syndrome, adrenal tumors).
polycystic ovarian syndrome, i.e. PCOS)
• Müllerian dysgenesis (uterovaginal agenesis) INVESTIGATIONS—GENERAL
• Chromosomal abnormalities (intersex, Turner’s
Pregnancy Test
syndrome, testicular feminizing syndrome)
• All patients require an initial pregnancy test
#Causes ‘false’ or ‘cryptomenorrhea’ — menstruation is
taking place but the patient is unaware of it as the outflow
(serum or urine hCG). Any woman with
is obstructed. amenorrhea is considered pregnant until proven
20
Physiological • Hormones
• Pregnancy • Glucocorticoid excess
• Breastfeeding • Opiates, cocaine
• Breast stimulation Altered Metabolism
• Sexual intercourse • Liver failure
• Exercise • Renal failure
• Stress (e.g. venesection, trauma, surgery, myocardial • Seizures
infarction) Ectopic production
Pathological (serum prolactin ≥ 100 ng/ml) • Bronchogenic (e.g. carcinoma)
• Pituitary disease (e.g. Prolactinoma, nonsecreting • Gonadoblastoma
adenoma, meningioma, metastasis) • Hypopharynx
• Hypothalamic and pituitary stalk disease (e.g. TB, • Ovarian dermoid cyst
sarcoidosis, craniopharyngioma, empty sella, meta- • Renal cell carcinoma
stasis, cranial irradiation) • Teratoma
Medications Others
• Oral contraceptive pills • Hypothyroidism
• Antipsychotics • PCOS
• Antidepressants • Addison’s disease
• Antihypertensives
• Antiemetics #Normal serum prolactin reference range – ≤25 ng/
• Histamine H2 receptor blockers ml; Hyperprolactinemia = serum prolactin ≥40 ng /ml
Contd... (40 mcg/l)
21
• Medications (Table 3.2) may induce hyper Table 3.3: Tanner staging for female secondary
prolactinemia. Post-pill amenorrhea may sexual characteristics
persist for several months Stages of breast (B) Stages of pubic hair (PH)
• Vigorous exercise—A history of excessive development development
activity level suggests the female athlete triad • B1 preadolescent, • PH 1 preadolescent, no
(i.e. amenorrhea, eating disorder, and elevated papilla, small pubic hair, fine vellus hair
osteoporosis: vide infra ↓↓) flat areola covers genital area
• Social history includes—Dietary habits, • B2 (age 11, range 8-13) • PH 2 (age 11) sparse
breast bud, papilla and distribution of long slightly
‘crash’ dieting, nutritional status, weight areola elevate, increased pigmented straight hair
loss, emotional and physical stress, and areolar diameter bilaterally along medial
sexual activity border of labia majora
• Family history includes—Family pattern of • B3 (age 12) continued • PH3 (age 12) pubic hair
sexual development (menarche of mother enlargement of breast increases in pigmentation,
bud, no separation of begins to curl and spread
and sisters), genetic anomalies, and endo- breast contours sparsely over mons pubis
crinopathies (diabetes, thyroid dysfunction) • B4 (age 13) areola and • PH4 (age 13) pubic hair
• Past history includes—Trauma, surgery papilla separate from continues to curl and
(hysterectomy), endometrial curettage, contour of breast to form becomes coarse, increase
infection (TB), chemotherapy, and irradiation secondary mound in number
• B5 (age 15, 13-18) • PH 5 (age 14) mature,
• Physical examination—This is guided by mature, areolar mound pubic hair attains triangular
history and should address the following: recedes into general pattern, spread to surface of
Psychologic status (stress, depression) contour of breast, papilla medial thigh
BMI,§§ nutritional status, height (short continues to project
stature in Turner’s syndrome)
Secondary sexual characteristics (Tanner • Pelvic examination—Physical findings may
staging: Table 3.3) be grouped as below:
• The type and stage of development of secon- In primary amenorrhea:
dary sexual characteristics such as breast — External genitalia (male or female)
and areola development, axillary and pubic — Clitoromegaly***
— Imperforate hymen
hair growth, provide most important guide
— Absent or blind ending vagina
to diagnostic work-up in patients with
— Uterus and cervix (present or
primary amenorrhea
absent)
• Associated symptoms and signs as clues to
In secondary amenorrhea:
the diagnosis include:
— Clitoromegaly
Signs of hirsutism (acne, excessive facial
— Atrophy of vulva and vaginal skin
and body hair), virilization (voice change,
— Uterine size
temporal baldness) are suggestive of
— Ovarian tumor
PCOS and ovarian or adrenal tumor.
• Systemic examination—For evidence of Tur-
Expressive galactorrhea suggests hyper- ner ’s syndrome, hypo- and hyperthyroi-
prolactinemia. dism, Cushing’s disease, panhypopitui-
Anosmia with hypogonadism suggests tarism, chronic hepatic or renal disease.
Kallmann’s syndrome. Evidence of autoimmune disorder (RA, SLE,
Visual field defects on confrontation and myasthenia gravis) is suggestive of
indicate pituitary adenoma. autoimmune ovarian failure
Features of Turner’s syndrome may be present. • Primary amenorrhea with normal secon-
dary sexual characteristics is commonly due
§§
Menstruation fails to occur regularly if BMI falls below
***
18-19 kg/m2 and it is estimated that 22% of female body Clitorimegaly defined as a length times width product
weight should be fat to ensure ovulatory cycle. of greater than 40 mm2.
24
to anatomical defects and rarely due to secondary amenorrhea and shortened luteal
androgen insensitivity syndrome, i.e. patient phases is much higher among women partaking
phenotypically female but genetically male in athletics, specifically in sports requiring low
with undescended testes. A karyotype body weight for per-formance and aesthetics. The
analysis is needed to determine proper hormone pattern seen in these amenorrheic
treatment. If testes are present, they should athletes includes a decrease in GnRH pulses from
be removed because of the high risk of the hypo-thalamus, which results in decreased
malignant transformation after puberty pulsatile secretion of LH and FSH and shuts down
• Primary amenorrhea with hypoplastic stimulation of the ovary. The recently dis-covered
secondary sexual characteristics is com-monly hormone leptin may also play a large role as a
due to HPO axis disorders; Turner’s syndrome significant mediator of reproductive function. The
is the commonest type of dysgenetic gonad. prevalence of eating disorders is high among female
athletes who practice sports which emphasize
RED FLAGS leanness. Consequently, the cause of menstrual
• Although primary pregnancy before men- irregularities is not due to the exercise alone, but
arche is extremely rare, it’s not impossible. to chronic inadequate or restrictive caloric intake
“Although the first few menstrual cycles that does not com-pensate for the energy
after menarche are often anovulatory, this expenditure. The most dangerous risk associated
is not always the case. Because it is no longer with amenorrhea for the female athlete is the
uncommon for girls to be sexually active in impact on the skeleton. Complications associated
their early to mid teens, a sensitive dis- with amenorrhea include compromised bone
cussion of this subject and a pregnancy test density, failure to attain peak bone mass in
are necessary in the initial investigation of adolescence and increased risk of stress fractures.
amenorrhea in women of almost any age”5 The diagnosis of exercise-associated menstrual
• Although ‘constitutional delay of menarche dysfunctions is one of exclusion. The most effective
and puberty’ is a common cause for primary treatment is to decrease the intensity of the
amenorrhea, it should not be assumed to exercise and increase the nutritional intake.
account for amenorrhea; periodic follow up Hormone replacement has also been under
to evaluate other pathological causes for investigation as a possible treatment”.6
delayed puberty (e.g. growth velocity for
skeletal age) is indicated REFERENCES
• In patients with secondary amenorrhea, 1. Tierney Lawrence M Jr, et al. Current Med Diag
physical and pelvic examinations must rule out and Treat 2006; 45th ed. 1184.
pregnancy before diagnostic testing begins 2. Kaplowitz PB. Link between body fat and the
• Oral contraceptives do not cause amenorrhea timing of puberty. Pediatrics 2008; 121 Suppl
3:S208-17. [PMID: 18245513: Abstract].
after discontinuation. Amenorrhea occurring 3. Baker ER. Body weight and the initiation of
after discontinuation of oral contraceptive puberty. Clin Obstet gynecol 1985;28(3): 573-9.
therefore needs the same investigations as [PMID: 4053451: Abstract].
amenorrhea temporarily unrelated to 4. Child Marriage: Girls 14 and Younger At Risk.
previous use of an oral contraceptive. Web site - http://www.iwhc.org/resources/
youngadolescents/childmarriage.cfm. Accessed
on 11-09-08.
SELECTIVE GLOSSARY 5. Bryan M, et al. Evaluation and Management of
Amenorrhea, Mayo Clin Proc 1997;72:1161-9.
Female athlete triad—Includes “amenorrhea, 6. Warren MP, et al. Exercise-induced endocrine
osteoporosis and eating disorders. The inci-dence pathologies. J Endocrinol Invest 2003 Sep;
of menstrual irregularities including primary and 26(9):873-8. [PMID: 14964440: Abstract].
CHAPTER
4 Anxiety
Table 4.1: Clinical features of anxiety: Table 4.2: Anxiety and anxiety-like state
emotional/psychological symptoms A-Medical conditions which can mimic or cause anxiety
• Apprehension/fearful • Behavioral problems • Hypertyroidism • Adrenal disorders
anticipation (especially in children and • Hypoglycemia • Temporal lobe epilepsy
adolescents) • Hyperventilation • Cardiac—acute coronary
• Irritability • Nervousness and jumpiness syndrome syndrome, MVP
• Impaired concentration/ • Exaggerated startle • Asthma • Psychiatric illnesses—
‘mind going blank’/ response • Sleep disorders depression
impatience • Trauma
• Feeling restless/on • Fear that you are dying/
B-Medications and substances which can induce anxiety
edge ‘going crazy’
• Stimulant drugs • Bronchodilators and
• Confusion
(Caffeine and respiratory inhalers
• Insomnia
other stimulants)
• Abuse drugs (heroin, • Herbal remedies (ephedra)
can be challenging because patients present with cocaine, amphetamine)
distress and concern about disease in the absence • Over-the-counter • Hypertensive medication
medications (decon- • Withdrawal from alcohol
of objective evidence. However, “...central to the gestants) • ADHD medications
whole issue of diagnosing anxiety disorders, it is • Steroids (amphetamine)
• Hormones (oral • Withdrawal from
usually not the illness that is masked but the
contraceptives, benzodiazepines
doctor who is blind. By confining enquiries to thyroid medication) (Diazepam)
physical systems, the correct questions are not
asked, and consequently the correct diagnosis is • Substance abuse (alcohol, benzodiazepines,
missed...”. 2 Also, anxiety and anxiety-like caffeine)
symptoms may be consequent to a variety of • Menopause.
medical aliments and their treatment (Table
Occasional
4.2).3 Therefore, a comprehensive, emphatic
understanding, and time to listen to the patient • Medications (bronchodilators, antipsycho-
permits a reasoned and often a therapeutically tics, amphetamine, insulin)
effective approach to the difficult problem. • Drug withdrawal (anxiolytics, sedatives,
hypnotics)
DIFFERENTIAL DIAGNOSIS • Chronic systemic disease (diabetes mellitus,
Common cardiac arrhythmia, hyperthyroidism,
rheumatoid arthritis, hepatitis B and C, post-
• Acute stress reaction (death; accident;
herpetic neuralgia)
traumatic diagnosis: HIV, ESRD, end-stage
• Psychiatric disorders (panic, phobia, obs-
COPD; cancer; assault; rape)
essive compulsive disorder, post traumatic
• Adjustment reaction with anxiety (inter-
stress disorder, hysteria, psychosis, demen-
personal conflict)
tia).
• Psychiatric disorder (generalized or chronic
anxiety state, depression, hyperventilation
Rare
syndrome)
• Acute systemic illness (acute coronary • Systemic disorders (mitral valve prolapse,
syndrome, bronchial asthma, stroke, pheochromocytoma, Cushing’s disease)
seizure, migraine) • Secreting tumors (carcinoid, insulinoma)
Anxiety 27
Table 4.3: Pathological anxiety: signs and symptoms critical to diagnose depressive disorders
Motor tension Autonomic overactivity because they are common, treatable, carry a
high risk of morbidity and mortality, and
Muscle tension or ache Dry mouth
Tension headaches Palpitation/tachycardia frequently coexist with anxiety. In addition
Tremors, twitches, Sweating/cold clammy skin DSM IV criteria may be used to determine
and jitters
Tiredness/fatigue Flushes/chills
specific psychiatric disorder.
‘Lump in throat’/difficult
swallowing RED FLAGS
Diarrhea/abdominal distress
Frequent urination Anxiety and depression frequently occur together,
Difficulty breathing/suffocating
Dizziness/light headedness which can complicate the clinical picture,
including suicidal attempts or self-medication
with alcohol or other illicit drugs.4-7
anxiety is dysfunctional, i.e. whether it is Cardiac arrhythmias, endocrinopathies
excessive and sustained and interferes with (insulinoma), and medication reactions consti-
daily living. History also helps to ascertain if tute significant number of undiagnosed psy-
medications, substance abuse, a medical chiatric referrals for ‘anxiety’.
illness, or associated psychiatric disorder is
aggravating patient’s anxiety. Historical data REFERENCES
from family members may indicate the cause
1. Hamilton M. Fish’s Clinical Psychopathology—
of acute anxiety
Signs and Symptoms in Psychiatry; 2nd ed.
• History of intermittent anxiety—Suggests (Indian), p. 72.
cardiac arrhythmia such as PSVT or AF, 2. Hodgkiss A. Anxiety; French’s Index of Diff. Diag.
psychomotor epilepsy, insulinoma, and 14th ed. P. 38.
pheochromocytoma 3. Härter MC, et al. Associations between anxiety
disorders and physical illness. Eur Arch
• Age—The young and the middle-aged patient
Psychiatry Clin Neurosci 2003; 253(6):313-20.
is more likely to suffer from a psychiatric [PMID: 14714121: Abstract].
disorder, while older patient may be suffering 4. Katon W, et al. The association of depression and
from vascular or some other form of dementia anxiety with medical symptom burden in patients
• Physical examination—Patient with anxiety with chronic medical illness. Gen Hosp
Psychiatry 2007; 29(2):147-55. [PMID: 17336664:
is restless, agitated; vital signs reveal tachy-
Abstract].
cardia and increased blood pressure and 5. Sareen J, et al. Anxiety disorders and risk for sui-
respiration; neurologic examination usually cidal ideation and suicide attempts: A population-
shows brisk tendon reflexes and tremors. based longitudinal study of adults.Arch Gen
Sustained tachycardia with weight loss makes Psychiatry 2005; 62(11):1249-57. [PMID:
16275812: Abstract].
hyperthyroidism a very likely possibility.
6. Hawgood J, et al. Anxiety disorders and suicidal
Presence of a thyroid bruit, auscultatory behaviour: An update. Curr Opin Psychiatry 2008;
systolic click indicates hyperthyroidism and 21(1):51-64. Review. [PMID: 18281841: Abstract].
mitral valve prolapse respectively 7. Petry NM, et al. Comorbidity of DSM-IV patho-
• Exclusion of other psychiatric disorders, logical gambling and other psychiatric disorders:
Results from the National Epidemiologic Survey
especially depression—The Mini Mental
on Alcohol and Related Conditions. J Clin Psychia-
State Examination (MMSE) protocol is useful try 2005; 66(5):564-74. [PMID: 15889941:
to screen patients for this purpose. It is Abstract].
CHAPTER
5 Arthralgia and
Arthritis
Table 5.1: Differentiating inflammatory arthritis from Table 5.2: Pattern of joint involvement and
noninflammatory (usually degenerative) arthritis differential diagnosis
Features Inflammatory Noninflammatory • Monoarticular—Acute
arthritis arthritis
– Septic arthritis (gonococcal, nongonococcal,
Synovial WBC >2000/μl <2000/μl or viral)
count
– Gout (due to uric crystal deposition)
-ESR, CRP - Elevated - Usually normal
-Early morning - Prolonged; >1 hr - ‘Gel phenomenon’ – Pseudogout (due to calcium pyrophosphate
stiffness observed, i.e. pain and cry-stal deposition)
stiffness lasting few – Hemarthrosis
minutes after a period of
– Acute presentation of seronegative spondylo-
joint immobility, and
improves with mild to arthropathies, e.g. Reactive arthritis
moderate activity. • Monoarthritis—Subacute or chronic
Nights worse than Yes No – Tuberculosis
days – Postinfective arthropathies (mostly viral)
Constitutional Yes, in certain No – Osteoarthritis
features (e.g. conditions
– Trauma
fever, fatigue,
weight loss) – Rheumatoid arthritis (i.e. palindromic onset)
Spontaneous Common Uncommon – Juvenile chronic arthritis
disease flares – Malignancy
• Polyarticular—Asymmetrical
chikungunya, dengue; bacterial—gonoco- – Seronegative spondyloarthropathies:
ccal, nongonococcal, e.g. staphylococcal, – Ankylosing spondylosis
streptococcal; tubercular) – Reiter’s disease
• Osteoarthritis – Psoriatic arthritis
• Rheumatoid arthritis – Enteropathic arthritis (associated with IBD)
• Polyarticular—Symmetrical
• Trauma.
– Rheumatoid arthritis
Occasional – Osteoarthritis
– Arthritis associated with autoimmune rheumatic
• Infection (Brucellosis; viral: HBV, HCV, HIV; disease:
Lyme disease) – Systemic lupus erythematosus
• Gout, pseudogout – Scleroderma
• Reactive arthritis (i.e. Reiter’s syndrome ^) – Vasculitis
– Sjögren’s syndrome (primary)
• Prosthetic joint arthritis (bacterial,
– Antiphospholipid syndrome
tubercular, fungal) – Dermatomyositis/polymyositis
• Adult onset Still’s disease (Juvenile rheuma- – Polyarticular septic arthritis
toid arthritis). – Poncet’s disease (vide infra ↓↓)
– Polyarticular gout–
Rare – Arthritis associated with malignancy
– Miscellaneous—sarcoidosis, amyloidosis
• Rheumatic fever with arthritis
• Spondyloarthropathies (ankylosing spon-
dylitis, i.e. AS; Reiter’s syndrome; Psoriatic • Collagen disease (SLE, PAN, PMR, sclero-
arthritis, IBD) derma)
^ • Immune-mediated (serum sickness, lepra
Of historical interest is the fact that this diagnosis shares
its name with the man who first described it, Hans Reiter, a reaction)
Nazi physician who tested unapproved vaccines and • Hematologic (hemophilia, sickle cell disease,
performed experimental procedures on victims in leukemia)
concentration camps. The infamous legacy of Reiter’s name
has led to the proposal that the syndrome be referred to by • Malignancy (hypertrophic pulmonary
another, more descriptive name such as Reactive arthritis. osteoarthropathy, i.e. HPOA; metastasis).
31
example, ‘pain in the knee’ as the patient may episode may be a harbinger of a chronic
complain, may actually be due to pain polyarticular disease, and a chronic condi-
because of bursitis over the knee; ‘pain in tion can present as an acute episode. There-
the shoulder ’ may be due to adhesive fore, chronic conditions such as RA, SLE, and
capsulitis as against arthritis in the shoulder gout should be considered, at least initially,
joint. The main features that differentiate in patients who present with acute poly-
arthritis and STR are explained in Table 5.4. articular or monoarticular joint pain
• The most useful information in evaluating • Inflammatory or degenerative etiology—
joint pain comes from history and physical Inflammatory features include the presence
examination. The relevant aspects are age; of all or some of the cardinal signs of
whether the underlying condition is inflammation (i.e. erythema, warmth, pain,
inflammatory or degenerative; type of onset swelling, and morning stiffness), and generally
(i.e. acute or otherwise); subsequent evolution associated with systemic symptoms (e.g. fever,
(i.e. self-limiting, monoarticular, polyarti- fatigue, weight loss). Common examples are
cular symmetrical, or polyarticular non- infections, RA, gout, and reactive arthritis.
symmetrical); and presence of associated or Degenerative (i.e. noninflammatory) features
complicating extra-articular features. include pain without swelling or warmth,
activity-related pain, minimal or absent
Table 5.4: Difference between arthritis and STR
morning stiffness, and absence of systemic
Clinical features Arthritis STR
symptoms. Common examples are OA,
Pain Deep, diffuse, around Superficial and localized
area of affected joint around affected bursa,
fibromyalgia, and neoplasms
tendon, muscle, etc. • Affected joints—Early OA can present in one
Tenderness Circumferential Localized to the site of
around the joint affected structure joint, most commonly the knee. Podagra, or
where capsule is pain in the first metatarsophalangeal joint,
accessible to surface
Effusion Develops with more Usually superficial is the classic presentation of gout, appearing
advanced disease swelling; effusion rare suddenly at night. Gout most commonly
Pain on active Present Absent
range of motion affects joints in the feet, ankles, hands, wrists,
(ROM) elbows, and knees; less commonly affected
Pain on passive Present Absent
ROM areas include the sacroiliac, sternoclavicular,
Instability/ Often present Absent and shoulder joints. Gout rarely affects the
deformity
hip and spine. Symmetrical involvement of
• Age—Infectious causes as well as trauma have metacarpal phalangeal, proximal interpha-
no particular age association. SLE presents langeal joints, wrist, and feet is more
between second and forth decades of life; RA is common in RA; involvement of knees and
more common between fourth and sixth decades; hips is unusual. OA favors knees, ankles, feet,
and OA peaks in the seventh and eighth decades and spinal column, but involvement is not
• Duration—Joint disorders are acute or chro- necessarily symmetrical. Depending upon
nic, i.e. either less or more than six weeks the underlying cause, the pattern of arthritis
respectively. Acute disorders are often may change overtime
traumatic, infectious, metabolic (gout), or • Lifestyle factors—Diet rich in purine foods
reactive; chronic disorders often include (liver, kidney, red meat) and alcoholism can
noninflammatory and immunologic dis- precipitate an attack of gout in susceptible
orders such as OA and RA. However, an acute individuals. High-risk behaviors, intravenous
34 Diagnosis: A Symptom-based Approach in Internal Medicine
drug use, past history of STD are risk factors Table 5.5: Clinical signs associated with
for infectious arthritis, including viral arthritis and systemic disease
Table 5.6: The red-hot joint disease remains a diagnosis of exclusion. Poncet’s
• Infectious disease is postulated to be an immunologic
– Bacterial reactive form of polyarthritis, and associated
– Gonococcal
with an excellent prognosis with rapid resolution
– Mycobacterial
– Virus on commencing antituberculous therapy and no
– Lyme disease sequelae. Therefore, recognition of Poncet’s
• Crystal-induced
– Gout disease can be important.
– Pseudogout (CPPD)
– Hydroxyapatite (acute calcific periarthritis) REFERENCES
• Hemarthrosis (hemophilia)
• Traumatic 1. Toivanen A. Alphaviruses: An emerging cause
• Septic bursitis (i.e. prepatellar bursitis) of arthritis? Curr Opin Rheumatol 2008; 20(4):486-
• Flare of rheumatoid joint (existing RA) 90. [PMID: 18525365: Abstract].
• Psoriatic arthritis 2. McGill PE. Viral infections: Alpha-viral arthro-
• Reactive arthritis pathy. Baillieres Clin Rheumatol 1995;9(1):145-
• Osteomyelitis secondary to septic arthritis 55. [PMID: 7728877: Abstract].
3. Szkudlarek M, et al. Ultrasonography of the meta-
tarsophalangeal joints in rheumatoid arthritis:
SELECTIVE GLOSSARY Comparison with magnetic resonance imaging,
conventional radiography, and clinical exami-
Poncet’s disease—In 1897, Poncet described nation. Arthritis Rheum 2004;50(7):2103-12.
polyarthritis in patients suffering from tuber- [PMID: 15248207: Abstract].
culosis which was not caused by tuberculosis 4. Wright SA, et al. High-resolution ultrasonography
of the first metatarsal phalangeal joint in gout:
infection of the joints. It is characterized by A controlled study. Ann Rheum Dis 2007;
polyarthritis that occurs during acute tuber- 66(7):859-64. Epub 2006;21. [PMID: 17185326:
culosis infection that affects persons with visceral Abstract].
5. Wright S, et al. Hand arthritis in systemic lupus
or disseminated tuberculosis. No mycobacterial
erythematosus: An ultrasound pictorial essay.
involvement can be found or other known cause Lupus 2006; 15(8):501-6. [PMID: 16942002:
of polyarthritis detected. Therefore Poncet’s Abstract].
CHAPTER
6 Back Pain
Table 6.1: Potentially serious conditions that may Table 6.2: Psychosocial barriers to back pain recovery
present as back pain
• Fear, financial problems, anger, or stress
Possible condition Findings from the medical history • Depressed or negative moods, social withdrawal
Fracture • Serious accident or injury • Overprotective family or lack of support
• History of even a minor trauma or strenuous • Problems at work, e.g. heavy work, unsociable
lifting in an older or osteoporotic patient hours, low job satisfaction
• Chronic oral steroid use • Belief that pain and activity are harmful
Tumor or infection • Age >50 years or <20 years • “Sickness behaviors” such as extended rest
• History of cancer • Problems with claim and compensation
• Constitutional symptoms (fever, chills,
unexplained weight loss)
• Bacterial infection – TB, UTI • Trauma/accident
• Intravenous drug use • Infective (TB, i.e. Pott’s disease, epidural
• Immunosuppression (corticosteroid use,
transplant recipient, HIV infection) abscess, brucellosis)
• Pain worse at night or ‘rest pain’
• Failure to improve after 4 to 6 weeks of
• Lumbar spondylosis (degenerative OA)
conservative low back pain therapy • Spinal dysfunction (intervertebral disk
Cauda equina • Saddle anesthesia
syndrome • Recent onset of bladder/bowel dysfunction
prolapse, i.e. IVDP)
• Abnormal gait/severe or progressive • Psychosocial (depression, anxiety, drug
neurologic deficit in lower extremity
Referred pain • Cardiac – Angina, MI seeking behavior)
• Vascular–Pneumothorax, pulmonary • Referred (lower cervical segments, renal
embolism, dissecting aneurysm
calculi, pyelonephritis)
Clinically backache is usually classified into: • Pelvis (in women—dysmenorrhea, pelvic
Acute backache—Usually lasting <4 weeks of inflammatory disease).
duration; mostly due to injury, strain, or
faulty posture; symptoms such as pain, and Occasional
restricted movements often confined to lower • Infective (osteomyelitis)
back, which are aggravated on coughing, • Spinal abnormalities (kyphosis, scoliosis,
straining, or bending. The main task is to secondary to poliomyelitis, Scheuermann’s
watch on events, e.g. any neurological deficit, disease)
and address them as indicated.
• Vertebral collapse (osteoporosis, osteom-
Chronic backache—Lasting >4 to 8 weeks of
alacia)
duration. At this point it is appropriate to
• Referred pain (cardiac—angina, MI; GI—
reassess the patient’s symptoms and physical
findings; perform selective investigations, duodenal ulcer, pancreas)
evaluate psychosocial barriers (Table 6.2), and a • Spondyloarthropathies (ankylosing spon-
surgical referral should be considered. dylitis, Reiter’s syndrome)
Since there is overlapping in the etiopatho- • Malignancies (usually secondaries: from
genesis and management between the UBP, LBP, lungs, breast, prostate, thyroid).
acute, and chronic disorders, their causes are
Rare
considered together for the purpose of practical
clinical approach. • Congenital (spina bifida, spondylolisthesis*)
• Malignancies (primary: myeloma, Hodg-
DIFFERENTIAL DIAGNOSIS kin’s)
• Referred pain (aorta, pulmonary embolism)
Common
• Faulty posture
* Spondylolisthesis, i.e. anteroposterior movement of
• Mechanical pain (muscle/ligamentous strain, one vertebral body upon another body or the sacrum,
sprain) commonly L4 on L5, occasionally L5 on S1.
38 Diagnosis: A Symptom-based Approach in Internal Medicine
or lumbar region which can be demon- Table 6.4: Limitations of X-rays in low back pain***
strated on US of abdomen and pelvis. • The radiation dose of one lumbar spine is equivalent to 150 chest X-
rays and potential of gonadal irradiation.
CT Spine • X-rays will not reveal a slipped disk.
• Even in well-established metastatic disease, the tumor must erode
• CT scanning is considered the imaging more than half of the vertebra before it is visible on plain X-ray.
• There is a high false-positive rate in lumbar spine.
modality of choice to evaluate patients for • Several X-ray findings are of questionable clinical significance
spinal trauma and vertebral fractures. and may be unrelated to back pain. These findings include:
– Disk calcification
– Mild to moderate scoliosis
HRCT Abdomen – Single disk space narrowing
– Spondylolysis
• To confirm abdominal US findings, and /or for – Lumbarization
– Sacralization
evidence of pancreatic, aortic, or pelvic lesions. – Schmorl nodes
– Spina bifida occulta
MRI Spine *** Diagnostic imaging practice guidelines for musculoskeletal
complaints in adults - an evidence-based approach. Part 3: spinal
• MRI is noninvasive, does not involve radia- disorders. Web site:
tion, covers a large area of the spine, and can http://www.guideline.gov/content.aspx?id=13009&search= adult+
low+back+pain#Section405
show changes within the disk and vertebral
body. It has become the imaging modality of
Histocompatibility Antigen Test (HLA-B 27)
choice in the diagnosis of radiculopathy, spinal
cord abscesses, spinal cord tumors, spinal • In suspected spondyloarthropathies, e.g.
stenosis, and nontraumatic vascular lesions. ankylosing spondylitis.
Is there a neurological deficit that may the interscapular region of the thoracic spine.
entail surgical evaluation? A clinical rule is to consider the cause of
Is there a psychosocial distress that is thoracic pain as cardiac until the examination
aggravating or prolonging the pain (see and investigations prove otherwise
below)? • Beware of herpes zoster in the thoracic
• The vast majority of LBP are mechanical, i.e. segments especially in old and immunocom-
muscular and ligamentous strains. They are promised persons
self-limiting and not severe • Beware of spinal canal stenosis, especially
• Diagnostic testing should not be a part of in middle-aged or elderly patient, with
their initial evaluation. However, a patient’s history of neurogenic claudication‡ such as back
failure to improve with conservative pain referred to hips, paresthesias worsened
treatment (within 4–6 weeks) is an by back extension, walking and relieved by
indication for further evaluation sitting, or lying with the trunk flexed (finds
• Absence of history of trauma does not exclude hills easier to climb than to descend)
mechanical causes, IVDP, or vertebral • In chronic cases, exclude significant pathology.
fractures. A seemingly insignificant episode, Focus on counseling; discussing preventive
such as a minor fall, may be a red flag for measures and patient education for self-
fracture in an elderly management of future episodes improves
• Examine the spine after its adequate prognosis. Avoid unnecessary, costly investi-
exposure and in good light. Sometimes an gations
unexpected finding such as midline mole, tuft • Suspect malingering, especially in patients
of hair, dimpling, or hemangioma will spot with legal, or mediclaim issues. False-positive
the diagnosis of spina bifida occulta physical findings such as positive SLR tests
• Palpation is an important component of may be seen, yet the person may not have
examination. Unlike the lumbar spine, the any problem while walking, sitting, or
thoracic vertebrae are superficial and it is climbing. However, when the diagnosis of
relatively easy to locate affected (painful) malingering is doubtful, it is safest to assume
segment a person is not, unless a contradictory sym-
• Sciatica usually involves L4 - L5, L5- S1 nerve ptom or sign is witnessed (Table 6.6)5
roots, either alone or together (Table 6.5) • Although any one episode of back pain may be
• IVDP is very uncommon in the thoracic spine started by a physical problem in the back, its
• Thoracic spine pain is frequently associated prognosis is vastly influenced by psychosocial
with the lower cervical spine lesions factors. The added morbidity of depression and
• The thoracic spine is the commonest site in anxiety with chronic pain is strongly associated
the vertebral column for metastatic deposits with more severe pain, greater disability, and
• Back pain that is unilateral may have a poorer health-related quality of life.6
urologic etiology such as pyelonephritis, or
obstructive nephropathy RED FLAGS
• Only congenital abnormalities which may
cause back pain are spina bifida and spon- • Back pain associated with severe or pro-
dylolisthesis. Sacralization† of L5 is gene- gressive neurological deficit is a medical
rally asymptomatic emergency; suspect IVDP, cord compression,
• The pain of myocardial ischemia, from angina,
‡
or myocardial infarction can be referred to Neurogenic claudication, i.e. presence of neurological
symptoms/deficit in lower extremities while walking with
†
Sacralization—fusion of the sacrum and L5 vertebra. normal peripheral pulses.
Back Pain 41
Table 6.5: Sciatica — Nerve root • Cauda equina syndrome—Back pain with
compression and symptoms bladder or bowel incontinence, saddle area
Level/ Nerve Pain Neurological Sciatica perineal numbness, disturbed gait is an
disk root radiation deficit emergent condition.
location involved
• Beware of patients, especially elderly, with
L3 – L4 L4 Lateral Patellar Uncommon weight loss, pain at rest, or constant pain at
thigh jerk(reflex);
and dorsiflexion
night; significant pathology, especially
inner of foot malignancy, must be ruled out.
aspect (motor) • In elderly men, especially over age 50 with
of leg
L4 – L5 L5 Anterola Extensor of Common back pain, per rectal examination is man-
-teral leg great toe datory; associated PSA estimation may be
and great (motor)
toe indicated to rule out prostate malignancy.
L5 – L6 S1 Posterior Ankle Common • Chronic back pain before the age of 20 years
leg and jerk (reflex);
lateral plantar flexion
is an indication to rule our primary spinal
toes (motor) tumors, e.g. osteosarcoma.
Midline Cauda Bilateral Saddle Uncommon
disk equina leg anesthesia
hernia weakness urinary REFERENCES
-tion retention
1. Mulconrey DS, et al. Interobserver reliability in
Table 6.6: What physical exam techniques are the interpretation of diagnostic lumbar MRI and
useful to detect malingering? nuclear imaging. Spine J 2006;6(2):177-84.
[PMID: 16517390: Abstract].
The Diagnostic and Statistical Manual of Mental 2. National Clearing House. Clinical Practice Guide-
Disorders (DSM-IV) defines malingering as: line. Web site - http://www. guideline. gov/
“The intentional production of false or grossly exaggerated summary/summary.aspx? doc_id=8599 and nbr =
physical or psychological symptoms motivated by external 004786 and string = low + and + back + and + pain.
incentives such as avoiding military duty, avoiding work, Accessed on 03.10.08.
obtaining financial compensation, evading criminal 3. Carragee E, et al. Are first-time episodes of
prosecution, or obtaining drugs.” serious LBP associated with new MRI findings?
Malingering is not considered a mental disorder Spine J. 2006;6(6):624-35. [PMID: 17088193:
because symptoms are intentionally produced for Abstract].
external incentives. 4. Chou R, et al. Clinical Guidelines: Diagnosis and
Several exam tests are commonly thought to detect treatment of low back pain: A joint clinical practice
nonorganic causes of low back pain such as Waddell’s guideline from the American College of Physi-
signs, Mankopf ’s test, Hoover’s test, Arm Drop test, cians and the American Pain Society. Ann
Midline Split test, etc. which have low diagnostic yield. Intern Med. 2007;147(7):478-91. [PMID:
Since no examination technique objectively proves 17909209: Abstract].
malingering, the DSM-IV recommends suspicion of Web site: http://www.annals.org/cgi/content/
malingering for patients who present with 2 or more of abstract/147/7/478? maxtoshow = and hits = 10
the following: and hits = 10 and Resultformat = and fulltext =
Diagnosis + and + Treatment + of + Low + Back +
• Medicolegal issues
Pain% 3A + Recommendations + from + the +
• Disagreement between objective and subjective
American + College + of + Physicians% 2F
stress or disability
American + Pain + Society and searchid Back = 1
• Noncompliance with evaluation or treatment, or
and first index = 0 and resource type = HWCIT.
• Antisocial personality disorder. Accessed on 04.10.08.
5. American Psychiatric Association. Diagnostic and
vertebral fracture, and viral myelitis (her- Statistical Manual of Mental Disorders, Fourth
Edition, Text Revision (DSM-IV-TR). Washington
pes, polio, HIV). Hospitalization is indicated. DC: American Psychiatric Press Inc; 2000:683.
• In a patient with acute back pain, who is 6. Bair MJ, et al. Association of Depression and
withering with pain and clinically unstable, Anxiety Alone and in Combination with Chronic
Musculoskeletal Pain in Primary Care Patients.
suspect intra-abdominal or vascular Psychosom Med. 2008. [Epub ahead of print].
process. Hospitalization is indicated. [PMID: 18799425: Abstract].
CHAPTER
7 Breast Lump
FNAC or FNA Biopsy (FNAB)†† Screening MRI may be helpful for women for
whom mammography is not optimal, such
• The material aspirated, either fluid from the
as young women at substantially increased
cyst or samples of solid lesions, are subjected
risk for breast cancer because of known
to cytological examination. Any finding that
BRCA1 or BRCA2 mutations.3
is suspicious for malignancy on FNA is
subjected to surgical excision for definitive
Core-needle Biopsy
diagnosis
• This procedure can be combined with US, • Mostly used to evaluate small or difficult-
i.e. US guided FNAC, to further assess poorly to-palpate lesions, or nonpalpable breast
defined palpable masses masses identified on mammogram with
• If FNA is done before mammography, the ultrasound guidance. A minimum of four
diagnostic mammography should be de- core samples are taken to achieve greater
layed for 2 weeks after needle aspiration so histologic accuracy.
as to avoid false-positive results due to
trauma and possible hematoma formation. Excision Biopsy
generation; a family member who has both Table 7.2: Risk factors for breast cancer
breast and ovarian cancers; a male relative • Early menarche, before age 12
with breast cancer; or a positive BRCA1 or • Age greater than 50 years
BRCA2 genetic test in a relative; may • Late menopause, after age 50
• Age greater than 30 at first birth
undertake genetic testing after proper genetic • Nulliparity
counselling to see if she actually do have a • Ionizing radiation exposure
• Family history in first degree relative (i.e. mother,
mutated gene. If a woman has mutations in
sister, daughter)
either of two breast cancer susceptibility • Previous history of breast cancer, breast biopsy
genes (BRCA1 and BRCA2), her risk of breast showing atypical hyperplasia
• Minor risk factors include: alcohol intake, obesity
or ovarian cancer is significantly higher than (BMI >= 30 kg per m2), high economic status,
that of a woman without such a mutation.## HRT, and use of oral contraceptive pills
• Tuberculosis of the breast, though an 17(8):1931-42. Epub 2007 Feb 14. [PMID:
uncommon disease, is still present and is also 17429645: Abstract].
3. Joann G, et al. Screening for Breast Cancer. JAMA
misdiagnosed with carcinoma or bacterial
2005;293:1245-56.
abscesses. Moreover, simultaneous occurrence 4. http://www.nci.nih.gov/cancertopics/ Genetic-
of these two major illnesses in the breast, i.e. Testing-for-Breast-and-Ovarian-Cancer-Risk/
tuberculosis and carcinoma has been reported print?page=&keyword= (accessed on 08-07-08).
5. Singletary SE, et al. Revision of the American
in the literature which can lead to many
Joint Committee on Cancer staging system
problems regarding diagnosis and treatment.6,7 for breast cancer. J Clin Oncol 2002;20(17):
3628-36. [PMID: 12202663: Free full text].
REFERENCES Web site - http://jco.ascopubs.org/cgi/content/
full/20/17/3628 (accesses on 09-07-2008).
1. Goodson WH, et al. Causes of physician delay in 6. Fadeei-Araqqhi M, et al. Breast tuberculosis:
the diagnosis of breast cancer. Arch Intern Med. Report of eight cases. Arch Iran Med 2008;
2002;162(12):1343-8. [PMID: 12076232: Free full 11(4):463-5.[PMID: 18588382: Free full text].
text]. 7. Alzaraa A, et al. Coexistence of carcinoma and
2. Bick U, et al. Digital mammography: What we do tuberculosis in one breast. World J Surg Oncol
and what we don’t know? Eur Radio 2007; 2008;6:29. [PMID: 18318914: Free full text].
CHAPTER
8 Chest Pain
Table 8.1: Physical findings in acute chest pain Location (diffuse, anterior retrosternal
Features Cause pain, chest pain, interscapular pain)
Altered mental state; cold Low cardiac output: MI; LVF Radiation (to the neck, jaw, shoulders or
extremities; pulsus alternans; arms)
tachycardia; hypotension; S4
Dyspnea; tachycardia; hypoxia; Acute pulmonary edema: MI; Aggravating factors (exertion, meals, cold
elevated JVP; rales; S 3 gallop LVF weather, and stress)
Pulse deficit; hypertension; Aortic dissection
BP difference between two arms; Duration (brief pain lasting few seconds
murmur of aortic insufficiency;
neurological deficit
to few minutes)
Tachypnea; hypotension; Pulmonary embolism Relieving factors (rest)
elevated JVP; right ventricular
lift; accentuated P2; pulmonary Associated symptoms (dyspnea, cough,
rales, consolidation, effusion diaphoresis, presyncope, syncope).
Dyspnea, dysphagia, hypoxia; Cardiac tamponade
elevated JVP; hypotension; • Common features of atypical chest pain are
tachycardia; pulses paradoxus; listed in Table 8.3
muffled heart sounds;
pericardial rub • Coronary risk factors include—Age, family
Dyspnea; hypoxia; tachycardia; Pneumothorax history of heart problems, diabetes,
mediastinal shift; hyperresonance;
absent/diminished breath sounds; hypercholesterolemia, smoking, hyper-
subcutaneous emphysema
Hamman’s sign (crunching, Pneumomediastinum;
tension, obesity, sedentary lifestyle, and
rasping sound, synchronous Pneumopericardium; stress or competitive occupation
with heartbeat) esophageal rupture
• Although cardiac risk factors are common
Table 8.2: Classification and examples of
in patients with ACS, they are not a pre-
chest pain based on duration requisite; absence of such risk factors does
Duration Examples not lower the risk of ACS14
Acute chest pain–lasting Cardiac: ACS; HCM; aortic stenosis; • The key distinctive point in the clinical
for few seconds to few pericarditis Vascular: Aortic diagnosis of chest pain caused by CAD is in
minutes dissection; PE; PH Pulmonary:
pneumonia; tracheobronchitis; its relation to physical exertion. If the chest
pleuritis; pneumothorax; mass lesion discomfort is not precipitated by physical
GI: GERD; PUD; biliary disease;
pancreatitis exertion, it is highly unlikely that coronary
Musculoskeletal: costochondritis;
cervical disk
artery disease of any significant degree is
Lesion; trauma present (Table 8.4)
Others: breast disorders; herpes zoster;
anxiety; emotional
• Occasionally, effort-induced ischemic pain
Recurrent chest pain – Cardiac: (same as in above) disappears while the activity continues; this
lasting for minutes vascular: PE; PH
pulmonary: (same as in above, except is known as walkthrough or second wind angina
pneumothorax) • Occasionally, diagnosis based solely on
GI / musculoskeletal, and others: (same
as in above) history may not be possible; e.g. descriptions
Persistent – lasting for hours Cardiac: pericarditis of chest pain of cardiac, upper gastroin-
and days together Pulmonary: ( same as in above, except
pneumothorax) testinal, or gallbladder origin can be identical.
GI / musculoskeletal, and others: Hence, although patient’s history is usually a
(same as in above)
valuable starting point, it may not provide a
• Careful assessment of patient’s history and definite diagnosis because of their poor
cardiac risk factors is often the most helpful specificity in diagnosis of chest pain15
starting point. Historical features generally useful • Symptoms of angina equivalents, i.e. cardiac
in the diagnosis of cardiac origin of chest pain ischemia without chest pain, such as
include:
54
Table 8.3: Symptoms of atypical chest pain • The pain of diffuse esophageal spasm may
• Features suggesting atypical, also called as non- mimic that of angina pectoris, including that
cardiac/ nonanginal pain includes: the relief in many cases is obtained with
• Pain—dull ache, sharp, shooting,’ knife-like’, pleuritic, nitroglycerine
pain brought on by respiratory movements or cough.
• Location—pain localized with one finger, left sub- • Severe chest pain, retrosternal, accompanied
mammary. by dyspnea, cough, and hemoptysis deve-
• Aggravating factors – body movements, respiration,
loping in a patient who has been immo-
swallowing, palpation of chest.
• Duration – brief episodes lasting a few seconds, or bilized or bedridden is suggestive of
constant lasting for days. pulmonary embolism
• Pulmonary hypertensive pain may resem-
Table 8.4: Questions to differentiate patients with non- ble angina in that it is precipitated by effort.
cardiac chest pain from those with coronary heart
disease # Associated moderate or severe dyspnea and
Response evidence of signs of pulmonary hypertension
Question Typical Atypical suggest its diagnosis
If you go up a hill (or other stressor) on 10/10 <10/10
• Chest discomfort due to pericarditis is typi-
10 separate occasions on how many cally retrosternal, aggravated by coughing,
do you get the pain?
Of 10 pains in a row, how many occur at rest? <2/10 ≥2/10 deep respiration, or change in position; worse
How many minutes does the pain usually last? <5 ≥5 in supine, and relieved in sitting upright and
When answers to all three questions are “atypical” the chance of leaning forward
coronary disease is only 2% in patients aged <55 years and 12% in • The acute onset of pleuritic pain and dyspnea
those aged ≥55
in a patient with a history of asthma or
#Christopher Bass et al. Clinical review ABC of psychological emphysema is suggestive of pneumothorax
medicine chest pain. BMJ 2002; 325:588-91.
• Psychogenic chest pain is often associated
breathlessness; profound, unexplained, with hyperventilation and other somatic
sudden-onset fatigue, especially in the symptoms such as chronic headache, diz-
elderly and diabetic patients is common ziness, sweating, paresthesia, and a sense of
• Pain that radiates to the left arm and ‘impending doom’.
shoulder is often assumed to indicate
coronary ischemia, whereas pain that RED FLAGS
radiates to the right shoulder is thought to
suggest a biliary source. However, chest pain • Lack of chest pain does not exclude IHD
that radiates to the right shoulder is more • Over-reliance on tests with poor sensitivity,
specific for pain of cardiac origin than pain such as ECG, or on the initial values of cardiac
that radiates to the left shoulder. Radiation biomarkers will miss many patients with MI
of chest discomfort to the right arm is also • In a patient with chest pain, the clinical
consistent with the diagnosis of acute IHD16 response to GI cocktail (a mixture of liquid
• Acute, sudden and severe chest pain described antacid, viscous lidocaine, and an
as ripping or tearing that is maximal at onset anticholinergic), or sublingual nitroglycerin
and radiates to interscapular area raises the (NTG), cannot reliably identify the source of
possibility of aortic dissection. Important pain. Failure to respond to NTG should not
diagnostic feature is the inequality in the pulses, be used to exclude the possibility of CAD7,17
e.g. carotid, radial and femoral, and a blood • A history of a psychiatric diagnosis or
pressure differential of greater than 20 mm Hg overwhelming anxiety in a patient with
55
acute chest pain does not preclude the therefore proposed as a pathogenic factor in
possibility of an acute coronary event. female patients. Recently, techniques such as
functional angiography, SPECT, and stress MRI
SELECTIVE GLOSSARY have been used to diagnose CSX. However, the
diagnosis remains one of exclusion. CSX has a
Cardiac syndrome X (CSX)§— It is a condition
low mortality rate and an excellent prognosis
defined by the presence of angina-like chest pain
despite variable symptomatic improvement.
with angiographically normal coronary arteries
which is observed in approximately 20–30% of
REFERENCES
angina patients undergoing coronary arterio-
graphy. To establish the diagnosis, patients 1. Dumville JC, et al. Non-cardiac chest pain: A
retrospective cohort study of patients who
must have evidence of stress-induced myo- attended a Rapid Access Chest Pain Clinic Family
cardial ischemia by exercise ECG, stress Practice Advance Access published on April 1,
scintigraphy, or stress echocardiography, in 2007; DOI 10.1093/fampra/cmm002. Fam. Pract.
24: 152-7.
conjunction with anginal chest discomfort. 2. Sheps DS, et al. Chest pain in patients with
Coronary angiography reveals normal or near cardiac and noncardiac disease. Psychosom
normal epicardial coronary arteries. Patients Med 2004;66(6):861-7. [PMID: 15564350: Free
full text].
with CSX are usually younger (mean age 49 3. Kachintorn U. How do we define non-cardiac
years) than patients with atherosclerotic CAD; chest pain? J Gastroenterol Hepatol 2005;20
Suppl:S2-5. [PMID: 16359344: Abstract].
more common in women (most of whom are
4. Eslick GD. Noncardiac chest pain: Epidemiology,
perimenopausal) than men. Pain, which usually natural history, health care seeking, and quality
occurs at rest, may have atypical features. The of life. Gastroenterol Clin North Am 2004;
33(1):1-23. [PMID: 15062433: Abstract].
exact pathophysiologic factors and mechanisms 5. Nora Goldschlager. Chest pain: Avoiding com-
of pain in these patients are unclear. However, mon pitfalls. Internal Medicine World Report: Aug
patients with chest pain and normal coronary 2007.
6. Wilhelmsen L, et al. “Nonspecific” chest pain
arteries have abnormal vasodilatory coronary
associated with high long-term mortality: Results
blood flow responses and an increased from the primary prevention study in Göteborg,
sensitivity of the coronary microcirculation to Sweden. Clin Cadiol 1998;(7):477-82. [PMID:
9669056: Abstract].
vasoconstrictor stimuli (microvascular angina).
7. Amany H Ahmed, et al. Silent myocardial ische-
Microvascular endothelial dysfunction appears mia: Current perspectives and future directions.
to be responsible for these coronary micro- Exp Clin Cardiol 2007;12(4):189-96. [PMID:
circulation abnormalities. Risk factors such as 18651003: Free full text].
8. Arslanian-Engoren C, et al. Symptoms of men
hypertension, hypercholesterolemia, increased and women presenting with acute coronary
plasma homocysteine levels, diabetes mellitus, syndromes. Am J Cardiol 2006;98(9):1177-
abnormal blood rheology, H. pylori infection, 81.Epub2006Sep7. [PMID: 17056322: Abstract].
9. Wilhelmsen L, et al. “Nonspecific” chest pain
and smoking can contribute to its development. associated with high long-term mortality: Results
Most patients with CSX are postmenopausal from the primary prevention study in Göteborg,
women and estrogen deficiency has been Sweden. Clin Cardiol 1998;21(7):477-82. [PMID:
9669056: Abstract].
10. Autore C, et al. Role of echocardiography in acute
chest pain syndrome. Am J Cardiol 2000;
§
CSX must be distinguished from metabolic syndrome x 86(4A):41G-42G. [PMID: 10997353: Abstract].
of insulin resistance (glucose intolerance), hypertension, 11. Nissen SE, et al. Intravascular ultrasound: Novel
hyperlipidemia, elevated BMI, and frequently associated pathophysiological Insights and current clinical
with abnormal coronary angiography. applications. Circulation 103:604-16.
56 Diagnosis: A Symptom-based Approach in Internal Medicine
12. DeFevter PJ, et al. Spiral multislice computed 15. Swap CJ, et al. Value and limitations of chest pain
tomography coronary angiography: A current history in the evaluation of patients with Suspected
status report.Clin Cardiol 2007;30(9):437-42. acute coronary syndromes. JAMA 2005;294:2623-
[PMID: 17803209: Abstract]. 29.
13. Fruergaard P, et al. The diagnosis of patients admit- 16. Berger JP, et al. Right arm and plain extension can
ted with acute chest pain but without myocardial
help to differentiate coronary diseases from chest
infarction. Eur Heart J 1996;17(7):1028-34. [PMID:
pain of other origin: A prospective emergency
8809520: Free full text].
14. Body R, et al. Do risk factors for chronic coronary ward study of 278 consecutive patients admitted
heart disease help diagnose acute myocardial for chest pain. J Inter Med 1990;227(3):165-72.
infarction in the emergency department? Resus- [PMID: 2313224: Abstract].
citation. 2008 Aug6 [Epub ahead of print. PMID: 17. Gibbons RJ. Nitroglycerin: Should We Still Ask?
18691797: Abstract]. Ann Intern Med 2003;1036-37.
CHAPTER
9 Constipation
• High blood glucose in uncontrolled chronic Table 9.1: Anorectal and pelvic floor function tests1
diabetes mellitus complicating autonomic • Ultrasonography
neuropathy. • Anorectal manometry
• Defecation proctography
Serum Calcium • Balloon expulsion test
• Rectal sensation – mechanical and electrical
• Elevated in malignancy, and hyperparathy- • Pudendal nerve terminal motor latencies
roidism. • Perineometry
• Measurement of rectoanal angle
• Sphincter/puborectalis electromyogram
AXR • Spinal evoked potentials by rectal stimulation
• Dilated bowel loops with multiple fluid • Cerebral evoked potentials by rectal stimulation
• Scintigraphic expulsion of artificial stool
levels in intestinal obstruction.
• May provide evidence for an excessive Anorectal manometry—Mainly to exclude
amount of stool in the colon. adult-onset or short segment Hirschsprung
US Abdomen disease.
Barium defecography—To evaluate evacu-
• To assess extrinsic abdominal or pelvic atory disorders such as rectal prolapse,
compression (e.g. pregnancy, fibroid, tumor). enterocele, and rectocele.
Colonoscopy Colonic transit studies (using radiopaque
marker)—To study colonic motility dis-
• Preferred procedure in patients at risk (i.e.
orders. In normal persons, most of the
with warning signs) for colon cancer or IBD.
markers should pass by day 5; in a patient
• Enables biopsy (Bx) of suspicious lesion, and
with slow colonic transit, the markers will
remove any high impaction.
be scattered throughout the colon. If the
Sigmoidoscopy/Barium Enema patient has pelvic outlet obstruction, more
than 20% of the markers will be held up in
• May be appropriate in younger patients
the rectum.
who are not at risk for colon cancer. Polyps,
Balloon expulsion studies—To demonstrate
diverticula, strictures, and luminal wall
impaired rectal evacuation.
lesions can be demonstrated.
Rectal Biopsy
MRI—Brain, Spine
• Helpful to diagnose Hirschsprung’s disease,
• As indicated in multiple sclerosis, spinal
ulcerative colitis, Crohn’s disease, and infil-
trauma, spinal disease.
trative diseases such as scleroderma, and
Expanded Physiological Studies (Table 9.1)1 amyloidosis.
• In patients with chronic constipation with
CLINICAL NOTES
no identifiable cause following initial
evaluation, and in whom initial treatment • The initial step is to define the nature of the
has failed, or in those patients wherein patient’s bowel habit, and how the current
subtypes of constipation are suspected, such problem differs from the normal pattern.
as colonic motility dysfunction, or pelvic History should include:
floor dysfunction, following studies may be Detailed inquiry into the patient’s normal
helpful:7 pattern of defecation
60 Diagnosis: A Symptom-based Approach in Internal Medicine
Amount of time spent on the toilet while weight loss, change in bowel habits (Table
waiting to defecate 9.2), nausea, vomiting, abdominal pain,
Whether the patient is c/o decreased distension, presence of blood in the stools,
frequency of stools, or painful/incom- family history of colon cancer is important.
plete evacuation Table 9.2: Differential diagnosis of change
Perceived hardness of the stools in bowel habit (constipation/diarrhea)
Whether the patient strains in order to Constipation dominant
defecate • Low-fiber diet
What maneuvers (pharmacological or • Drug effect — For example codeine, iron, laxative abuse
• IBS
physical) are used to facilitate this • Diabetic neuropathy (autonomic neuropathy)
process • Fecal impaction
• Carcinoma of colon, rectum, or anus
Any other symptoms (pain, protruding
• Neurologic disease such as spinal cord injury
mass, bleeding) the patient may be
Diarrhea dominant
experiencing • Viral gastroenteritis
• Is the constipation acute or chronic—Consti- • Food poisoning
pation is generally considered to be acute or • Parasite infection (giardiasis)
• Traveler’s diarrhea (usually Escherichia coli infection)
occasional if it’s less than three months, and • Change in resident bacterial flora, e.g. antibiotic
chronic if it lasts thee months or more associated diarrhea
• In acute constipation there is abdominal pain • Antibiotic-related diarrhea (Clostridium difficile colitis)
• Hyperthyroidism
and vomiting, suggesting the possibility of • Diabetic neuropathy (autonomic neuropathy)
intestinal obstruction. The most common • Drug effect
cause of acute constipation in the elderly is • Lactose intolerance
• Gluten sensitivity (celiac sprue)
fecal impaction. The diagnosis is made by • Crohn’s disease
DRE by the presence of firm, clay-like mass • Diverticulitis (infection of a diverticulum)
indicating impaction • Food intolerance
• IBS
• The most common cause of chronic habitual • Ulcerative colitis
constipation is usually a combination of poor • Whipple’s disease
• Malabsorption syndrome
diet low in fiber (fast foods/eat on the run),
decreased fluid intake, physical inactivity,
and failure to acknowledge “call to toilets”‡ • Depression—Constipation can be a significant
• Diet—Inquiry about a typical day’s diet symptom in all types of depressive illness
should include the type and quantities of and may be aggravated by treatment with
fiber, fluid, fruits, vegetables, as well as any depression
recent change in diet • IBS—With IBS the patient may c/o consti-
• Medications—Reviewing medications and pation or diarrhea or both alternating. Asso-
discontinuing any responsible drug will ciated somatic and psychological complaints
relieve constipation such as anxiety, depression, chest pain,
• Risk factors—In adults inquiry about risk headache, fatigue, myalgias, and gynecologic
factors for colon cancer such as unintentional symptoms strongly favor the diagnosis of
IBS
‡
‘Dyschezia’ or lazy bowel is the term used to describe a • Systemic disease—Diabetic neuropathy may
rectum that has become unresponsive to fecal content
and this usually follows repeated ignoring of calls to
result in constipation due to chronic dys-
defecate. motility, and slow transit time. Symptoms
61
such as cold intolerance, hair and skin changes Significant weight loss
suggest myxoedema. Any cause of Therapy resistant constipation
hypercalcemia, e.g. hyperparathyroidism, New onset constipation in elderly
and malignancy may cause constipation. The without obvious cause
patient may also c/o abdominal pain, Family history of IBD
vomiting, nocturia, and mental symptoms Family history of colon cancer.
associated with this condition. A neurolo- • Intermittent colicky abdominal pain with
gical examination may detect signs of CVA, distension and progressive constipation or
dementia, Parkinson’s disease, spinal cord obstipation is an urgent indication to
disease, or multiple sclerosis evaluate the cause of intestinal obstruction
• Past history—A long history of bowel • Sexual abuse is a known cause of chronic
obsession§ , abdominal surgery, radiation constipation and needs to be excluded in
therapy, may suggest the cause of constipation. patients especially with psychosexual
• Physical examination—For weight, nutritio- problems.
nal status, thyroid, and abdomen (tender-
ness, mass, distended bowel loops) SELECTIVE GLOSSARY
• PR—It is an important procedure because
Hirschsprung’s disease (Congenital Mega-
about one-forth of cancers are within reach
colon)—Abnormally large or dilated colon due
of the examining finger. Lesions such as
to congenital absence of myenteric ganglion cells
hemorrhoids, fissure, ulcer, impaction,
in a distal segment of the large bowel, and
growth, fecal occult blood are obvious
resultant loss of motor function in this segment
• Anal wink— Sensation of the perianal area
causes massive hypertrophic dilatation of the
and the ‘anal wink’ (a reflex constriction
normal proximal colon, appears soon after birth,
upon pinprick sensation of the perianal area;
mediated by S2, S3, S4) reflex should be tested is called “Hirschsprung’s disease”. Signs and
in spinal cord disease or lumbosacral roots symptoms (abdominal distension, vomiting,
• Constipation from infancy may be due to constipation, etc.), may vary with the severity
Hirschsprung’s disease. Occasionally symp- of the condition. Sometimes they appear
toms may present for the first time in adult after birth; other times they may not be
life apparent until the child becomes a teenager or
• Lifelong constipation (severe refractory adult.
constipation) is sometimes due to megacolon. Pelvic floor dysfunction (PFD)—The pelvic floor
muscles support the pelvic organs, bladder and
RED FLAGS rectum, and their function is critical to activities
• Alarm symptoms and signs in patients with such as urinating, having bowel movements,
constipation include: and sexual intercourse. PFD has traditionally
Persistent anemia been described as resulting from laxity or poor
Positive FOBT tone of the pelvic floor musculature and/or
Hematochezia ligaments. Damage of this nature usually results
from aging, straining, or trauma, resulting in
§
The older generation considers defecation every day a complaints such as poor urine stream, consti-
sign of good health. pation, low back pain, pain with ejaculation or
62 Diagnosis: A Symptom-based Approach in Internal Medicine
vaginal penetration, pelvic pain or pressure, or 4. Ashraf W, et al. An examination of the reliability
of reported stool frequency in the diagnosis of
urinary frequency and urgency.
idiopathic constipation. Am J Gastroenterol 1996;
91(1):26-32. [PMID: 8561138: Abstract].
REFERENCES 5. Marshall JB. Chronic constipation in adults. How
far should evaluation and treatment go? Postgrad
1. Camilleri M, et al. Clinical management of intrac-
Med 1990;88(3):49-51,54,57-9,63. [PMID:
table constipation. Ann Intern Med 1994;
121(7):520-8. Full Text [PMID: 8067650: Abstract]. 2169048: Abstract].
2. Herz MJ, et al. Constipation: A different entity for 6. Locke GR, et al. American Gastroenterological
patients and doctors. Fam Pract. 1996;13(2):156- Association Medical Position Statement: Guide-
9. [PMID: 8732327: Free full text]. lines on constipation. Gastroenterology 2000;
3. Chang L, et al. Gender, age, society, culture, and 119(6):1761-6[PMID: 11113098: Abstract].
the patient’s perspective in the functional gastro- 7. Rantis PC Jr, et al. Chronic constipation—is the
intestinal disorders.Gastroenterology. 2006; work-up worth the cost? Dis Colon Rectum. 1997;
130(5):1435-46. [PMID: 16678557: Abstract]. 40(3):280-6. [PMID: 9118741: Abstract].
CHAPTER
10 Convulsions
Table 10.2: Nonepileptic seizures (NES): Differentiation • CNS infection (bacterial, TB, viral-HIV,
Two major types of NES are recognized; their differen- cerebral malaria, cysticercosis)
tiating features being as follows: • Seizures (generalized tonic-clonic, partial-
• Psychogenic NESs are symptoms of an underlying simple, status epilepticus)
psychiatric disorder, without a physiologic basis,
e.g. conversion disorder, anxiety disorder, PTSD,
• Cerebrovascular accident (TIA, stroke)
psy-chotic disorder, factitious disorder. • Head injury (early or late)
• Physiologic NESs are caused by physiologic dys- • Hypoglycemia
function, such as cardiac arrhythmias, hypotensive • Malignant hypertension (hypertensive
episodes, cerebrovascular disease, complicated mig-
raine, parasomnias, tics, and spasms. Such conditions encephalopathy)
may result in loss of consciousness, with or without • Toxemia of pregnancy.
associated motor manifestations. A detailed history
and appropriate investigations (e.g. Holter moni- Occasional
toring, noninvasive carotid artery studies, or tilt-table
testing) will usually reveal the true diagnosis. • Migraine (complicated)
Note: Most of the discussion in this article pertains to • Alcoholism/withdrawal (rum fits)
psychogenic NESs, i.e. PNES. • Metabolic (electrolyte imbalance, hypo-
calcemic, DKA, uremia, hepatic encephalo-
Epilepsy‡ is a symptom complex in which
pathy, cardiac arrest)
there is a tendency to have repeated (two or
• Drug toxicity (aminophylline, theophylline,
more), unprovoked seizures, requiring definitive
ephedrine, terbutaline, bupropion, penicillin,
diagnosis and treatment. Not everyone who has
insulin, metronidazole, pentazocine, lidocaine)
seizures has epilepsy, but everyone who has
• Substance abuse (amphetamines, ‘ecstasy’,
epilepsy has seizures.
antidepressants, antipsychotics, cocaine).
Neither convulsions, seizures, nor epilepsy
are a final diagnosis, but are symptom complexes Rare
requiring a search for underlying etiologic
• Pseudoseizure§ (i.e. PNES)
factors. Further, it is extremely important to
• Infections (tetanus, rabies)
differentiate epileptic seizures, including various
• Brain tumors (primary/secondary)
simple partial seizures, complex partial seizures,
• Degenerative disorders (dementia, multiple
typical and atypical absence seizures from NES,
sclerosis)
because misdiagnosis leads to inappropriate
• Sleep disorders (parasomnias)
treatment with antiepileptic drugs, leading to
• Poisoning (organophosphate insecticides,
toxic side effects, causing additional disability
cyanide, strychnine).
and frustration.
INVESTIGATIONS—GENERAL
DIFFERENTIAL DIAGNOSIS
CBC
Common
• Leukocytosis may suggest CNS infections.
• Syncope (vasovagal, orthostatic hypoten-
• Erythrocytes may show sickled cells.
sion, cardiac arrhythmia)
• Polycythemia with elevated hematocrit in
‡
The word ‘epilepsy’ is derived from the Greek word for hypercoagulable states.
‘attack’, (presently meaning seizure). People once thought
§
that those with epilepsy were being ‘attacked’ by demons The term nonepileptic seizure is preferred to pseudoseizure,
or Gods. However, in 400 BC Hippocrates suggested because the former term is nonjudgemental, and describes
that epilepsy was a disorder of brain. problem without implying causation.
65
• Listen to the eyewitness—An accurate record Table 10.3: Differentiation between syncope and seizure
from an observer is invaluable, particularly Parameter Syncope Seizure
if there is evidence that his/her attack was Onset Gradual Sudden
the first one. This record should include: Attack Rapid, but never Loss of
Details of the circumstances of the attack absolutely consciousness
sudden; may with absolute
(anxiety, panic, pain, prolonged standing, be averted suddenness;
physiological acts, e.g. micturition). by lying down cannot be
Any prodromal symptoms (aura, e.g. odd promptly averted
Position at Usually erect or Any
behavior, repetitive actions). onset on change to
Details of the sequence of events of the attack erect; rarely
recumbent
itself (e.g. a rhythmic flexion-extension
Warning Light Unusual
movement of the extremities, loss of symptoms headedness sensations,
consciousness, incontinence, tongue biting). dizzy, giddy, sounds, smells,
nausea,vomiting blurred vision,
The aftermath - whether the episode was hallucinations,
followed by period of (postictal) con-fusion. tingling,
• These observations, especially presence or twitching
of muscles
absence of aura, and postictal confusion are Convulsions Rare Common
critical and help to differentiate seizures Accompani- Incoherence, Confusion,
from syncopal and other common physiologic ments incontinence, enuresis,
tongue bruising tongue
NES, such as postural hypotension, TIA, rare bruising
complicated migraine, sleep disorders, and common
psychogenic NES (Table 10.3) Duration Variable—seconds About a
to few minutes minute
• What is the cause of seizure? Knowledge of Sequela No sequela Confusion,
patient’s medical history, including family after recovery headache,
history, aids in the understanding the cause of from attack drowsiness,
often deep
convulsion or seizure. A history of head trauma, sleep;postictal
fever, infection, alcoholism, and systemic disease paralysis
may be present
such as diabetes mellitus, hypertension, EEG Normal Normal or
cerebrovascular disease, and metabolic abnormal
disturbances suggest the cause of seizure
• Medications and substance abuse—A review possibility of pseudoseizure should be care-
of patient’s medications is important. Bron- fully considered as prompt recognition can
chodilators (aminophylline, theophylline, prevent subsequent intervention.
terbutaline, ephedrine); antidepressants • Physical examination—A focused exami-
(bupropion, amitriptyline, imipramine); nation should be done soon after a paroxys-
antipsychotics (thioridazine, clozapine, mal event and should include:
haloperidol); opioids (tramadol); anes- Evidence for injuries, including head
thetics (lidocaine, pentazocine, fentanyl); injury.
antimicrobials (penicillin, metronidazole, Check oxygen saturation.
isoniazid); antineoplastics (vincristine, Chest auscultation for possible aspiration.
methotrexate), ‘ecstasy’, etc. are known to Heart rate, rhythm, BP, ECG (hypertensive
provoke seizure. encephalopathy), and orthostatic changes
• Pseudoseizure, i.e. PNES (Table 10.4)—The (syncope, arrhythmias).
Convulsions 67
11 Cough
• Sputum eosinophilia in asthma and non- Table 11.2: Causes of chronic cough among adults with
asthmatic eosinophilic bronchitis (NAEB)† normal CXR
Diagnosis Differential diagnosis with normal CXR
CXR Environmental Tobacco exposure; industrial
pollutants; occupational allergens
• Helpful in evaluating for:
Infections— Postinfectious cough; chronic
Pneumonia (consolidation) respiratory bronchitis; TB; bronchiectasis;
Bronchiectasis (dilated tubular or cystic tropical pulmonary eosinophilia;
mucus filled bronchi) whooping cough
COPD (hyperinflation, flat diaphragm) Infections/ Cerumen; Otitis media with
disorders—ENT effusion; chronic sinusitis; nasal
TB (upper lobe infiltrates, hilar lympha- polyp; vocal cord dysfunction/paralysis;
denopathy, cavitary lesions, pleural aspiration
effusion) Asthma Cough-variant asthma; postinfectious
Sarcoid (hilar lymphadenopathy) hyperactivity airways
CHF (pulmonary edema, vascular conges Cardiac CHF; mitral stenosis
tion, Kerley B lines, peripheral infiltrates, GI disorders Gastroesophageal reflux
pleural effusion, cardiomegaly) Neoplasia Bronchial adenoma; mediastinal mass
Bronchogenic carcinoma (hilar mass or a with tracheal compression; laryngeal
papilloma, hemangioma
single coin shadow).
Iatrogenic Drug induced; Foreign body – nose;
• A normal CXR in an immunocompetent patient ear; trachea; larynx; bronchus
with chronic cough usually excludes tuber- Psychogenic Habit cough; tic cough; psychoge-
culosis, bronchiectasis, persistent pneumonia, nic cough
bronchogenic carcinoma, and sarcoidosis.
However, chronic cough can be a cause of many
Pulse Oximetry
disorders in spite of a normal CXR; a few of such
conditions are given in Table 11.2. • To monitor arterial O2 saturation in patients
with asthma or COPD.
Peak Expiratory Flow Rate (PEFR)
• Serial measurements of peak flow rates on pH Studies
waking, i.e. early morning, during day, and
• Ambulatory 24-hour esophageal pH monitoring
before bed, demonstrating wide variations
is the most reliable but invasive test for GERD.
in airflow limitation is seen in asthma, and
It should, therefore, be performed only after
facilitates monitoring its treatment.
failure of empiric GERD treatment, and a
INVESTIGATIONS—SPECIFIC negative evaluation for asthma and sinusitis.
the posterior pharynx. Its role in chronic • In a patient with chronic bronchitis, any
cough, though controversial, is supported change in the character of the cough or
by response to therapy — usually an sputum may be the presenting feature of a
antihistamine-decongestant combination superimposed bronchogenic carcinoma
drug or nasal corticosteroid spray8 • Smoker’s cough should not be neglected; it may
• Cough due to ACE inhibitors is a class effect be an early symptom of bronchogenic
and has been documented with all ACE carcinoma. Conversely, bronchogenic
inhibitors in use; changing to another agent carcinoma is known to occur in nonsmokers
will not ameliorate the symptoms or in patients with other pulmonary
• A past history of recurrent lung infections conditions, such as chronic bronchitis
from childhood is suggestive of cystic fibrosis • When a patient has a cough lasting for >2
and bronchiectasis; a history of hay fever and weeks without another apparent cause and
eczema suggests asthma; while tuberculosis, it is accompanied by paroxysms of coughing,
emphysema (alpha1-antitrypsin deficiency) posttussive vomiting, and/or an inspiratory
asthma, cystic fibrosis have a familial whooping sound, the diagnosis of a B.
predisposition pertussis infection should be made unless
• In a healthy individual, cough, following another diagnosis is proven
URTI and persisting for at least 3 weeks, but • In patients with unexplained cough, evaluate
no more than 8 weeks, consider the diagnosis the possibility of drug-induced cough.
of postinfectious cough. In some patients,
transient bronchial hyperreactivity may be REFERENCES
demonstrated
1. Senzilet LD. Pertussis is a frequent cause of
• In all patients with chronic cough, even in prolonged cough illness in adults and adolescents.
the absence of clinical signs or symptoms, Clin Infect Dis. 2001;32(12):1691-7. Epub 2001
consider UACS, asthma, and GERD, as they May 21. [PMID: 11360208: Abstract].
2. Birkebaek NH. Bordetella pertussis in the
may present only as cough, and no other aetiology of chronic cough in adults. Diagnostic
associated clinical findings, i.e. ‘silent’ UACS, methods and clinic.Dan Med Bull 2001;48(2):77-
cough-variant-asthma, and ‘silent’ GERD 80. [PMID: 11414122: Abstract].
3. Tomasz J, et al. Chronic Cough From the Patient’s
respectively Perspective. Mayo Clin Proc 2007;82:56-60.
• In a nonsmoking patient with a clear chest 4. Kalpaklioglu AF, et al. Evaluation and impact of
radiograph who does not use ACE inhibitors, chronic cough: Comparison of specific vs generic
quality-of-life questionnaires.Ann Allergy Asthma
one or more of the following four causes of Immuno 2005;94(5):581-5.[PMID: 15945562:
chronic cough account for the overwhelming Abstract].
majority of cases; namely, UACS, asthma, 5. Brignall K, et al. Quality of life and psychosocial
aspects of cough. Lung. 2008; 186 Suppl 1:S55-
NAEB, or GERD. 8. Epub 2007. [PMID: 17939003: Abstract].
6. Braman SS. Postinfectious cough: ACCP evidence-
RED FLAGS based clinical practice guidelines. Chest. 2006;
129(1 Suppl):138S-146S. [PMID: 16428703: Free
• A normal lung examination does not exclude full text].
7. Pratter MR, et al. Chronic upper airway cough
asthma, bronchitis, COPD, GERD or lung syndrome secondary to rhinosinus diseases
malignancy (previously referred to as postnasal drip
• Failure to improve with appropriate manage syndrome): ACCP evidence-based clinical practice
guidelines. Chest. 2006;129(1 Suppl):63S-71S.
ment over 4 weeks signals a need for detail [PMID: 16428694: Abstract].
work up to exclude TB, cough variant asthma, 8. O’Hara J, et al. “Postnasal drip syndrome”: Most
resistant pulmonary infections, malignancy, patients with purulent nasal secretions do not
complain of chronic cough.Rhinology. 2006;
and immunosuppression 44(4):270-3. [PMID: 17216744: Abstract].
CHAPTER
12 Dementia
Mood (e.g. growing apathy, depression, Table 12.2: Potentially treatable/reversible dementias
withdrawal, anxiety, hallucinations); and • Alcoholism: Chronic
Behavior (e.g. repetitive actions, or • Connective tissue disorders: Temporal arteritis,
questioning; purposeless hyperactivity; vasculitis, SLE
• Drug toxicity
wandering, agitation). • Endocrine: Thyroid disease, hyperglycemia, hypo-
These clusters of symptoms and disabilities glycemia, insulinoma, adrenal disease, pituitary
compromise the successful performance of activities disease, parathyroid disease
• Infections: Viral encephalitis, postencephalitis
of daily living in a demented individual (e.g. syndrome, chronic meningitis, AIDS, neurosyphilis
neglecting household chorus, neglecting self-care, • Mass lesion: Chronic subdural hematoma (bilateral), tumor
mistakes at routine work, difficulty handling money, • Metabolic: Dehydration, electrolyte disturbance,
uremia, hepatic encephalopathy, hypercalcemia,
trouble with shopping, and difficulty in driving). hypoxia
Dementia does not occur de novo, but probably • Normal-pressure hydrocephalus
• Nutritional: Vit. B12, folate, thiamine deficiency
represents the end of a spectrum from normal aging
• Others: Blindness, chronic seizures, CHF, dialysis
through an intermediate state called mild cognitive encephalopathy, hearing loss, obstructive sleep
impairment (MCI - vide infra ↓↓). Early identification of apnea, radiation-induced
• Psychiatric: Depression
MCI is important because some of the disorders
that cause dementia might be treatable, reversible, NOTE: Dementia due to alcoholism, HIV, TB, drugs,
nutritional deficiency, and head trauma are preventable;
and preventable (Table 12.2). On the other hand, the rest are amicable to therapy.
dementia tends to be progressive, cognitive
functions tend to decline steadily, vegetative Table 12.3: Typical features differentiating mild
cognitive impairment and dementia
symptoms such as change in appetite, weight,
Mild cognitive impairment
sleep, and fatigue are often absent, and there is little • Insidious onset – always
or no response to medications. The typical • Deficit involves memory
differentiating features between MCI and • Cognition remains intact
• No interference with social and occupational
dementia✝ are given in Table 12.3. functioning
The task of a physician caring for a demented • May or may not eventually lead to dementia
patient, therefore, is twofold:
Dementia
Early identification of those dementias • Insidious onset – generally
that are treatable, especially because more • Impaired memory and one or more of the features
treatment options are now available, and of aphasia, apraxia, agnosia, and impaired executive
functioning
Educate and support the family of the • Cognitive deficits significantly interfere with work
patient with incurable dementia. Much or social activities
can be achieved by careful analysis of the • Deficit represents major decline from previous level
of functioning
problems, defining what can be restored • Deficit cannot be explained exclusively by delirium,
and what cannot, even if the condition is CNS disorders, or major psychiatric illness
irreversible.
DIFFERENTIAL DIAGNOSIS
Common
✝
There are a variety of ‘dementias’ which most frequently
are categorized as cortical or subcortical. AD is the most • Degenerative disorders (e.g. Alzheimer’s
well-known example of a cortical dementia. Subcortical disease, i.e. AD; Parkinson’s disease, i.e. PD)
dementias include Parkinson’s, Huntington’s, and AIDS
dementia. The presentation of these two types of
• Vascular dementia (i.e. VaD; e.g. multi-infarct
dementias differs. dementia; single strategic infarct, lacunar state,
75
highly sensitive to AD, and may be useful in 1. Memory loss that is getting worse, e.g.
helping to make initial distinctions between cannot remember recent information,
patients experiencing cognitive changes forget names and appointments;
related to the normal aging process, and those 2. Difficulties with familiar activities, e.g.
experiencing cognitive deficits related to housewife to prepare a meal;
dementing disorders such as AD. It has 3. Language problems, e.g. has trouble expressing
reasonable inter-rater and test-retest thoughts, difficulty finding right words;
reliability, can be administered in a brief 4. Problems with spatial and temporal
period, and requires no clinical judgement orientation, e.g. get lost at familiar place;
and minimal training.11-13 5. Impaired capacity of judgement, e.g.
• Unless the patient has obvious and profound dress inappropriately;
cognitive impairment, it is generally 6. Problems with abstract thinking, e.g.
advisable to first interview him or her alone, financial mistakes, simple miscalculations;
followed by an interview with a close family 7. Leaving things behind, losing things;
member or caregiver (Table 12.4).14 8. Mood swings and behavioral changes,
Table 12.4: Questions for relatives to detect possible e.g. sudden mood swing without
early dementia
discernible cause, explosive outbursts;
• Have you noticed any change in personality? 9. Personality change, e.g. a friendly person
• Have you noticed increased forgetfulness or anxiety
about forgetting things (such as using lists more, etc)? becomes unexpectedly angry, jealous; and
• Have any activities been given up (hobbies and 10. Loss of initiative, e.g. lose interest in hobbies,
interests, shopping, dealing with finances) and why?
excessive procrastination, failure to thrive.
• Have you noticed nocturnal confusion or muddling
when out of usual routine or environment, or • Some of the potentially reversible causes of
unusual avoidance of new circumstances? dementia should be considered before a
• Have you noticed surprising failure to recognize
people (such as more distant relatives)?
diagnosis of AD is made (Table 12.2).
• Have you noticed undue difficulty in speech? • History should include drug list, head
• Have changes been gradual or has there been trauma, alcoholism, gastric surgery, risk
sudden worsening?
factors for HIV, functional disabilities, degree
• In an elderly with suspected dementia, of social support, and familial disorders.
cognitive testing should be ideally performed • Family history— As many as 40-50% of patients
after assessing their visual and hearing status. with FTD have an affected family member.
Their visual and hearing deficit may add to • Drug therapy of dementia—Although some
confusion and misinterpretation of end result, drugs have shown low risk for causing
leading falsely being classified them as cognition disorders in research studies, risk
demented. Patients with early or doubtful may be increased in frail older adults taking
dementia should be screened periodically up to several medications, and each case should
six months and possibly at intervals thereafter be reviewed carefully.15
• Ten early warning signs—Due to time constraint, • As cognitive decline is a feature of number of
it is difficult to perform screening test on all elderly medical conditions, the physical and systemic
patients coming to the office. Therefore, particular review must be thorough and detailed. Special
attention to the presence of warning signs attention must be paid for signs of common
suggestive of cognitive impairment is a useful problems at the patient’s age, including:
adjunct to maximize the gain: Nutritional status, anemia
Dementia 79
patients (e.g. cold intolerance, weight gain in Table 12.6: Comparison of features of delirium
hypothyroidism; and tremor, nervousness, and dementia
polyphagia, increased sweating in hyperthy- Delirium Dementia
roidism) are absent in elderly patients. Also, Acute onset Insidious onset
apathetic hyperthyroidism (i.e. paradoxical Profound confusion, clouding Clear consciousness
of or impaired consciousness,
presentation of hyperthyroidism with fatigue, drowsy, anxiety, agitation,
psychomotor slowing, depression, and weight bewilderment
Perceptual abnormalities Global impairment of cerebral
gain) may also occur in this population. (illusions, hallucinations, functions (e.g. recent memory,
Moreover, the common clinical features of imaginary conversations intellectual impairment, personality,
or activities) and behavior abnormalities)
hypothyroidism (e.g. fatigue, constipation, Paranoid ideas/delusions; Progressive course
cognitive loss) are often attributed to normal fluctuating course with
lucid intervals
aging. These factors, along with the fact that
Reversible Irreversible
hypothyroidism has an insidious onset and
affects multiple organ systems, may cause • “Despite the reemergence of syphilis with
considerable delay and difficulty in diagnosis. the AIDS epidemic, neurosyphilis is often
Therefore, it is important to have a high index neglected in the differential diagnosis of
of suspicion and a low threshold for screening patients with aseptic meningitis and mental
for thyroid dysfunction in elderly patients who status changes who are negative for the HIV.
present with vague, nonspecific symptoms The high mortality rate associated with
associated with MCI. delay in recognition, diagnosis, and
treatment of neurosyphilis obligates its
RED FLAGS inclusion in the differential of young
• Dementia and delirium can appear in the patients with cognitive decline.”19
same patient; however, it is important to • The mere presence of cerebral atrophy on a
distinguish dementia from delirium (acute scan should not be taken as evidence of
metabolically induced state of fluctuating dementing process. Atrophy can occur in
consciousness).Table 12.6 compares the individuals with no cognitive impairment.
features of delirium with those of dementia
• When dementia and delirium coexist, SELECTIVE GLOSSARY
making it difficult to separate them
Normal pressure hydrocephalus—NPH
clinically, it is not appropriate to give a
describes hydrocephalus in the absence of
patient a new diagnosis of dementia during
papilledema and with normal CSF opening
a state of delirium. With serial observations
as the delirium resolves, it becomes possible pressure on lumbar puncture. The clinical
to differentiate them symptom complex is characterized by
• HIV dementia may manifest with acute- abnormal gait, urinary incontinence, and
onset psychotic symptoms including dementia. It is an important clinical diagnosis
delusions and hallucinations, and these because it is a potentially reversible cause of
patients are at a higher risk for suicidal and dementia. The features of raised intracranial
homicidal ideation. The initial interview pressure are generally absent. The syndrome
should include screening for possible suicidal mainly occurs in the seventh or eighth decades
and homicidal ideation of life. Possible etiologic factors include head
Dementia 81
13. Mathew R, et al. Issues in evaluation of cognition Sacramento Area Latino Study of Aging study. J
in the elderly in developing countries. Ann Indian Am Geriatr Soc 2007;55(5):758-62. [PMID:
Acad Neurol [serial online] 2008 [cited 2008 Oct 1749319].
11];11:82-88. 18. Moretti R, et al. Risk factors for vascular dementia:
Available from: http://www.annalsofian.org/ Hypotension as a key point. Vasc Health Risk
text.asp?2008/11/2/82/41874 Manag 2008;4(2):395-402. [PMID: 18561514].
14. Macdonald AJD. ABC of mental health: Mental 19. Schiff E, et al. Neurosyphilis. South Med J 2002
health in old age. BMJ 1997;315:413-7. Sep;95(9):1083-7. [PMID: 12356119].
15. Lenzer J. FDA warns about using antipsychotic 20. Gauthier S, et al. Mild cognitive impairment. Lancet
drugs for dementia. BMJ 2005;330:922, doi:
2006 Apr 15;367(9518):1262-70. [PMID:
10.1136/bmj.330.7497.922-c
16631882].
16. Ho RC, et al. Metabolic syndrome and cognitive
decline in Chinese older adults: Results from the 21. Gimzal A, et al. Mild cognitive impairment. Turk
Singapore longitudinal ageing studies. Am J Psikiyatri Derg 2004 Winter;15(4):309-16. [PMID:
Geriatr Psychiatry. 2008;16(6):519-22. [PMID: 15622511].
18515697]. 22. Portet F, et al. What is a mild cognitive
17. Yaffe K, et al. Metabolic syndrome and cognitive impairment? Rev Prat 2005;55(17):1891-4. [PMID:
decline in elderly Latinos: Findings from the 16396229].
CHAPTER
13 Diarrhea
Rectal Swab for c/s suspicion of fat malabsorption (part one of the
test - stool fat greater than 5 to 7 g. / 24 hr.), and
• Useful only if the patient has persistent fever,
it has the added advantage of being able to
bloody diarrhea, immunocompromised, or
suggest maldigestion of dietary triglyceride
occasionally in traveler’s diarrhea. Routine
(part two of the test). If both part two and part
cultures will detect Shigella, Salmonella, and
one of the Sudan Test is positive, it indicates
Campylobacter species. Special media and
maldigestion of dietary triglyceride (pan-
conditions are required for pathogens such
creatic insufficiency, small bowel resection). A
as E. coli-057: H, Vibrio cholerae, yersinia, etc.
negative part two of the Sudan Test does not
FOBT exclude pancreatic insufficiency. Mineral oil,
• Positive fecal occult blood may indicate and the unabsorbable fat substitute, sucrose,
inflammatory, neoplastic disease, or ischemic polyester could cause false-positive Sudan
colitis. Tests (parts one and two).
• Important features in the history which help Table 13.1: The Manning criteria to distinguish IBS from
guiding the evaluation and management of organic disease
patients with acute diarrhea are: 1. Onset of pain associated with more frequent
Stool characteristics-frequency, consis- bowel movements
2. Onset of pain associated with looser bowel
tency, quantity, bloody, mucus-filled,
movements
purulent, or greasy; 3. Pain relieved by defecation
Presence of dysentery—fever, tenesmus, 4. Visible abdominal bloating
5. Subjective sensation of incomplete evacuation
blood, mucus, or both; more than 25% of the time
Symptoms of dehydration—thirst, 6. Mucorrhea more than 25% of the time
lethargy, postural giddiness, decreased
Table 13.2: Physical signs in diarrhea
urination; and
Physical signs Significance
Presence of associated symptoms—
General exam—Fever, Infection, IBD
nausea, vomiting, abdominal cramps,
weight loss, tachycardia, Alcohol abuse,
and significant upper or lower gastro- tremor, lymphadenopathy hyperthyroidism
intestinal bleeding (coffee ground emesis, TB, malignancy
hematemesis, melena, hematochezia). Skin — Erythema nodosum, IBD
dermatitis herpetiformis, Celiac sprue
• Some typical features of diarrhea and stools flushing, Carcinoid syndrome
associated with common diseases are: venous telangiectasis, Carcinoid syndrome
hyperpigmentation Addison’s disease,Peutz-
Nocturnal diarrhea—autonomic neuro- Jeghers syndrome
pathy, e.g. diabetes mellitus; Kaposi sarcoma AIDS
Diarrhea alternating with constipation - Punch’ purpura Amyloidosis
TB abdomen, laxative abuse, diverticu- Eyes—Iritis,uveitis IBD
losis, carcinoma of colon; Neck—Goiter Hyperthyroidism
Chronic bloody or melanotic stools with Lungs—Bronchospasm Carcinoid syndrome
Abdomen—mass, Crohn’s disease
weight loss - IBD, colonic malignancy; RLQ mass Colonic ischemia
Pale, bulky, greasy, frothy, foul-smelling Bruit
stools, which float in toilet, and associated PR—Rectal fistula, Crohn’s disease
painless fissure,
with nutritional deficiency, weight loss - perianal abscess
malabsorption syndrome; and
Diarrhea worsened by eating fatty foods - patient with new-onset bloody diarrhea.
steatorrhea. Development of the hemolytic uremic
• The Manning criteria (Table 13.1) are helpful to syndrome (HUS) or thrombotic thrombocy-
differentiate IBS from organic causes of diarrhea topenic purpura (TTP) should raise strong
• Table 13.2 illustrates common findings on suspicion of E. coli O157:H7 infection and
physical examination and their significance should lead to prompt evaluation
in patients with diarrhea. • Nocturnal diarrhea, unless occurring in a
known diabetic patient, usually points to an
RED FLAGS organic cause
• Abdominal TB (intestinal or peritoneal) can
• Infection with E. coli O157: H7 presents with mimic IBS and must be considered in chronic
many clinical manifestations and should be diarrheal disease, especially due to rising
included in the differential diagnosis for any HIV incidence
88
• In general, a patient with any of the following Melanosis coli—It is a pigmentation of the
warrants thorough work up: rectal and colonic mucosa due to use (or abuse)
Symptoms of dehydration: Particularly of anthraquinone type laxatives, and occurs
postural giddiness, diminished urine because of the deposition of a brown black
output, and excessive thirst; pigment called lipofuscin in the lamina propria
Advanced age (> 70 years); of the colon. The initial event is mucosal cell
Clinically suspected neoplasm, carcinoid death or apoptosis resulting from anthraqui-
syndrome, colonic ischemia; none laxative abuse. These cells are then
Compromised immune system; and phagocytosed by macrophages in lamina
Inflammatory diarrhea: fever, blood and propria producing lipofuscin, which gives a
mucus in stools. dark color to the colonic mucosa. Its incidence is
understandably higher in older population and
SELECTIVE GLOSSARY people who suffer from conditions like IBS and
chronic constipation, and is rising because of
Hemorrhagic colitis (E. coli O157:H7)— Entero-
the popularity of the herbal remedies containing
hemorrhagic E. coli (EHEC) strain designated E.
anthraquinone. Melanosis coli is a benign
coli O157:H7 serotype, causing Hemorrhagic
reversible condition with no malignant
colitis, is a gram-negative rod-shaped bacterium,
potential. The main importance of diagnosing
capable of producing potent toxins [verotoxic
Melanosis coli correctly lies in the fact that if it’s
(VT), shiga-like toxin] that cause severe damage
extensive, there may be difficulty in differentiating
to the lining of the intestine. Undercooked or raw
it from ischemic colitis. Withdrawal of the
hamburger (ground beef) has been implicated in
offending laxative, which nearly always can be
many of the documented outbreaks, however, E.
substituted with a bulk laxative, is sufficient
coli O157:H7 outbreaks have implicated alfalfa
treatment.
sprouts, unpasteurized fruit juices, milk, dry-
cured salami, lettuce, game meat, and cheese Peutz-Jeghers Syndrome (Pronunciation: p u tz
curds. The illness is characte-rized by severe
j a ’g e rz)—It is a hereditary disease caused by
cramping abdominal pain, and diarrhea which autosomal dominant mutations involving
is initially watery but becomes grossly bloody. Chromosome 19. It is characterized by the
Occasionally vomiting occurs. Fever is either presence of intestinal polyps, consistently in the
low-grade or absent. The illness is usually self- jejunum, and mucocutaneous pigmentation
limited and lasts for an average of 8 days. The with melanin spots (small, flat, brown or dark
majority of infections resolve completely; some blue spots with an appearance of freckles) of the
victims, particularly the very young, have lips, buccal mucosa, and digits. Isolated
developed HUS, characterized by renal failure melanotic mucocutaneous pigmentation
and hemolytic anemia. In the elderly, it may be without gastrointestinal polyps has also been
complicated by TTP with high mortality rate. described because of the genetic variability of
Because person-to-person transmission of E. coli the syndrome. History includes:
O157:H7 is not uncommon, and infection with • Family history of Peutz-Jeghers syndrome
this organism may cause severe disease, stool • Repeated bouts of abdominal pain in patients
specimens from all patients with a history of younger than 25 years
acute bloody diarrhea should be cultured for • Unexplained intestinal bleeding in a young
E. coli O157:H7. patient
Diarrhea 89
• Prolapse of tissue from the rectum antibiotic therapy, or can occur up to 6 weeks after
• Menstrual irregularities in females (due to discontinuation. Other causative factors for PMC
hyperestrogenism from sex cord tumors are abdominal surgery, colonic obstruction,
with annular tubules) uremia, and prolonged hypotension causing
• Gynecomastia in males (possible due to the hypoperfusion of the bowel. PMC also has been
production of estrogens from Sertoli cell described with lymphoma, leukemias, and
testicular tumors) advanced HIV infection. Diagnosis is primarily by
• Precocious puberty the detection of C. difficile, or its toxins in stool by
• Gastrointestinal intussusception with ELISA techniques, or direct culture of C. difficile from
bowel obstruction. the stool. CT scanning of the abdomen can be helpful
The risk of cancer remains elevated with by revealing the presence of bowel wall edema (>4
disregard to the presence or the absence, as well
mm) and inflammation, particularly in cases
as the number, of gastrointestinal polyps.
involving the right colon. Although these findings
Pseudomembranous colitis—PMC is a descriptive are nonspecific, imaging studies are helpful in
term for colitides associated with pseudo- patients with severe disease in detecting
membrane formation (or plaques) on the colonic or complications (e.g. toxic dilation, perforation).
small intestinal mucosa. Although small intestine
can be involved in PMC, most cases encountered in
REFERENCES
the modern era involve only the colon. Clostridium
difficile infection is responsible for virtually all cases 1. Achkar E. What is a practical approach to outpatient
of PMC; the basic mechanism in its pathogenesis evaluation of diarrhea in a previously healthy,
middle-age patient? Cleve Clin J Med 2001;68:104.
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(toxin A is an enterotoxin, while toxin B is a mean?Am J Gastroenterol 1994;89(8):1160-4.
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3. Fernández-Bañares F, et al. Systematic evaluation
spectrum of illnesses, ranging from mild diarrhea of the causes of chronic watery diarrhea with
to life-threatening PMC. The anaerobes that are functional characteristics. Am J Gastroenterol 2007
normally present in the colon control colonization Nov; 102(11):2520-8. Epub 2006. [PMID:
17680846 : Abstract].
by C. difficile; therefore, antibiotics that are most 4. Bertomeu A, et al. Chronic diarrhea with normal
active against anaerobic organisms are more stool and colonic examinations: organic or
commonly associated with PMC. Although functional? J Clin Gastroenterol. 1991;13(5):531-
6. [PMID: 1744388: Abstract].
clindamycin and lincomycin classically have been
5. Fine KD, et al. AGA Technical Review on the
linked to PMC, virtually all antibiotics can cause Evaluation and Management of Chronic Diarrhea.
PMC; its onset being within days after initiation of Gastroenterology 1999;116:1464–86.
CHAPTER
14 Dyspepsia
or “is there anything that you are worried Any associated chest pain, dyspnea, or
about regarding these symptoms?”, may sweating
help elicit concerns, relieve worries, and Pain radiation to arm, jaw, shoulder, back
improve patient satisfaction. Associated with dizziness, syncope, or
Does the patient accept stressful lifestyle transient mental status changes
and/or stressful life events playing a History of IHD or cardiac risk factors
contributing role? Pulse and blood pressure abnormality.
Is there a concurrent psychiatric diag- • Alarm symptoms and signs suggestive of
nosis such as anxiety, depression, organic cause in dyspeptic patients, and in
somatization, alcoholism, and drug whom endoscopy is indicated, irrespective
dependency? of their age, include:
What is the family’s involvement in Progressive unintentional weight loss >
terms of emotional and moral support? 3 kg (malignancy)
When healthy and supportive behaviors Constant or severe abdominal pain,
are present, the family members can be nocturnal pain (malignancy)
recruited to help the patient toward Pain that radiates to the back (posteriorly
recovery; or else counseling may be located ulcer, pancreatitis)
indicated. Persistent heartburn, regurgitation,
Unless the clinical data (e.g. occult blood in vomiting (obstruction)
the stool, significant weight loss, or Hematemesis, melena, anemia (chronic
abnormal physical findings) suggest the GI bleeding)
possibility of other disorders, the diagnostic Progressive difficulty in swallowing
studies ordered on the first visit should be (esophageal lesion)
limited. The choice depends on the nature Jaundice (alcoholic liver disease,
and severity of symptoms and associated
metastasis)
clinical factors (see below - alarm signs and
Epigastric mass or suspicious barium
symptoms). However, in the majority of
meal
patients with functional dyspepsia,
Unresponsive to the sequential treat-
wherein a variety of emerging therapies
ments for H. pylori eradication
are being developed, but unfortunately,
Previous peptic ulcer
to date, all of these therapies have yielded
Family history of cancer.
only marginal results. Therefore, the
physician’s most effective approach is to
SELECTIVE GLOSSARY
maximize the physician-patient
relationship to help them cope with their Frontotemporal dementia (FTD)— It is a group
symptoms.15 of diseases in which parts of the brain (the
frontal and temporal lobes) shrink, or atrophy,
RED FLAGS causing changes in personality and behavior.
• It is prudent to consider any dyspeptic People with FTD may have:
symptoms as IHD, especially under follo- • Loss of social component—Not express any
wing circumstances: caring for others.
Dyspepsia 95
Ulcers that is refractory to standard therapy 5. Tally NJ, et al. The Rome III Classification of
dyspepsia: Will it help research? Dig Dis 2008;
Multiple ulcers
26(3):203-9. Epub 2008. [PMID: 18463436:
Giant ulcers, larger than 2 cm Abstract].
Recurrent ulcers 6. Suzuki H, et al. Therapeutic strategies for
functional dyspepsia and the introduction of the
Ulcers with unexplained diarrhea
Rome III classification. J Gastroenterol 2006;
Strong family history of ulcers 41(6):513-23. [PMID: 16868798: Abstract].
Hypercalcemia 7. Malfertheiner P. Current concepts in dyspepsia:
Duodenal ulcer that is not related to A world perspective. Eur J Gastroenterol Hepatol
1999; 11 Suppl 1:S25-9. [PMID: 10443909:
Helicobacter pylori infection or nonsteroidal Abstract].
anti-inflammatory drug use. 8. Wang A, et al. The clinical overlap between
A family history of nephrolithiasis, hyper- functional dyspepsia and irritable bowel
syndrome based on Rome III criteria. BMC
parathyroidism, and gastrinoma also may be
Gastroenterol 2008;8:43.[PMID: 18808723 : Free
present. Fasting serum gastrin (serial measure- full text].
ments on different days) is the best single 9. Geeraerts B, et al. Functional dyspepsia: Past,
screening test. To localize the gastrin-secreting present, and future. J Gastroenterol
2008;43(4):251-5. Epub 2008 May 6. [PMID:
tumor, computer-assisted tomography, endos- 18458839: Abstract].
copic ultrasound, and somatostatin receptor 10. Van kerkhoven LA, et al. Functional dyspepsia:
scintigraphy provide useful help; but most Not All Roads Seem to Lead to Rome. J Clin
Gastroenterol 2008. [PMID: 18719513: Abstract].
recently endoscopic ultrasound with high 11. Lundquist P, et al. Symptom criteria do not
resolution transducers appear to improve distinguish between functional and organic
preoperative site localization. dyspepsia. Eur J Surg 1998;164(5):345-52. [PMID:
9667468: Abstract].
12. Sander JO Veldhuyzen van Zanten. Treating non-
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9, doi: 10.1136/bmj.321.7262.648.
1. Bytzer P, et al. Dyspepsia. Ann Intern Med 2001;
13. Hansen JM, et al. Management of dyspeptic
815-22.
patients in primary care. Value of the unaided
2. Heading RC. Definitions of dyspepsia. Scand J
clinical diagnosis and of dyspepsia subgrouping.
Gastroenterol Suppl. 1991;182:1-6. [PMID:
Scand J Gastroenterol 1998;33(8):799-805.
1896823: Abstract].
3. Drossman DA, moderator. AGA Clinical [PMID: 9754725: Abstract].
Symposium — Rome III: New Criteria for the 14. Tally NJ, et al. Lack of discriminant value of
Functional GI Disorders. Program and abstracts dyspepsia subgroups in patients referred for upper
of Digestive Disease Week; May 20-25,2006; Los endoscopy. Gastroenterology. 1993;105(5):1378-
Angeles, California. [Sp461-469]. In: From Rome 86. [PMID: 8224642: Abstract].
to Los Angeles – The Rome III Criteria for the 15. Saad RJ, et al. Review article: Current and
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http://www.medscape.com/viewarticle/533460. Aliment Pharmacol Ther 2006;24(3):475-92.
Accessed on 13-11-08. [PMID: 16886913: Abstract].
4. Tack J, et al. Functional gastroduodenal disorders. 16. Jennifer Lynn Bonheur. Gastrinoma. Web site -
Gastroenterology. 2006;130:1466-79. [PMID: http://www.emedicine.com/med/ TOPIC2678.
16678560: Abstract]. HTM. Accessed on 15-11-08.
CHAPTER
15 Dysphagia
strictures — benign (smooth) or malignant function. However, patients with mass lesion
(irregular and tortuous ‘rat-tail’ deformity); or other lesions identified by barium
esophageal dysmotility or spasm (‘corkscrew’ swallow should undergo EGD with cytology
deformity); achalasia cardia (‘bird’s beak’ and biopsy(Bx) to confirm the diagnosis
deformity with dilated proximal esophagus, • EGD allows certain therapeutic interven-tions:
and air-fluid level); hiatus hernia; and To remove an impacted food bolus or
dysphagia due to external compression such foreign body,
as mediastinal growth or aortic aneurysm. It To dilate strictures with balloons or
also reduces the risk of endoscopic perforation dilators,
in these disorders, especially in those having To destroy a lesion by laser, cautery, or
pouch or diverticulum. Different consistencies photodynamic therapy, and
of barium (solid, semisolid, or liquid; barium To assist placing of implants or stents for
pill, or a standard marshmallow) further assess advanced esophageal malignancy.
swallowing disorders, as delays in transport
may not be apparent with simple liquid barium. Esophageal Manometry (Stationary and
If the patient has noted a problem with a specific Ambulatory)
solid food, a mixture barium paste plus the
• Indicated to assess EMDs, especially if no
offending food may provide definitive
obstructing lesion is identified by EGD or
information.5 The disadvantage of barium X-
barium swallow. Esophageal peristaltic
rays is that they are relatively insensitive in
contractions—their amplitude, duration,
detecting mucosal disease, even if air contrast
velocity, and coordination, as well as upper
technique is added. Fluoroscopy can detect
and lower end sphincter pressure studies,
GERD.
and their temporal correlations between
EGD symptoms and reflux can be evaluated. On
• Fiberoptic endoscopy directly visualizes the some patients esophageal manometry is used
esophageal mucosa as well as other areas of in combination with 24 hours pH monitoring
the upper GI tract. Its direct view is superior to evaluate uncommon causes of dysphagia,
to barium X-rays for assessing mucosal e.g. DES, NE, achalasia, unexplained chest
disease of the esophagus, and the esophago- pain, and scleroderma.
scope permits assessment of structural
Esophageal 24-hours pH Reflux Study‡‡ 6
lesions that are identified. Furthermore,
punch biopsies and/or brush cytology of • Accepted as the most accurate method for
specific lesions are easily obtained through diagnosing reflux. It is, however, uncomfor-
the endoscope. Microscopic evidence of table and expensive investigation. Therefore,
esophagitis may be found even when the indicated especially:
mucosa looks grossly normal If barium swallow or EGD studies are
• Endoscopy is the single most useful test in negative,
the evaluation of patients with reflux In patients being considered for antire-
symptoms, as it permits one to establish the flux surgery, and
presence or absence of esophagitis or
Barrett’s esophagus. Endoscopy gives little ‡‡
This technique has been revolutionized by a catheter-
reliable information regarding esophageal less, wireless pH system.
101
In the evaluation of patients with chest transit time in the upper, middle and lower thirds
pain of undetermined origin. of the esophagus. Scintigraphy also can be
• An abnormal result is indicated by a pH of combined with 24-hour pH manometry to
<4 for more than 3% of the time when the check the cause of chest pain between
patients are supine, and for > 8% of the time esophageal and possible cardiac factors.
when they are erect.
CT Scan/MRI
Videofluoroscopic Swallowing Function
• In suspected structural CNS abnormalities, e.g.
Study (VSFS)‡‡
primary or secondary tumors, MS; or, aortic
• The VSFS—performed jointly by a physician
vascular lesions, e.g. aneurysm, lusorian artery.
(typically a radiologist) and a speech-
language pathologist—is the gold standard Muscle Enzymes
for evaluating the mechanism of swallo- • Elevated serum CK may be observed in
wing. For this study, the patient is seated motor neuron diseases, e.g. polymyositis,
comfortably and given foods mixed with dermatomyositis.
barium to make them radiopaque. The
patient eats and drinks these foods while TFTs
radiographic images are observed on a video • To detect hypothyroid or hyperthyroid
monitor and recorded on videotape. disorders causing dysphagia, e.g. Graves’
• VSFS permits close observation of all structures
disease or thyroid carcinoma.
involved in swallowing process, i.e. lips,
tongue, palate, pharynx, larynx, and proximal RF, ANA
esophagus; indicated especially in patients at • In patients with autoimmune disorders, e.g.
risk for silent aspiration, e.g. patients with
RA, SLE, scleroderma.
stroke, or neurologic impairment such as
cerebral palsy, MS, PD, MG, motor neuron
Antiacetylcholine Antibodies
disease, systemic sclerosis, and connective
tissue disorders such as SLE, and RA. • Antiacetylcholine receptor antibody activity
• VSFS not only allows estimation of risks of may be elevated in patients suspected with
aspiration and respiratory complications, MG, and polymyositis.
but also helps in determining dietary
modifications and training in swallowing Genetic Analysis
techniques and maneuvers. • For example, in familial forms of ALS, or
muscular dystrophy.
Radionucleotide Study7 (Tc-99m Sulfur Colloid
Bolus) CLINICAL NOTES
• These assess gastroesophageal reflux, esophageal
motility disorders, or to identify silent aspiration. • It is important to ascertain that the patient
In GERD, reflux is present if the isotope is seen to truly has dysphagia, because some may
travel back up into the esophagus. In esophageal misinterpret ‘lump in the throat’ (globus) as
motility disorders, computer programs measure dysphagia
• The clinical features of ‘globus’ sensation may
‡‡
The VSFS is similar to the MBS, except that the protocol occur with organic disease in the neck, pharynx,
for the MBS specifies quite small bolus volumes and does
or cervical esophagus; hence this diagnosis
not include drinking from a cup. In practice, the terms
“VSFS” and “MBS” are often used interchangeably. should only be made after a complete evaluation
102 Diagnosis: A Symptom-based Approach in Internal Medicine
• By asking following specific questions, the Table 15.2: Types of bolus causing dysphagia
cause of dysphagia can usually be identified: Bolus Cause of dysphagia
Do you have difficulty swallowing? In what Dysphagia with both Muscular or neural control
way? liquids and solids from disorders of swallowing
the outset (bulbar, pseudobulbar palsy);
Do you have this sensation without motility disorders
swallowing food? Dysphagia initially for Esophageal obstructive
solids lesions (rings, webs,stricture)
Can you localize dysphagia? Intermittent, non- Benign obstructive lesions
Do you have trouble with solids or liquids? progressive dysphagia, (rings, webs, stricture);
more for solids than esophageal spasm
Is the swallowing difficulty greater for liquids
solids or liquids? Progressive dysphagia Obstructive inflammatory
first for solids, then for stricture; achalasia;
Is the dysphagia intermittent or progressive? semisolids and liquids malignancy (carcinoma
Do you have heartburn? esophagus); scleroderma
Cold food or beverages Esophageal dysmotility,
Any eating habits adopted to relieve precipitating dysphagia especially spasm
symptoms? or causing chest pain
Are there any associated problems, e.g. stress, Table 15.3: Signs and symptoms of causes for dysphagia
cough, chest pain, dysphonia, collagen
Signs and symptoms Diagnostic clues
disease, immunosuppression, weight loss? Sudden dysphagia Obstructive dysphagia,
• Generally, dysphagia at the very beginning esophagitis, brainstem
stroke, acute thyroiditis,
of swallowing characterizes oropharyngeal Intermittent symptoms Rings and webs, DES, NE
dysphagia; whereas dysphagia a few seconds Progressive symptoms Obstructive lesions,
carcinoma, scleroderma
after starting to swallow indicates an esopha- Difficulty initiating swallow Oropharyngeal dysphagia
geal cause Food ‘sticks’ after swallow Esophageal dysphagia
Pain with dysphagia Esophagitis—infection, pill-
• Onset—Acute dysphagia is commonly due induced
to oropharyngeal causes such as infection, Regurgitation of old food, Zenker’s diverticulum
halitosis
inflammation, food bolus impaction, or Ulcers on the tongue; Lesions obvious on
stroke (see above). Intermittent dysphagia tonsillar infection/abscess; examination of the oral
retropharyngeal abscess cavity
suggests esophageal dysmotility syndrome, Tongue fasciculations ALS
webs, or rings. Progressive dysphagia Pallor, koilonychia, Plummer-Vinson syndrome
indicates an organic cause such as achalasia, hypochromic microcytic
anemia
carcinoma, mediastinal expanding lesion, or Mask-like facies, saliva Parkinson’s disease
other systemic disorder, e.g. PD, scleroderma drooling from the mouth,
tremors, cog-wheel rigidity
• The type of bolus that elicits symptoms of Drooping of eyelids, Myasthenia gravis
dysphagia may indicate its cause (Table 15.2) diplopia, swallowing
becomes more difficult
• Odynophagia often accompanies dysphagia in as meal progresses,
esophagitis, pharyngitis, opportunistic extreme weakness
infections, pill esophagitis, diffuse esopha- Palpable mass medial to Pharyngeal pouch
sternomastoid
geal spasm, rheumatoid arthritis (inflam- Hoarseness of voice, Mediastinal syndrome,
mation of cricoarytenoid joint), or malignant visible neck, goiter, recurrent laryngeal nerve
tracheal compression palsy, retrosternal goiter
process involving the mucosa Puckered and narrow
• Associated signs and symptoms as impor- mouth, inability to open Scleroderma, progressive
mouth, thickened-hard-and systemic sclerosis
tant clues for possible cause of dysphagia tight skin, Raynaud’s
are given in Table 15.3 Phenomenon
Dysphagia 103
endoscopy to aid in cancer detection to identify furrows, adherent white plaques, or a friable
abnormal mucosa, may be used as a means of (crepe paper) mucosa, prone to tearing with
esophageal cancer screening. In patients who minimal contact; or even normal looking
are at increased risk for squamous cell esophagus. Frank esophagitis is not part of the
carcinoma, the dye stains the glycogen in macroscopic endoscopic picture of eosinophilic
normal squamous epithelium a dark brown esophagitis. The most important element in the
color. Areas that are unstained, particularly diagnosis of eosinophilic esophagitis is to know
those that are larger than 5 mm in size, are its macro- and micromorphological character-
likely to be dysplastic or malignant, and can be istics. Biopsies from the proximal to the distal
readily targeted for endoscopic biopsy. esophagus demonstrating > 15-20 eosinophilic
Dysphagia lusoria—This is caused by a rare granulocytes per high powered field favor the
anomaly of the subclavian artery. This artery diagnosis. With increasing recognition, this
arises from the aortic arch distal of the left entity is taking its place as an established cause
subclavian artery, crossing the midline, behind of solid food dysphagia.
the esophagus. This abnormality is generally Progressive systemic sclerosis—Patients with
silent and often an incidental X-ray finding, but progressive systemic sclerosis usually present
can result in dysphagia, which generally with heartburn, dysphagia, and regurgitation. The
appears after the age of 40 years. The diagnosis oral, pharyngeal, and esophageal phages of
can be overlooked at endoscopy, but barium swallowing can all be affected. Progressive
contrast examination of the esophagus shows a atrophy and fibrosis of esophageal smooth muscle
characteristic diagonal impression at the level is usually prominent. Gastroesophageal reflux is
of the fourth thoracic vertebra. CT with contrast frequent. Esophageal manometry typically shows
study or MR angiography confirm the diagnosis lower pressures and sometimes aperistalsis. Poor
and exclude aneurysms. peristalsis, decreased lower esophageal sphincter
Eosinophilic esophagitis—This is an emerging pressures, and gastroesophageal reflux can result
cause of dysphagia, typically seen in young in a transition from a patulous dilated esophagus
adults. Often, the history of dysphagia dates to to one that is strictured and scarred. Barrett
adolescence. In children it is responsible for esophagus may develop. The presence of
feeding disorders, vomiting, reflux symptoms oropharyngeal disease is usually accompanied by
and abdominal pain, and in adults it causes pulmonary disease. Patients with progressive
intermittent solid food dysphagia or food systemic sclerosis may also have xerostomia
impaction. The natural history of this disorder (which is frequently due to medications), dental
has not been well-characterized, but appears problems (due to fibrosis of the ligamentous tooth
to be marked by periods of spontaneous attachments), trigeminal nerve involvement
remission and exacerbations that are not linked (decreased bolus sensation), and lingual atrophy
to specific factors, although food allergies and that can also contribute to dysphagia.
exposure have been implicated. Some have a Schwartz ring (pronounced - shats-ke or schatz·ki’s
history of atopy. Endoscopy may reveal a ring)—This is narrowing in the lower part of the
number of subtle features that include a esophagus, consisting of a membrane-like
‘corrugated’ esophagus with fine rings; a structure, lined by squamous epithelium on its
diffusely narrowed esophagus that may have superior aspect and columnar epithelium
proximal strictures; the presence of linear inferiorly. Such a ring is quite common, being
106 Diagnosis: A Symptom-based Approach in Internal Medicine
16 Dyspnea—Acute
17 Dyspnea—Chronic
measure functional capacity. The six minute Thoracic Society. Am Rev Respir Dis 1991;
144(5):1202-18. [PMID: 1952453].
walk distance (6MWD) can be correlated with 7. Aggarwal AN, et al. Comparison of Indian
patient’s height, BMI, Borg scale, spirometric reference equations for spirometry interpret-
parameters and diffusion capacity. Absolute ation. Respirilogy 2007;12(5):763-8. [PMID:
17875069].
contraindications to the test include an history 8. Yap LB, et al. Natriuretic peptides, respiratory
of unstable angina or MI during the previous disease, and the right heart. Chest 2004;
month; relative contraindications include 126(4):1330-6. [PMID: 15486400: Free full text].
9. Tsuchida K, et al. Plasma brain natriuretic peptide
resting tachycardia (heart rate >120/mit), concentrations and the risk of cardiovascular
uncontrolled hypertension, or arthritis and events and death in general practice. J Cardiol
2008;52(3):212-23. Epub 2008 Aug 26. [PMID:
other musculoskeletal disease.
19027599: Abstract].
10. Sirithunyanont C, et al. Role of the plasma brain
REFERENCES natriuretic peptide in differentiating patients with
congestive heart failure from other diseases. J
1. Enright PL. Respiratory Care: The Six-minute Med Assoc Thai 2003;86 Suppl 1:S87-95. [PMID:
Walk Test. 2003;48(8):783-5. 12866774: Abstract].
2. Al Ameri HF. Six minutes walk test in respiratory 11. Kontrus M, et al. Spiral-CT [corrected] in chronic
diseases: A university hospital experience. Ann lung thromboembolism. Radiologe 1996 Jun;
Thorac Med 2006;1:16-19. 36(6):496-502. Erratum in: Radiologe 1996;
3. Kervio G, et al. Intensity and daily reliability of 36(8):645. [PMID: 8767120: Abstract].
the six-minutes walk test in moderate chronic heart 12. Remy-Jardin M, Remy J. Spiral CT angiography
failure patients. Arch Phys Med Rehabil 2004; of the pulmonary circulation. Radiology 1999;
85(9):1513-8. [PMID: 15375827]. 212(3):615-36. [PMID: 10478224: Abstract].
4. Pereira de Sousa LA, et al. Six-minute Walk Test 13. Singh RB, et al. Tobacco consumption in relation
in Patients with Permanent Cardiac Pacemakers. to causes of death in an urban population of north
Cardiopulm Rehabil Prev 2008;28(4):253-7. India. Int J Chron Obstruct Pulmon Dis 2007;
[PMID: 18628656: Abstract]. 2(2):177-85. [PMID: 18044690: Abstract].
5. Roul G, et al. Does the 6-minute walk test predict 14. Woloshin S, et al. The risk of death by age, sex,
the prognosis in patients with NYHA class II or III and smoking status in the United States: Putting
chronic heart failure? Am Heart J 1998;136(3):449- health risks in context. J Natl Cancer Inst 2008 Jun
57. [PMID: 9736136: Abstract]. 18; 100(12):845-53. Epub 2008 Jun 10. Erratum in:
6. Lung function testing: Selection of reference J Natl Cancer Inst 2008;100(16):1133. [PMID:
values and interpretative strategies. American 18544745: Abstract].
CHAPTER
18 Facial Asymmetry
and Weakness
• Bell’s palsy (HSV-1,CMV, EBV, rubella, and • To evaluate for diabetes mellitus.
mumps)
• Cerebrovascular accidents (stroke) VDRL
• CNS infections (bacterial, TB, abscess, • Indicated in neurosyphilis.
malignant otitis media)
• CNS tumors (posterior fossa tumors, CXR
acoustic neuroma)
• To exclude sarcoidosis or to rule out TB in
• Diabetic neuropathy
selected patients before treating with steroids.
• Head trauma (fractures of the temporal bone).
Occasional INVESTIGATIONS—SPECIFIC
• Ramsay Hunt syndrome CT Skull
• Guillain-Barré syndrome (GBS)
• CT scan of the temporal bone for evidence of
• Infections (HIV, cerebral malaria, Lyme
temporal bone fracture.
disease, chickenpox) • Associated anomalies of the external ear,
• Tumors invading temporal bone (cholestea- middle ear, inner ear, etc. can be assessed.
toma).
MRI with Gadolinium
Rare
• Generally indicated in patients with
• Infections (tetanus, leprosy, poliomyelitis, atypical features such as:
diphtheria) Hearing loss
• Multiple sclerosis (MS) Multiple cranial nerve deficit
• Myasthenia gravis Signs of limb paresis or sensory loss
• Motor neuron disease Lesion suggesting a posterior fossa lesion
• Sarcoidosis as the cause of CN VII palsy
• Metastasis to temporal bone (from carci- To exclude neoplasms, stroke, MS, or
noma breast, bronchus, prostate) other structural lesions.
• Neoplasm of base of the skull or parotid gland CSF
• Carcinomatous or leukemic meningitis • Indicated only in inflammation, granuloma,
• Surgery of mastoid, parotid or malignancy is a consideration.
• Melkersson-Rosenthal syndrome (MRS: vide • A mild pleocytosis of the CSF may be seen in
infra ↓↓). Bell’s palsy.
122 Diagnosis: A Symptom-based Approach in Internal Medicine
elevating one eyebrow at a time. UMN lesion is appearance. It is an important physical sign, as
usually unilateral as in CVA and neoplasm and it is most often seen in cases of multiple sclerosis
rarely bilateral as in GBS and MS. LMN lesion and with neoplastic and inflammatory lesions
may be unilateral or bilateral (Table 18.3) of the brainstem, and if noted makes brain
• Facial myokymia is a rare form of involuntary imaging (MRI) mandatory
movement affecting the facial muscles. It is • Mimic palsy, also known as emotional facial palsy
clinically defined as continuous twitching of (EFP) refers to weakness or abolition of facial
small bands or strips of muscles that give an movements during emotions like smiling or
undulating or rippling appearance to overlying weeping, while voluntary movements do not
skin, descriptively called as ‘bag of worms’ show any deficit. EFP has been described in
124 Diagnosis: A Symptom-based Approach in Internal Medicine
Table 18.2: Difference between UMN and LMN type of CN VII palsy
UMN type LMN type
• Upper face escapes; only lower face • Whole face is involved on one side
affected, i.e. eyes can be closed,
forehead wrinkled but teeth cannot
be shown with weakness of lips
and buccinator muscles
• Emotional movement retained. • Emotional movements are lost
In bilateral UMN lesions whole face
is paralyzed and emotional movements
are also affected
• Bell’s phenomenon*—absent • Bell’s phenomenon*—present
• Facial muscles—not atrophied • Facial muscles—fasciculations/atrophy on the affected
side may be present
• Taste sensation—preserved • Taste sensation—may be lost
• Corneal reflex—present • Corneal reflex—lost
• Hemiplegia—usually associated with • Hemiplegia—may be an isolated phenomenon; and
ipsilateral hemiplegia or hemiparesis or if associated with hemiplegia, it is always crossed
monoplegia
• Plantar response—extensor on the • Plantar response—flexor on the paralysed side of the face;
paralysed side of the face may be extensor on the opposite side
• Examples—CVA, CNS neoplasms, MS, • Examples—Bell’s palsy, acoustic neuroma, GBS,
syringobulbia, motor neuron disease Lyme disease
* Bell’s phenomenon, i.e. if the patient tries to close his affected eye, the eyeball turns upwards and inwards.
Table 18.4: Etiology for bilateral facial weakness of HIV, paralysis can be directly due to the
Bilateral nuclear lesions: Pontine viral infection. In later stages paralysis is
• Infarction more likely to be associated with the
• Hemorrhage opportunistic infections or tumors associated
• Multiple sclerosis, vasculitis
• Tumor with severe immune deficiency.8
• Infection • Dissatisfaction with facial appearance seems
• Syringobulbia
to be a factor in many suicides. In a patient
• Motor neuron disease
• Möbius syndrome, i.e. facial paresis with ophthal- with facial asymmetry (Table 18.5), negative
moplegia coping strategies may include avoidance of
Bilateral infranuclear lesions: social contact, alcohol misuse, and
• Bell’s palsy aggression. It is dangerous for the physician
• GBS
• HIV
to dismiss a complaint of this type or
• Poliomyelitis labelling these patients as ‘psychiatric’.9
• Postdiphtheritic palsy
• Bilateral parotid disease
SELECTIVE GLOSSARY
• Bilateral otitis media
• Leukemia
• Melkersson syndrome, i.e. recurrent facial palsy
Melkersson-Rosenthal syndrome—MRS is an
with facial edema, unilateral or bilateral; and lingua uncommon condition of unknown cause.
plicata (scrotal tongue) Several factors, such as infection, autoimmunity,
Muscle disease: neurotropic factors, atopy, and hypersensitivity
• Myasthenia gravis
to food additives have been implicated in the
• Myotonic dystrophy
• Fascioscapulohumeral dystrophy pathogenesis, but none of them are proven. An
autosomal dominant inheritance with variable
Table 18.5: Differential diagnosis of altered facial counter expression has been proposed in some cases of
• Trauma, burns, contractures MRS.
• Hemiatrophy (e.g. localized scleroderma, Parry-
Romberg syndrome)
Although early manifestations of the
• Hemihypertrophy· syndrome can start at any age, MRS generally
• Lipodystrophy develops at the end of the second decade of life.
• Unilateral postural edema
• Paget’s disease, fibrous dysplasia The classical triad includes recurrent orofacial
• Massive parotid gland swelling edema involving predominantly the lips
• Acromegaly (macrocheilitis), peripheral facial palsy and
• Cushingoid faces (moon face)
• Micrognathia scrotal tongue, although it is accepted that the
• Congenital — absence of condyle of mandible presence of two manifestations is sufficient to
make the diagnosis. Facial palsy can be
• Bilateral facial palsy seen in pregnancy may be a unilateral or bilateral; may tend to be recurrent
sign of serious underlying disease. Some to such an extent that it’s sometimes described
authors suggest that Bell’s palsy increases the as intermittent. Recurrences don’t follow any
risk of hypertension and toxemia of pregnancy, pattern—each recurrence can be on the same
whereas the pregnant state, in turn, may affect side, alternating side, or bilateral. Disturbances
the course and severity of disease.7 of salivary, lacrimal and nasal secretion,
• Peripheral facial palsy has been considered disorders of taste and vision, migraine, and
as a possible neurological complication of the febrile symptoms occasionally accompany the
early stages of HIV infection. In the early stage condition. MRS is an unusual cause of facial
126 Diagnosis: A Symptom-based Approach in Internal Medicine
swelling that can be confused with angioedema. 3 . Cohen Y, et al. Bell palsy complicating pregnancy:
A review. Obstet Gynecol Suey 2000;55(3):184-
Diagnosis of this syndrome can easily be missed, 8. [PMID: 10713984: Abstract].
as the obvious symptoms may look like Bell’s palsy. 4. Mari I, et al. Facial diplegias during pregnancy.
Presse Med 2000;29(40):2213-5. [PMID:
However, unlike MRS, Bell’s palsy recurrences tend 11196051: Abstract].
to be separated by wide time spans. 5. Gbolade BA. Recurrent lower motor neurone
facial paralysis in four successive pregnancies. J
Laryngol Otol 1994;108(7):587-8. [PMID:
REFERENCES 7930897: Abstract].
6. James DG. Differential diagnosis of facial nerve
1. Leigh W, et al. Are human preferences for facial
palsy. Sarcoidosis Vasc Diffuse Lung Dis 1997;
symmetry focused on signals of developmental 14(2):115-20 [PMID: 9306501: Abstract].
instability? Behavioral Ecology Advance Access 7. Mylonas I, et al. Idiopathic facial paralysis (Bell’s
published on September 1, 2004, DOI 10.1093/ palsy) in the immediate puerperium in a patient
beheco/arh099.Behav. Ecol. 15: 864-71. Web site: with mild preeclampsia: A case report. Arch
http://beheco.oxfordjournals.org/cgi/reprint/15/ Gynecol Obstet 2005;272(3):241-3. Epub 2005
5/864. Accessed on 09-11-08. May 3. [PMID: 15868184: Abstract].
2. Michael ER, et al. Detecting hemifacial asym- 8. Abboud O, et al. Isolated bilateral facial paralysis
metries in emotional expression with three- revealing AIDS: A unique presentation.
dimensional computerized image analysis. Proc Laryngoscope. 2008;118(4):580-4. [PMID:
Biol Sci 2004;271(1540): 663-8. Web site: http:// 18197137: Abstract].
w w w. p u b m e d c e n t r a l . n i h . g o v / p i c r e n d e r. 9. McGrouther DA. Facial disfigurement. BMJ
fcgi?artid=1691649&blobtype=pdf. Accessed on 1997;314(7086):991. [PMID: 9112836: Free full
09-11-08. text].
CHAPTER
19 Facial Swelling
INVESTIGATIONS—GENERAL INVESTIGATIONS—SPECIFIC
CBC TFTs
• Elevated THS values indicate hypothyroi-
• Leukocytosis in infections, cellulitis, dental
dism, cretinism.
abscess.
• Eosinophilia in allergic disorders, trichinosis. ANA
• Anemia of iron, folate deficiency in chronic
• To screen for underlying autoimmune
disease.
disorder.
ESR
Parotid Sialography
• Elevated in infection, and autoimmune
• To detect any abnormality and obstruction
disorders.
of the Stensen’s duct.
Urinalysis
CT/MRI Brain
• Proteinuria, hematuria, and RBC casts in
• For evidence of cavernous venus thrombosis,
renal disease.
Cushing’s syndrome (pituitary microadenoma
Plasma Protein secreting ACTH tumor).
• In hypoproteinemic edema, total plasma • In patients with CNC signs and symptoms
protein level is less than 5 g/dl and the plasma due to trichinellosis.
albumin content is below 1.5-2.5 g/dl.
CT/MRI Lungs, Abdomen
Urea, Creatinine • To confirm CXR lesions, and adrenal adenoma.
• Elevated in renal failure.
CT/MRI PNS
Blood Glucose • For detailed evaluation of PNS; obscure
• In diabetic patients, especially in Type 1 DM, lesions such as polyps, tumors may be
insulin therapy may be associated with the evident causing recurrent sinusitis and facial
development of transient edema. edema.
129
20 Fever of Unknown
Origin
Table 20.1: Minimum diagnostic work-up to fungal lesions, and Pneumocystic carinii
qualify as FUO** pneumonia may be suspected.
• Comprehensive medical history
• Repeated physical examination Plain X-ray of Bones
• Complete blood count and differential • In osteomyelitis, periosteal reaction and
• Microscopic examination of blood film, routine
blood chemistry (including lactic dehydrogenase, sequestration develop 10-15 days later; for
bilirubin, and liver enzymes) earlier diagnosis radionucleotide bone scan
• Blood sedimentation rate
is preferred.
• Urinalysis and microscopy
• Chest radiography
• Blood and urine culture (before initiation of
US Abdomen, Pelvis
antibiotic treatment) • To rule out intra-abdominal masses or
• Antinuclear antibodies
• Rheumatoid factor
abscesses of liver, spleen, kidney, and pelvic
• Serology for CMVs and Epstein-Barr virus organs.
• HIV antigen and antibody tests
• Hepatitis serology (if abnormal liver enzyme tests LFT
result)
• Angiotensin converting enzyme • Hepatic involvement in FUO is common;
• CT scan of abdomen significant elevated values of transaminase
• Q fever serology (if exposure risk factors exist)
• Examination for specific endemic infectious disease
levels indicate hepatitis; elevated alkaline
in returning travellers or persons living in such phosphatase levels point to infiltration of the
geographic areas (e.g. systemic leishmaniasis in liver.
India, Mediterranean area, etc.)
• Tuberculin test Sputum
• Evaluation of any abnormal symptoms and findings
** Source: Siegenthaler Walter. Siegenthaler’s Differential
• Gram’s stain, AFB, and culture.
Diagnosis in Internal Medicine From Symptoms to
Diagnosis, Thieme, 1st English ed. Chapter-4-Fever of Stool Microscopy and Culture
Unknown Origin-Table 4.2 - Minimum Diagnostic work- • Ova, parasites, cysts, and occult blood on
up to qualify as FUO, p. 114.
microscopy.
sustained may prove to be helpful but rarely antineoplastics, atropine and its compounds,
diagnostic; it may aid in diagnosing cases of barbiturates, iodides, phenytoin, quinidine)
tertian or quartan malaria, or Hodgkin’s must be considered in patients who are taking
disease (with Pel-Ebstein fever characterized medications, including OTC drugs, because
by 5-10 days of fever alternating with 5-10 elimination of the offending agent may solve
days of afebrility) the problem and eliminate the need for
• A single record of temperature in a febrile extensive investigations. If fever persists
patient gives very little information. In all beyond 72 hours of stopping all possible
cases of fever, a serial record of temperature is offending drugs then the likelihood of fever
essential; four-hourly in acute cases and eight- being drug-induced is markedly reduced
hourly in all other cases. A simultaneous • History of high risk sexual activity and I V drug
record of pulse rate and respiration gives abuse need screening for HIV, viral hepatitis,
additional information that may be clinically and infective endocarditis. History of alcohol
useful abuse indicates cirrhosis, and hepatoma
• The duration of fever prior to seeking medical • A past history of intermittent illness over a
help may give some clues. The longer the period of years involving multiple organ
duration of the fever, the less likely there is systems suggests the possibility of connective
an infectious etiology; if it is of month’s tissue disease
duration, then autoimmune or malignant • Fundoscopic examination may provide the
disorders are the possibilities; when it’s more first clue to the diagnosis of tuberculosis if
than a year or so, then granulomatous choroid tubercles are demonstrable. Ocular
diseases are the probabilities manifestations of systemic diseases such as
• Naproxen test15: The response to fever to scleritis, uvulitis in connective tissue disorders
naproxen sodium may be helpful in that may provide clues to the diagnosis of obscure
fever due to solid tumors and many fever. Hence, referral to an ophthalmologist in
rheumatologic diseases (most notably Still’s
the early stages of FUO is particularly useful
disease) usually subside promptly, while
• Physical examination—Must be thorough
fever due to other causes may persist
and often repeated. Symptoms and signs of
• History of recent travel (malaria, SARS); pets,
common diseases causing FUO are given in
animal and insect contacts (toxoplasmosis,
Table 20.2
brucellosis, leptospirosis, Lyme disease);
• Fever associated with rash may be a viral
occupation (brucellosis in abattoir workers,
exanthem (e.g. rubella, varicella) or a clue to
anthrax in leather workers); and recent
a serious disease (e.g. meningococcemia,
contact with persons exhibiting similar
thrombocytopenia, erythema multiforme).
symptoms (viral hepatitis, TB) are important
aids in the diagnosis
RED FLAGS
• The family history should also be carefully
elicited for hereditary causes of fever, such • Rule out habitual hyperthermia, i.e. exaggerated
as familial Mediterranean fever. Diseases circadian rhythm, characterized by
such as rheumatic fever, tuberculosis, temperature between 100 and 100.5°F in the
lymphoma, etc. in other family members afternoon hours; other febrile symptoms
must be enquired (chills, sweats, and tachycardia) are absent
• Drug-induced fever (antihistamines, antibiotics, and initial tests are normal
136 Diagnosis: A Symptom-based Approach in Internal Medicine
Table 20.2: FUO—Common causes • Rule out factitious fever. Clues to the diagnosis
Symptoms and signs Cause are a patient with medical knowledge or
Skin—Mucous membrane— Meningococcemia training, inconsistent histories, excessively
petechial eruptions, high temperatures (105°-107°F, which are a
Erythema chronicus migrans Lyme disease
Pruritus Hepatitis, Hodgkin’s lymphoma, rare occurrence), normal pulse and respiratory
hepatic -tumor
Scalp—Tender cranial arteries Temporal arteritis
rates at the time of fever, and rapid
Seborrheic dermatitis HIV defervescence unaccompanied by diaphoresis
Face— Butterfly rash SLE
Eyes—Subconjunctival petechial, IE • A high index of suspicion of temporal (or
splinter hemorrhages giant cell) arteritis, characterized by
Dry eyes RA
Conjunctiva—Icterus Hepatitis, leptospirosis, hepatic/ headache, fever, jaw claudication, visual
pancreatic-malignancy
Fundi—Roth spots IE
symptoms, polymyalgia rheumatica, and
Choroidal tubercle Miliary TB constitutional symptoms must be
Retinal hemorrhages, Leukemia, lymphoma
infiltrates maintained, since failure to do so, and to
Oral cavity—Ulcers SLE institute appropriate treatment may lead
Ears—Ear pain, diminished hearing; Otitis media, mastoiditis
tympanic membrane- to permanent vision loss
erythema,
effusion
• FUO should be presumed to be secondary to
Neck—Stiffness Meningitis an infection (bacterial, parasitic, fungal,
Thyroid—Tenderness Thyroiditis
Lymphadenopathy TB, infectious mononucleosis, viral, rickettsial, and chlamydial) until
lymphoma, sarcoidosis proven otherwise because infections cause
Hands—Clubbing, Raynaud’s IE, SLE, RA
phenomenon the majority of FUOs and can be life-
Arms—Drug injection sites IV drug abuse
Chest—Cough, hemoptysis, dyspnea, TB, lymphoma, malignancy
threatening
consolidation, effusion, rub • The diagnosis of TB may be delayed despite
Cardia—Dental procedure, IE, pericarditis
skin lesion, ‘varying’ murmurs, a high index of suspicion because of normal
conduction disorder, rub CXR, negative skin and sputum test, and
Abdomen–Tenderness, guarding, Hepatitis, cholecystitis, abscess,
hepatosplenomegaly, mass kala-azar, infective endocarditis, inconclusive histopathologic examination.
malignancy
Scrotum—Swelling, tenderness, mass Orchitis, seminoma, TB
Repeated examination and work-up is
epididymitis indicated in patients with strong clinical
Penis—Discharge, rash, ulcer HIV
Digital rectal examination— Prostatitis, perianal abscess suspicion of TB
Tenderness, mass • A high index of suspicion and familiarity
Pelvic examination—Discharge, Pelvic inflammatory disease
dysuria with the rapidly changing epidemiology of
Bones and joints—Pain, tenderness, RA, PMR, Osteomyelitis,
swelling, metastatic deposits
SARS is extremely useful in its early diagnosis
restricted and minimizing transmission
movements
Lower extremities—Calf Thrombophlebitis • Patients who are elderly, immunocom-
swelling, promised, talking steroids or NSAIDs may
tenderness,
palpable cord not show evidence of fever, even in the
Back—Tenderness, swelling over Spinal TB, Paravertebral/spinal presence of a severe infection
spine, restricted painful epidural abscess, metastatic
movements deposits • Patients who present with rash associated
with FUO should have a skin biopsy (Bx)
CNS—Altered consciousness Encephalitis; TB, cryptococcal unless the diagnosis is straightforward
Focal deficit meningitis
Brain abscess, mass lesion
• Patients who are immunosuppressed (on
corticosteroids, chemotherapy) or who have
Fever of Unknown Origin 137
altered immune response due to disease 8. Shamsuzzaman SM, et al. Thoracic amebiasis.
Clin Chest Med 2002;23(2):479-92. [PMID:
(Hodgkin’s, HIV), are likely to have fever due 12092041: Abstract].
to infection caused by atypical organisms. 9. Victor F, et al. Pacemaker lead infection:
Echocardiographic features, management, and
outcome. Heart 1999;81(1):82-7. [PMID:
REFERENCES 10220550: Abstract].
1. Knockaert DC, et al. Fever of unknown origin in 10. Haaker R, et al. Osteomyelitis after endoprostheses.
the 1980s. An update of the diagnostic spectrum. Orthopade. 2004;33(4):431-8. [PMID: 15146838:
Arch Intern Med 1992;152(1):51-5. [PMID: Abstract].
1728929: Abstract]. 11. Sharif MA, et al. Prosthetic stent graft infection
2. Ophry M, et al. A comprehensive evidence-based after endovascular abdominal aortic aneurysm
approach to fever of unknown origin. Arch Intern repair. Vasc Surg 2007;46(3):442-8. [PMID:
Med 2003;163:545-51. 17826231: Abstract].
3. Vanderschueren S, et al. From prolonged febrile 12. Meller J, et al. 18F-FDG PET and PET/CT in fever
illness to fever of unknown origin: The challenge of unknown origin. J Nucl Med 2007;48(1):35-
continues. Arch Intern Med 2003;163(9):1033-41. 45. [PMID: 17204697: Free full text].
4. Cunha BA. Fever of unknown origin. Infect Dis 13. Keidar Z, et al. Fever of unknown origin: The
Clin North Am 1996;10:111-27. role of 18F-FDG PET/CT. J Nucl Med 2008;
5. Roth AR, et al. Approach to the adult with fever 49(12):1980-5. Epub 2008 Nov 7. [PMID:
of unknown origin. Am Fam Physician 2003;
18997040: Free full text].
68:2223-8.
14. Corrado G, et al. Pacemaker-induced infection:
6. Barbado FJ, et al. Fever of unknown origin: Classic
Diagnosis by multi-plane transesophageal
and associated with human immunodeficiency
virus infection: A comparative study. J Med 2001; echocardiography. Cardiologia 1997;42(10):
32(3-4):152-62. [PMID: 11563813: Abstract]. 1083-6. [PMID: 9534285: Abstract].
7. Kasper DL, et al. Harrison’s Principles of Internal 15. Agarwal PK, et al. Fever of unknown origin. J of
Medicine 16th ed. Vol.I:p.106. Assoc Phy of India, (52),2004;317.
CHAPTER
21 Gait Disorders
in which the patient is asked to stand up from take longer than 30 seconds tend to need
a sitting position without use of hands, walk assistance with many mobility tasks
10 feet, turn around, walk back, and sit down, • Gait disorders worse in the dark are due to
is a valid procedure to readily assess gait lesions of the posterior column, e.g. Friedreich’s
disorders.2,3 Patients who take less than 10 ataxia, pernicious anemia, MS, or tabes dorsalis
seconds are usually normal, patients who • Romberg’s test (eyes-open-eyes-closed): Cerebellar
Gait Disorders 143
ataxia can be differentiated from sensory his walking, the psychogenic patient is found
ataxia by Romberg’s test, where removal of to perform well on the chair test (sitting
the visual input dramatically reduces versus standing), showing improved ability
compensatory ability in sensory ataxia. to propel a chair forward than when seated.
Ask the patient to stand in one place with By contrast, a normal person performs
his feet together. If he is able to stand with equally when walking or propelling utilizing
his eyes open as well as eyes closed, the the chair.
test is negative, i.e. normal.
If he is able to stand with eyes open, but RED FLAGS
tends to fall with eyes closed (i.e.
• In the elderly:
removing visual input), the test is
Three “Ds” contribute to gait disorder;
positive. The cause may be posterior
viz. drugs, depression, and dementia;
spinal column lesions due to tumor, vit
these must be specifically looked for and
B12 deficiency, cervical spondylosis, or
excluded before any other intervention.
tabes dorsalis.
Acute onset gait disorder is likely to be
If he is unable to stand with eyes open
due to acute systemic decompensation,
and feet together, it indicates severe
such as MI, stroke, or sepsis; a careful
unsteadiness, commonly involving the
systematic evaluation is indicated to
peripheral and central vestibular system
exclude such catastrophic presentations.
and the cerebellum.
It is often not advisable to attribute gait
• Fukuda test: Marching in place for 50 steps;
disorder to a single disease because many
abnormal if patient deviates close to 90° or
different conditions (e.g. degenerative
more, either to left or right. If abnormal, it
joint disease, postural hypotension, and
reflects vestibular disorder
stroke) can present in similar gait
• Hoover sign: It is a maneuver aimed to
abnormalities.
separate organic from nonorganic lower limb
• In a patient with history suggestive of
paralysis. The physician takes a position at
secondary gain and normal neurological
the foot of the supine patient and places one
examination, except bizarre gait, strongly
hand under the heel of the patient’s ‘weak’
favors malingering.
leg while pressing down with the other hand
on the good leg. Now the patient is asked to
SELECTIVE GLOSSARY
attempt to raise the affected ‘weak’ leg. In
organic disease, the associated movement Brown-Séquard syndrome—It is associated with
causes the unaffected heel to press injury to the lateral half of the spinal cord
downward; in hysteria, the associated (involving interruption of the lateral corticospinal
movement is absent tracts, posterior white column, and lateral
• The chair test to aid in the diagnosis of spinothalamic tracts), usually as a result of
psychogenic gait disorders: In this procedure penetrating trauma to the cervical or thoracic
of ‘chair testing’ patient is asked to walk 20- spine. Multiple causes of Brown-Séquard
30 feet forward and backward toward the syndrome have been described in the literature.
examiner. The patient is then asked to sit in a The most common cause remains traumatic injury,
swivel chair with wheels and to propel the often a penetrating mechanism, such as a stab or
chair forward and backward. Compared with gunshot wound or a unilateral facet fracture and
144 Diagnosis: A Symptom-based Approach in Internal Medicine
dislocation due to a motor vehicle accident or fall. slow and clumsy walking, which often begins
The condition is characterized by the following after normal walking has developed. Diagnostic
clinical features (which are found below the level criteria of typical FA include: disease duration at
of the lesion): contralateral hemisensory least 5 years, onset < 25 age, progressive ataxia of
anesthesia to pain and temperature, ipsilateral gait and limbs, absent knee and ankle jerks, and
loss of proprioception, and ipsilateral motor extensor plantar responses ‡ . As the disease
paralysis. Tactile sensation is generally spared. progresses, ataxia affects the trunk, legs, and arms.
The pure Brown-Séquard syndrome reflecting As the arms become grossly ataxic, both action
hemisection of the cord is not often observed. A and intention tremors may develop. Eventually,
clinical picture comprising fragments of the the patient is unable to walk because of the
syndrome or the hemisection syndrome plus progressive weakness and ataxia, becoming
additional symptoms and signs, known as wheelchair bound and ultimately bedridden.
‘Brown-Séquard–plus syndrome’, is more With disease progression, dysarthria and
common.4 In the absence of trauma, this condition dysphagia appear, incapacitating the patient by
needs to be differentiated from acute poliomyelitis, 20, and death by 25 (40 in autosomal dominant
Guillain-Barré syndrome, cervical disk disease, form), especially due to cardiac failure.
vertebral artery dissection, infection and
Normal pressure hydrocephalus (NPH)—It is
inflammatory causes. MRI is helpful to define
characterized by Adam’s triad (impaired gait,
the extent of spinal cord injury and is also helpful
urinary incontinence and dementia) — and an
when differentiating among nontraumatic
anatomic abnormality, i.e. enlargement of the
etiologies. CT myelography may be useful if MRI
cerebral ventricles, which can be seen on CT or
is contraindicated or not available.
MRI of brain. The gait is typically wide-based
‘Fear of falling’ gait—It is largely a psychogenic with reduced step height, stride length, and
gait disorder of the elderly that is often velocity, which gradually progresses to so-called
unrecognized. It usually begins after a fall and is ‘magnetic’ gait (‘feet stuck to ground’ – due to
characterized by a shuffling or sliding stride and simultaneous contraction of opposing muscles
an intense need to hold on for support. It appears while walking), it becomes almost impossible for
to be most common in elderly women, can be the patient to initiate gait. The urinary
reversed by education, suggestion, and physical incontinence is of ‘urge’ type. The precise
therapy, and is often mistaken for Parkinson pathogenesis of NPH is not known, but it is well-
disease, or other gait disorders in the elderly. known that despite the absence of increased
intracranial pressure, the drainage of CSF
Friedreich’s ataxia—FA is the most common
regularly induces transient clinical improvement,
autosomal recessive ataxia; the major
and ventriculosystemic shunting usually results
pathophysiologic finding in FA is a “dying back
in prolonged remissions. Recently, another
phenomena” of axons, beginning in the periphery
anatomic abnormality was described in NPH—
with ultimate loss of neurons and a secondary
a decrease in midbrain diameter on MRI that is
gliosis. Classic FA is the result of a gene mutation
restored to normal by ventriculosystemic
at the centromeric region of chromosome 9 (9q13-
shunting. The criteria to define cerebral
21.1) at the site of the gene encoding for the 210-
aminoacid protein frataxin. Onset of FA is early, ‡
Only diseases with decreased deep tendon reflexes and
with gait ataxia being the usual presenting positive Babinski signs are Friedreich’s ataxia, amyotrophic
symptom. Gait ataxia manifests as progressively lateral sclerosis, B12 deficiency and syphilis.
Gait Disorders 145
ventriculomegaly precisely are vague and rheumatica. Later symmetric proximal muscle
difficult to establish, and enlarged ventricles are weakness in the upper and lower extremities
surprisingly common. Other disorders of elderly develops. Weakness of pharyngeal and laryngeal
people such as Alzheimer’s disease, Parkinson’s muscles, interstitial lung disease, and inflam-
disease, and cerebral atrophy may show mation of the myocardium may also occur. Serum
enlarged ventricles, and demential disorders CK levels are usually elevated from 5-50 times
may be difficult to differentiate from each other. the normal value. Other muscle enzymes — lactic
dehydrogenase, aspartate aminotransferase,
Polymyositis—It is an idiopathic inflammatory
alanine aminotransferase, and aldolase — may be
myopathy with symmetric proximal muscle
elevated. Muscle biopsy is crucial in helping
weakness, characterized by subacute or slowly
diagnose PM and in excluding other rare muscle
progressing symmetrical weakness, primarily
diseases. MRI can be used to guide the site of
affecting the proximal limb and trunk muscles.
biopsy.
The illness may occur at any age, but is most
frequent in the fourth to sixth decade of life,
REFERENCES
women being more frequently affected than
men. Although the initial inciting agent remains 1. KurlanR.”Fear of falling” gait: A potentially
reversible psychogenic gait disorder. Cogn Behav
unknown, possibilities include virus-mediated Neurol 2005;18(3):171-2. [PMID: 16175021:
muscle injury, e.g. Coxsackie virus B1, HIV, Abstract].
Human T-lymphotropic virus 1 (HTLV-1) 2. Podsiadlo D, et al. The timed “Up & Go”: A test of
basic functional mobility for frail elderly persons.
Hepatitis B, influenza, echovirus, and adenovirus. J Am Geriatr Soc 1991; 39(2):142-8. [PMID: 1991946:
Many drugs are known to cause myopathy, e.g. Abstract].
3. Morris S, et al. Reliability of measurements
hydroxychloroquine, D-penicillamine, hyd-
obtained with the Timed “Up & Go” test in people
ralazine, procainamide, phenytoin, ACE with Parkinson disease. Phys Ther 2001;81(2):810-
inhibitors, and statins. Patients may report 8. [PMID: 11175678: Free full text].
4. Koehler PJ, et al.The Brown-Séquard syndrome.
muscle pain and tenderness, arthralgias or True or false? Arch Neurol 1986;43(9):921-4. [PMID:
arthritis that may be confused with polymyalgia 3741208: Abstract].
CHAPTER
22 Gastrointestinal
Bleeding
Table 22.1: Differential diagnosis of occult GI bleeding Table 22.2: Differential diagnosis of obscure GI bleeding
Inflammation • Aortoenteric fistula
• Peptic ulcer (esophagus, stomach, duodenum, • Dieulafoy’s lesion
surgical anesthemosis) • Diverticula
• Erosive esophagitis/gastritis • Extraesophageal varices (gastric, small bowel,
• Cameron lesion# colonic)
• IBD (ulcerative colitis, Crohn’s disease) • Hemobilia
• Meckel’s diverticulum
Infections
• Neoplasms (small bowel)
• Hookworm/ ascariasis/ whipworm/ strongyloidosis
• Vascular ectasias
• Amebiasis/ giardiasis
• TB enteritis
Neoplasms
• Carcinoma, lymphoma, polyp recurrence is a substantial problem, especially for
elderly patients with LGI bleeding.2 Additionally,
Vascular
• Portal hypertension the stability of the patient and the rate of bleeding
• Hemangioma dictate the order in which various diagnostic
• Dieulafoy’s lesion (ruptured mucosal artery: vide procedures should be conducted. Therefore, the
infra ↓↓) goal is to identify, and if necessary, treat the source
• Watermelon stomach##
• Vascular enteric fistula of bleeding, while maintaining hemodynamic
stability of such patient.
Superstitious
• Hemoptysis
• Oropharyngeal (epistaxis) DIFFERENTIAL DIAGNOSIS
Miscellaneous As noted above, the source of GI bleeding may
• Long distance running be categorized into two broad groups: viz. UGI
• Factitious
• Hemobilia bleeding and LGI bleeding.
#
Cameron lesions are linear gastric ulcers or erosions
positioned on the crests of mucosal folds at the A—UGI BLEEDING
diaphragmatic impression in patients with large hiatus
hernia. Common
##
Watermelon stomach is the popular name for Gastric
Antral Vascular Ectasia (GAVE) in which the lining of the
• Peptic ulcer disease (PUD; H. pylori infection)
stomach bleeds, causing it to look like the characteristic • Esophagitis (due to chronic GERD)
stripes of a watermelon when viewed by endoscopy; it • Erosive gastritis (NSAIDs, aspirin, steroids,
can occur in patients with diffuse systemic sclerosis. stress, alcohol).
Rare LFTs
• AST, ALT, and Alk. Phosphatase — elevated
• Colitis – ischemic, radiation
in hepatitis, cirrhosis, and neoplasm.
• Solitary rectal ulcer syndrome (SRUS: vide
infra ↓↓)3,4 ECG
• Diverticulosis/pseudodiverticulosis • To rule out cardiac ischemia due to
• Colonic neoplasm (adenocarcinoma) hypovolemia and related factors, especially
• Carcinoid tumor in the elderly.
• HIV/AIDS colitis (Cytomegalovirus colitis,
colonic histoplasmosis, Kaposi’s sarcoma of EGD
the colon, and bacterial colitis) • Diagnostic procedure of choice for acute UGI
• Colonic arteriovenous (AV) malformation bleeding; can demonstrate most lesions, e.g.
(i.e. vascular ectasias, angiomas, angiodys- varices, esophagitis, PUD, gastric erosions,
plasias, and Heyde’s syndrome†) MV tear, and carcinoma
• Systemic/iatrogenic bleeding disorder • Screening procedure in patients with
• Vasculitis (PAN, Wegener granulomatosis). cirrhosis and portal hypertension, but
without prior variceal hemorrhage
†
The Heyde’s syndrome consists of the association of • Advantages of early EGD include: confirmation
gastrointestinal bleeding from angiodysplasia with aortic
valve stenosis. of bleeding source in UGI tract; obtaining
Gastrointestinal Bleeding 149
99m
biopsy (Bx), and providing therapeutic Tc RBC Scanning
measures which lessen transfusion require-
• Like angiography, it is only of value in
ments, need for surgery, and hospitalization.
patients with active bleeding. The newer
techniques involving dynamic imaging
INVESTIGATIONS—SPECIFIC
(more frequent acquisition of data), extra
Sigmoidoscopy large field-of-view gamma cameras, and cine
scintigraphy, or movie-mode displays have
• Useful primarily in patients < 40 years of age for
proved to have an accuracy of nearly 90% in
minor bleeding due to low-lying anal disease.
the localization of the bleeding site
• Also most often employed in confirming
Colonoscopy5,6
Meckel’s diverticulum.
• First procedure of choice in LGI bleeding
Abdomen US/HRCT
diagnosis; may be performed urgently or
electively depending on patient’s hemodyna- • May be indicated to diagnose associated
mic status and risk-stratification criteria such disorders such as pancreatitis, aortic
as positive FOBT in patient > 40 years of age aneurysm, ascites, metastasis, and aortic graft
• Though colonoscopy is recommended for infection.
patients with LGI bleeding, it may also be used Double-contrast Barium Enema
in combination with EGD (i.e. bidirectional
• May be an alternative in patients with
endoscopy) for patients with upper GI bleeding,
contraindications to colonoscopy.
OGIB, or nondiagnostic EGD
• Advantages include: direct visualization; access Small Bowel Imaging
for tissue biopsy (Bx), and ability to treat • When endoscopy is undiagnostic, the small
bleeding lesions primarily with heat probe, bowel is evaluated. Common procedures
laser therapy, band ligation, or hemoclipping. employed are contrast radiography, i.e. UGI
barium follow-through series, and push
Angiography (Mesenteric) enteroscopy, which is an extension of EGD that
• Used for active, heavy bleeding and/or if allows visualization up to 160 cm. of small
colonoscopy is inconclusive bowel distal to ligament of Treitz; allows tissue
• The main advantage include: accurate biopsy (Bx), and treatment of bleeding lesions
localization of bleeding sites that are not up to 160 cm. of the proximal small bowel.
identified by endoscopy Capsule Endoscopy10,11
• It may also permit therapeutic interventions,
• It is a noninvasive visual evaluation of the entire
e.g. vasopressin infusion and embolization.
small bowel and esophagus, indicated in:
Complications such as renal failure,
Suspected small intestinal bleeding in
rebleeding may occur.
persons with objective evidence of
recurrent, obscure gastrointestinal bleeding
Multidetector Computed Tomographic (MDCT)
(e.g. iron-deficiency anemia, positive fecal
Angiography7-9
occult blood test, or visible bleeding) who
• MDCT angiography is a promising first-line have had EGD and colonoscopy within the
modality for fast and accurate localization of past 12 months that have failed to identify
acute GI and intraperitoneal bleeding. a bleeding source.
150 Diagnosis: A Symptom-based Approach in Internal Medicine
tional endoscopy may be essential depen- surface of skin and to mucous membranes often
ding on clinical suspicion, and to ascertain rupture and bleed after slight trauma. The most
that these lesions have not been overlooked. common clinical manifestation is spontaneous and
recurrent epistaxis beginning at approximately 12
SELECTIVE GLOSSARY years of age. About 25% of individuals with HHT
have GI bleeding, which most commonly begins
Dieulafoy’s lesion—It is an abnormally large
after age 40 years. Large AVMs often cause
artery that penetrates the gut wall, mainly in the
symptoms when they occur in the brain, lungs,
proximal stomach, causing massive bleeding.
or gastrointestinal tract, causing complications
The lesion bleeds into the GI tract through a
from bleeding or shunting, which may be
minute defect in the mucosa, which is not a
sudden and catastrophic. The diagnosis of HHT
primary ulcer of the mucosa, but erosion
is based on family history and the presence of
probably caused on the submucosal surface by
cutaneous or mucocutaneous telangiectases or
the pulsatile arteriole protruding into the
large visceral AVMs. HHT is caused by a
mucosa. Dieulafoy’s lesion is most commonly
mutation in ENG, the gene encoding endoglin
located in the proximal stomach (75% of cases).
or ACVRL1 (ALK1), the gene encoding the activin
Lesion typically occurs within 6 to 10 cm of the
receptor. Molecular genetic testing of these genes
esophagogastric junction, generally along the
detects mutation in 60-80% of individuals with
lesser curvature of the stomach. Detection and
HHT and is available on a clinical basis.
identification of the Dieulafoy’s lesion as the
source of bleeding can often be difficult, Mallory-Weiss syndrome—It is characterized by
especially because most present with massive UGI bleeding secondary to longitudinal mucosal
bleeding. Because of intermittent nature of lacerations at the gastroesophageal junction or
bleeding, initial endoscopy is diagnostic in 60% gastric cardia; may occur after any event that
of the cases, so repeated endoscopies are often provokes a sudden rise in intragastric pressure
necessary. Similar lesions have been identified in or gastric prolapse into the esophagus secondary
the duodenal bulb, jejunum, ileum, colorectum, to precipitating factors such as retching or
anal canal, and even in bronchus. With the vomiting. The classic presentation consists of an
advances in endoscopy and awareness of episode of hematemesis following a bout of
Dieulafoy’s lesion as the cause of massive retching or vomiting. Hematemesis is present
bleeding that can cause a high fatality rate if the in 85% of patients. Less common presenting
condition remains unrecognized, it has gained symptoms include melena, hematochezia,
the reputation of an unusual but important cause syncope, and abdominal pain. Excessive alcohol
of bleeding, especially LGI hemorrhage. use has been reported in 40-75% of patients, and
aspirin use in up to 30%.
Hereditary hemorrhagic telangiectasia (HHT /
Rendu-Osler-Weber Syndrome)—It is a Peutz-Jeghers syndrome—It appears to be a
hereditary disease of vascular malformation germline mutation of the STK11 gene, located on
transmitted as an autosomal dominant trait band 19p13.3. ; characterized by the combination
affecting men and women, characterized by the of pigmented lesions in the buccal mucosa and
presence of multiple arteriovenous malformations gastrointestinal polyps. Mucocutaneous pigmen-
(AVMs) that lack intervening capillaries and result tation and melanin spots are typical, and are
in direct connections between arteries and veins. present in more than 95% of cases. They appear
Small AVMs (or telangiectases) close to the as small, flat, brown, or dark blue spots with an
Gastrointestinal Bleeding 153
appearance of freckles, most commonly in the and clinical presentations may be confusing. The
peribuccal area. The number, as well as the size lesions may mimic other rectal pathologies,
and the location of polyps may vary from patient including primary or metastatic malignancy, and
to patient. Isolated melanotic mucocutaneous lead to wrong diagnosis.
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14. Batur P, et al. Increased prevalence of aortic stenosis 17630077: Abstract].
in patients with arteriovenous malformations of the 17. Boley SJ, et al. On the nature and etiology of
gastrointestinal tract in Heyde syndrome. Arch vascular ectasias of the colon. Degenerative lesions
Intern Med 2003;163(15):1821-4. [PMID: 12912718: of aging. Gastroenterology 1977 Apr; 72(4 Pt 1):650-
Free full text]. 60. [PMID: 300063: Abstract].
CHAPTER
23 Headache
Therefore, the clinician’s prime concern while • Ocular (acute narrow angle glaucoma,
examining headache patients is, to try and refractory errors)
distinguish the more common benign from the • Lumbar puncture headache.
less common serious life-threatening causes of
headache † , while maintaining a balanced Rare
approach to diagnostic testing.
• Thunderclap headache (i.e. TCH – vide infra ↓↓).
• Giant cell arteritis (GCA)
DIFFERENTIAL DIAGNOSIS
• Benign intracranial hypertension
Common • Cerebral venous thrombosis
• Coital/sexual headache.8
• Systemic illness (febrile episodes: viral,
typhoid, malaria)
INVESTIGATIONS—GENERAL
• Migraine
• Tension headache CBC
• Chronic daily headache
• Rarely useful or definitive, except in a febrile
• Psychogenic (depression, anxiety)
patient.
• Vascular (subarachnoid hemorrhage, i.e.
SAH; intracerebral hemorrhage)
ESR
• CNS infections (i.e. meningitis: bacterial-
Streptococcus pneumoniae, H. influenzae type b, • Elevated ESR (61-80 mm/hr) is useful to
N. meningitidis; TB; viral – HIV, HSV2, EBV; support the diagnosis of GCA.
parasitic – toxoplasma; fungal – cryptococcal‡)
• Post-traumatic headache Skull X-ray
• Premenstrual headache
• Immediately after head injury; CT scan is
• Drug induced (nitrates; calcium channel
superior.
blockers; phosphodiesterase type 5 inhibitors:
sildenafil; insulin: hypoglycemia) X-ray PNS
• Substance abuse (alcohol, caffeine, nicotine) • Useful if sinusitis is suspected – opacification,
• Analgesic rebound headache (analgesics, fluid level, mucosal thickening may be
NSAIDs, ergotamine) visualized.
• Cervical spondylosis
• Referred pain (sinus, dental, aural). INVESTIGATIONS—SPECIFIC
Occasional Blood Culture
Table 23.3: Headache features suggestive of a space Table 23.4: Typical findings in symptomatic/secondary
occupying lesion headache
• New onset in adult life (>40 yr of age) or significant • Pressure pain/tenderness (sinus, temple)
change in established pattern • Pathologic murmurs (neck, orbits)
• Progressive in nature • Meningism (i.e. clouding of consciousness, vomiting)
• Association with any of the following: • Meningitis (i.e. altered consciousness, neck
Nausea or vomiting not explained by migraine or stiffness, fever, photophobia, etc.)
systemic illness • Cranial nerve palsy and other local motor/sensory
Nocturnal occurrence or morning awakening deficits
Precipitation or worsening by changes in posture, • Horner’s syndrome (triad of miosis, i.e. constricted
Valsalva maneuver pupil; partial ptosis; and loss of hemifacial sweating,
Confusion, seizures, or weakness in extremities i.e. anhidrosis
• Papilledema/retinal hemorrhage
• Typical physical findings that may be noted
in secondary or symptomatic headache are listed
in Table 23.4 • An acute headache with papilledema and
• The presence of nuchal rigidity should make focal neurologic signs, one should consider
one think of a subarachnoid hemorrhage, cerebrovascular accident/hemorrhage,
cerebral hemorrhage, meningitis, or cerebral cerebral abscess. With a chronic headache
abscess and papilledema or focal neurologic signs,
• An acute onset of a headache can be a serious one should consider a SOL such as a primary
problem. It should be taken seriously because brain tumor or metastatic neoplasm
an abrupt onset of a severe (worst headache • Headache that is always on the same side,
ever experienced) occipital or generalized associated with seizures, visual distur-
headache in a patient with no past history bances, focal neurological deficit, and audible
of headache may mean a subarachnoid cranial bruit strongly indicates an arteriov-
hemorrhage or meningitis enous malformation
160 Diagnosis: A Symptom-based Approach in Internal Medicine
• The presence of a tender superficial temporal Table 23.5: Which patients with headache require
neuroimaging?
artery should make one think of GCA (temporal
arteritis), particularly in the elderly • Patients with older age (over 50-60 years old) with
new headache
• Cranial nerve palsies in the elderly are • Occipital location of pain
usually due to ischemia, but when they occur • Worsening headache with valsalva
in conjunction with an elevated ESR and • Headache waking patient from sleep
• Headache associated with syncope, nausea, or
headache, they could be associated with sensory distortion
GCA. However, when assessing an older • Sudden onset severe headache (reaching maximum
person with a headache, the information intensity over seconds to a minute
• HIV/AIDS patients with new or different headache
obtained from the patient should be • Pregnant patients
considered as carefully as any ESR result • Abnormal finding on neurologic examination
• In complicated migraine such as ophthalmic / Source: The American College of Emergency Physicians
hemiplegic/basilar artery migraine, signi- (ACEP) June 2008, Guidelines for evaluation of patients
ficant neurologic complications may outlast with acute headache.
14. Goadsby Peter J. To scan or not to scan in 16. Matharu MS, et al. Thunderclap headache: An
headache. BMJ 2004;329:469-470, doi: 10.1136/ approach to a neurologic emergency. Curr Neurol
Neurosci Rep. 2007;7(2):101-9.[PMID: 17324359
bmj.329.7464.469.[Free full text]
Abstract]
15. Banerjee A. Coital emergencies. Postgrad med J. 17. Schwedt TJ. Clinical spectrum of thunderclap
1996;72(853):653-6. [PMID: 8944205 Free full headache.Expert Rev Neurother. 2007;7(9):1135-
text]. 44. [PMID: 17868012 Abstract].
CHAPTER
24 Hearing Loss
Table 24.1: WHO grades of hearing impairment Other common symptoms which may be
Grade of Audiometric ISO value Impairment associated with hearing loss include headache,
impairment (average of 500, 1000, to description otalgia, otorrhea, tinnitus, vertigo, development
2000, 4000 Hz)
of weakness or asymmetry of the face, and an
0 (no impairment) 25 dBHL or less No or very slight
(better ear) problems. Able to abnormal sense of taste.
hear whispers The significance of hearing loss and its
1 (slight 26-40 dBHL or less Able to hear and
impairment) (better ear) repeat words spoken impact on the health and productivity of those
in normal voice at
1 meter
affected by it often go unrecognized. Although
2 (moderate 41-60 dBHL or less Able to hear and loss of vision is readily acknowledged and
impairment) (better ear) repeat words using
raised voice at 1 meter vigorously treated, loss of hearing is often denied,
3 (severe 61-80 dBHL or less Able to hear some minimized, or ignored.2 Since either ignored or
impairment) (better ear) words when shouted
into better ear undiagnosed hearing loss—both in the young
4 (profound 81 dBHL or greater Unable to hear and and the old—besides causing physical disab-
impairment (better ear) understand even a
including deafness) shouted voice ility, can also lead to multiple consequences,
including social isolation and depression, it is
This distinction is important, because sensory vital that early diagnosis is made, particularly
hearing loss is sometimes reversible and of reversible causes, in addressing these issues.
seldom life-threatening. A neural hearing loss
is rarely recoverable and may be due to a DIFFERENTIAL DIAGNOSIS
potentially life-threatening brain tumor—
commonly a cerebellopontine angle tumor. Common
Mixed hearing loss (MHL) may be caused by severe • Cerumen impaction
head injury, with or without fracture of the skull • Foreign body
or temporal bone, by chronic infection, or by one • Otitis externa (secondary to obstruction),
of many genetic disorders. It may also occur furuncle
when a transient conductive hearing loss, • Otitis media with effusion (secretory)
commonly from otitis media, is superimposed • Eustachian tube dysfunction
on a sensorineural hearing loss. • Tympanic membrane perforation/retraction
• Presbycusis TFTs
• Labyrinthitis—viral, bacterial • Hypothyroidism and hyperthyroidism are
• Noise induced hearing loss (NIHL).3, 4 causes of SNHL.
Occasional
INVESTIGATIONS—SPECIFIC
• Ménière’s syndrome
• Otosclerosis Pure Tone Audiometry
• Barotrauma
• Useful test for discriminating the cause of
• Ototoxic drugs (aspirin, loop diuretics, amin-
oglycosides, phosphodiesterase-5 inhibitors, hearing loss. It measures the threshold levels
and chemotherapeutic agents) (i.e. the intensity at which the patient is able
• Systemic disease (diabetes mellitus, hypoth- to perceive sound correctly 50% of the times)
yroidism, meningitis, syphilis). by presenting pure tones (i.e. electronically
generated sounds of specific frequencies), the
Rare intensity of which can be increased or
• Acoustic neuroma decreased in 5dB steps. Air conduction and
• Cholestatoma bone conduction thresholds for preset
• Ear trauma, head injury frequencies for both the ears are assessed and
• Systemic disease (multiple sclerosis, autoim- charted in the form of a graph called
mune disorders) audiogram. The threshold for bone conduc-
• Sickle cell disease tion is a measure of cochlear function. The
• Genetic (autosomal dominant and autoso- difference in the thresholds of air and bone
mal recessive) conduction (A-B gap) is a measure of degree
• Psychogenic (pseudohyperacusis). of conductive deafness. The normal thre-
shold is considered 0 dB hearing level (Hl);
INVESTIGATIONS—GENERAL hearing loss is considered present if the
CBC patient’s threshold is >25 dB Hl. When
hearing loss is such as to require loud test
• Leukocytosis in bacterial ear and labyrinth
infection tones, intense tones presented to one ear may
• Sickle cells may be seen on peripheral blood be heard in the other ear. In such cases, a
smears. masking sound, usually narrow band noise,
is presented to the nontest ear to isolate it.
ESR
Speech Audiometry
• Elevated with inflammation and autoim- • In this test the patient’s ability to hear and
mune hearing loss.
understand speech is measured. Here
Blood Glucose phonetically balanced words (single syllable
words, e.g. pin, thin, day, bus) and words
• Recurrent otitis externa raises suspicion of
diabetes mellitus and warrants blood glucose with two equally accented syllables
monitoring. (spondees), such as railroad, staircase, and
baseball are delivered at 30 or 40 dB above
Serology for Syphilis the patient’s speech reception threshold (SRT)
• SNHL is caused by both congenital and and the percentage of words correctly heard
acquired syphilis. by the patient is his discrimination sore (DS).
166
diverse degree of hearing loss, and their causes such as presbycusis, noise trauma,
communication may be unintelligible. ototoxicity, tumor, or autoimmune disorders.
Patience, understanding, and conversing Some forms may be intermittent, e.g. Ménière’s
slowly and clearly (do not follow the natural syndrome. Unilateral hearing loss is most often
instinct to shout) in patient’s first language associated with conductive causes, Ménière’s
are extremely important in establishing disease, trauma and acoustic neuroma. Bilateral
meaningful communication hearing loss is common with presbycusis,
• Screening in adults can be successfully ototoxic drugs, noise trauma, and autoimmune
carried out using the questionnaire from the disorders. History of fever, ear discharge, pain
Hearing Handicap Inventory for the Elderly is associated with ear infection
Screening (i.e. HHIE-S) Version (Table 24.3).5-7 • Associated neurological symptoms—Tinnitus is
common with Ménière’s syndrome; vertigo
Table 24.3: Hearing handicap inventory for the elderly—
screening (HHIE-S) version-questionnaire is associated with labyrinthitis. Focal
In this test, the patient is asked the following questions: neurologic deficit suggest CNS tumor or
1. Does a hearing problem cause you to feel embarrassed vascular insufficiency, whereas fluctuating
when you meet people? neurologic deficit may suggest multiple
2. Does a hearing problem cause you to feel frustrated
when talking to a family member? sclerosis
3. Do you have difficulty hearing when someone • Work history—Factory workers, pilots,
whispers?
4. Do you feel handicapped by a hearing problem?
firefighters, engine drivers, and those
5. Does a hearing problem cause you difficulty when exposed to chronic, recurrent loud sound are
visiting friends, relatives, or neighbors? prone to hearing loss, especially without the
6. Does a hearing problem cause you to attend
religious services less often than you would like? use of protective equipment
7. Does a hearing problem cause you to have • Current and past medications should be
arguments with family members?
8. Does a hearing problem cause you difficulty when
reviewed. Aspirin, loop diuretics, aminogly-
listening to television or radio? cosides, chemotherapeutic agents, etc. are
9. Do you feel that any difficulty with your hearing known to be ototoxic. FDA has received
hampers your personal or social life?
10. Does a hearing problem cause you difficulty when reports of cases of sudden decreases or loss
in a restaurant with relatives or friends? of hearing following the use of PDE-5
The patient responds to each question with “no” (0 inhibitors (sildenafil, tadalafil, and
points), “sometimes” (2 points), or “yes” (4 points).
vardenafil) for the treatment of erectile
Interpretation of Total Scores: 0-8 = no handicap;
10-24 = mild to moderate handicap; 26-40 = severe dysfunction and for the treatment of
handicap. Scores >10 suggest significant hearing pulmonary arterial hypertension8
impairment and necessitate follow-up.
• Family history—May be positive in
• History—Onset - age of onset helps to differentiate presbycusis, Ménière’s syndrome, otoscle-
congenital and acquired causes of hearing loss, rosis, and acoustic neuroma
e.g. unilateral hearing loss since birth is most • Physical examination—Evaluation of the external
likely congenital, whereas adult onset unilateral ear to detect obvious causes of CHL, e.g.
hearing loss should raise suspicion of a tumor. congenital malformations, atresia, obstruc-
Sudden onset may due to viral infection, tion, infection, and tympanic membrane for
perilymphatic fistula, barotrauma, stroke, or perforation, otitis media, and cholesteatoma.
hemorrhage. A gradual onset is suggestive of A pneumatic bulb (pneumoscopy) is required
168 Diagnosis: A Symptom-based Approach in Internal Medicine
to accurately assess the tympanic membrane and Weber’s test are performed to differentiate
and the aeration in the middle ear between CHL and SNHL. Table 24.2 illustrates
• Cranial nerve testing—Particular attention common causes of CHL and SNHL
should be paid to facial nerve function, • The characteristics of CHL are:
because cranial nerves VII and VIII are closely 1. Negative Rinne test, i.e. BC > AC
associated at the brainstem and in the 2. Weber’s lateralized (i.e. sound will be
temporal bone. Unilateral V, VII and VIII heard better) to worst ear
involvement suggests a cerebropontine angle 3. Normal absolute bone conduction
lesion (usually a tumor). The trigeminal (V) 4. Speech discrimination is good
and lower cranial nerves (IX through XII) can • The characteristics of SNHL are:
also be affected by a lesion at the brainstem, 1. A positive Rinne test, i.e. AC> BC (normal
such as acoustic neuroma presenting as pattern will be retained)
hearing loss 2. Weber lateralized to better ear
• Basic tests of hearing—Auditory acuity can 3. Reduced absolute bone conduction
be assessed very crudely as follows: 4. Speech discrimination is poor.
1. Stand behind the patient, 3 feet away, i.e.
about an arm’s length and request him RED FLAGS
to close his eyes. (It is important that he • Earwax impaction should never be missed,
cannot see your face as many deaf but it is common9, 10
patients can lip read). • Otitis media in the adult is uncommon; such
2. You need to mask the nontest ear, say by presentation in an elderly should be referred
inserting your finger into it. for further evaluation to rule out an underlying
3. Whisper a few words at random from obstructive lesion of the eustachian tube, e.g.
behind the test ear, (e.g. 31, 45, 17, 64, etc). nasopharyngeal carcinoma
4. The patient should be able to repeat these • Suspicion of cholesteatoma warrants
back accurately. surgical consultation
5. Then perform the same test for the other • If patient is elderly and diabetic, be
ear to get a rough measure of their hearing. suspicious of malignant otitis externa
You could report this as (for example) “able • Patients who present with sudden SNHL
to hear a quiet whisper (i.e. 0-20dB) at arms should have a CT/MRI scan to exclude
length on the right ear, but only able to hear vascular ischemic event, acoustic neuroma,
a loud conversational voice (i.e. 40-60dB) at arms multiple sclerosis, perilymph fistula, and
length on the left”. other CNS disorders
• Alternately, place your fingers approxi- • In elderly people, physical examination and
mately 5 cm from one ear and rub them investigations should be focused to search for
together. The patient should be able to hear alarming symptoms, which may suggest the
the sound generated. Repeat for the other ear. cause of hearing impairment is something
However, hearing levels are objectively and other than age-related presbycusis
accurately assessed by pure tone audiometry • An individual’s confused behavior, poor job
• Tuning fork tests—To assess air conduction performance, social isolation, depression, etc.
(AC) and bone conduction (BC). Rinne’s test may be atypical presentation of hearing loss
Hearing Loss 169
25 Hematuria
US IVP/IVU
• Often the first choice for renal imaging. It can • For evaluation of urolithiasis, renal tumors,
differentiate cysts from solid lesions. The bladder tumors, and renal trauma
renal size, position, collecting system, • Studies have suggested that the omission of
prostate, and bladder can be visualized. IVU as a routine investigation for painless
Other abdominal and pelvic organs can also hematuria does not dramatically reduce the
be assessed for their disorders detection rate of malignant conditions10
• Very helpful if the patient is allergic to IVP • Not indicated in patients with history of allergy
dye, has compromised renal function, and for to IV contrast and compromised renal function.
evaluating hematuria in pregnancy
• In prospective studies, when US was Cystoscopy
combined with a single plain abdominal • Important procedure to evaluate lesions
radiograph, it proved to be superior to affecting urethra and bladder mucosa;
urography as the primary imaging study in
especially indicated in:
this series.8, 9
All patients older than age 40 with gross
X-ray KUB hematuria
• Plain X-ray can detect radiopaque calcium Patients older than age 40 with negative
stones (>2 mm in size), occasionally cystine microscopic hematuria, IVP, and US reports
stones, and foreign bodies Patients suspected of having bladder
• Radiolucent uric acid xanthine stones can not carcinoma even with negative IVP or
be detected. cystourethrogram results.
Hematuria 173
26 Hemoptysis
CBC INVESTIGATIONS—SPECIFIC
• Hb% reduced in chronic hemoptysis resulting
HRCT Scan
in IDA
• Leukocytosis in upper and lower respiratory • This procedure is of immense value for the
tract infections detection of bronchiectasis and undiagnosed
• Eosinophilia in mycosis (allergic broncho- lung malignancy, i.e. when clinical suspicion
pulmonary aspergillosis) or collagen-vascular for malignancy exists, but sputum and
disease (Churg-Strauss syndrome: vide infra ↓↓, bronchoscopy reports are noncontributory
PAN) or equivocal
• Platelets decreased in thrombocytopenia. • HRCT with IV contrast is presently
ESR considered as an adjunct diagnostic
modality in patients with high probability
• Elevated in infection, inflammation, and
of PE presenting with hemoptysis
collagen-vascular disease.
• Current opinion favors HRCT to bronch-
Coagulation Screen oscopy as the first-line procedure for
• Prothrombin time (PT) or partial prothr- screening patients with large and those with
ombin time (PPT) increased in disorders of massive hemoptysis.13-15
coagulation, and in patients with anticoagu-
lation therapy. Multidetector CT (MDCT)16-19
smelling sputum suggests a lung abscess; • History of coexisting disorders like cardiac
pink, frothy sputum is suggestive of (valvular disease, heart failure); renal
pulmonary edema; slight blood streaking in (nephrotic syndrome); SLE; or previous
the sputum is most common with bronchitis; malignancy may give clues to the cause of
frankly bloody sputum is seen in TB, PE, and hemoptysis, which may indicate additional
bronchogenic carcinoma investigations to arrive at the diagnosis
• Associated symptoms—History of cough, • Hemoptysis since childhood is likely due to
dyspnea, sputum production over several congenital heart defects, bronchiectasis,
years may suggest chronic bronchitis or cystic fibrosis, or blood dyscrasias
bronchiectasis. Weight loss and fatigue may • Hemoptysis that accompanies menstrual
suggest an underlying malignancy; fever and periods suggests pulmonary endometriosis
night sweats might indicate TB • Medications, especially anticoagulants,
• History of smoking†, occupational exposures might contribute to bleeding. Patients
(e.g. asbestos, silica), drug abuse (crack lung), belonging to this class of hemoptysis are
etc. are strong risk factors for massive those suffering from PE, cardiac valvular
hemoptysis defects, or CHF
• Physical examination—Besides the vital signs
†
Especially in a male sex, older than 40 years, and smoking (tachycardia, tachypnea, and hypotension
history of more than 40 pack-years.
Hemoptysis 181
that causes inflammation in blood vessels medical history, but discrepancies are detectable
(vasculitis), which restricts blood flow to upon careful evaluation. They usually and readily
various organs. The disease can occur at any provide consent for all invasive procedures,
age, but it’s more commonly diagnosed in including thoracotomy.
middle-aged people. People older than 65
years are unlikely to develop Churg-Strauss Paragonimiasis (pulmonary)—Caused by
syndrome. Although the disease may involve Paragonimus westermani, a common lung fluke in
any organ, including lungs, skin, gastroin- humans, commonly found in Asia, Africa, and
testinal system, kidneys, muscles, joints and Latin America. Human infections occur where local
heart, most commonly it affects lungs and people consume improperly cooked freshwater
skin. The restricted blood flow to these crustaceans such as lobsters and crabs. Usually no
organs can cause temporary or permanent symptoms are observed when the parasites
damage. There are three stages of Churg- migrate in the peritoneal cavity. When parasites
Strauss syndrome, namely, allergic (asthma, invade the lung, several symptoms including
itching, polyp); hypereosinophilia (fever, weight loss, pleuritic and chest pain, cough, and rusty sputum
abdominal pain, GI bleeding); and systemic vasculitis may be present. Pulmonary complications of
(cough, dyspnea, diarrhea, hematuria). Churg- untreated heavy infection include interstitial
Strauss syndrome is progressive, but not pneumonia, bronchitis, and bronchiectasis.
everyone develops all three phases, and the Secondary complications may include
phases don’t always develop in order. Without bronchopneumonia, lung abscess, pleural effusion,
treatment, this disease may be fatal. or empyema. Ectopic paragonimiasis results in
granulomatous lesions in the organs other than
Cocaine lung—Popularly called as crack lung, the lung. The most commonly affected organs
(the term crack characterizes the crackling sound include liver, spleen, omentum, and ovary. The most
heard when cocaine freebase is smoked); cocaine serious illness is cerebral paragonimiasis.
has multisystemic effects, and virtually every
organ system may be a site of action. Crack lung, REFERENCES
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CHAPTER
27 Hiccups
specially advanced tumors of the digestive tract.3 • Sudden emotional excitement (laughing)
Symptomatic relief to the exasperated patient while • Sudden temperature changes (hot then cold
conducting a judicious evaluation to determine the liquids, hot then cold shower)
cause is the initial approach in the management with • Psychogenic (anxiety)
persistent hiccups. • Alcohol excess (acute or chronic).
Occasional
DIFFERENTIAL DIAGNOSIS • Metabolic (Uremia, diabetic ketoacidosis,
Common electrolyte imbalance)
• Neck (goiter)
• Abdominal distension (aerophagy, carbonated • Thorax (pneumonia, reflux esophagitis,
beverages, excess smoking, hurried-eating) cardiomegaly)
186 Diagnosis: A Symptom-based Approach in Internal Medicine
ESR INVESTIGATIONS—SPECIFIC
• ALT, AST values elevated in hepatitis, and • Indicated in patients with intractable hiccups
cirrhosis (with or without neurological signs), e.g.
Hiccups 187
Table 27.2: Symptoms and signs of common pathologic disorders associated with hiccups
Symptoms and signs Possible disorders
• Cough, sputum, fever, chest pain; lung consolidation, • Pneumonitis
effusion, pleural rub
• Above symptoms, dyspnea, weight loss, with possible • Bronchial tumor
hemoptysis in a smoker; clubbing, lymphadenopathy
• Above symptoms, stridor, hoarse voice, neck/chest • Extrinsic compression by mediastinal
swelling, engorged veins over chest and neck, night mass (lung carcinoma, lymphoma, aortic aneurysm,
sweats; Horner’s syndrome retrosternal goiter, dermoid cyst)
• Bovine cough, hoarse voice, stridor, weight loss; • Intrinsic laryngeal lesion/Extrinsic compression (benign/
neck mass malignant)
• Heartburn, regurgitation • Gastroesophageal reflux disease, hiatal hernia, acid-
peptic disease
• Progressive dysphagia, dyspepsia, weight loss • Esophageal compression (carcinoma of the esophagus),
carcinoma stomach
• Pain abdomen, referred to shoulder/scapula, fever, • Cholecystitis, hepatitis, subdiaphragmatic abscess
• Alcohol excess, icterus, back pain, weight loss, • Hepatomegaly, pancreatitis/malignancy
• Headache, neck stiffens, fever, altered • Meningitis, encephalitis, CNS mass lesion
consciousness, seizures
• Sudden onset headache, aphasia, visual defects, • Stroke, basilar artery insufficiency
motor/sensory deficit
• Oliguria, edema, hypertension • Uremia
• Amelioration of hiccups by sleep, bizarre • Hysteria
accompanying symptoms
188 Diagnosis: A Symptom-based Approach in Internal Medicine
28 Insomnia
INVESTIGATIONS—SPECIFIC Actigraphy5
Sleep Diary† • A new technique that records individual’s
activities during sleep and waking; useful in
• Maintained for a period of two weeks to
the diagnosis of primary sleep disorders,
collect information on bedtime and time of
hypersomnia, and parasomnia.
rising, duration and quantity of sleep, timing
and quantity of meals and exercise, and CT/MRI Brain
ingestion of alcohol, drugs, and caffeine. The • In special circumstances such as history of
findings are correlated with the patient’s trauma, Alzheimer’s disease, PD, MS, seizure
subjective assessments of insomnia, and help disorder, and mass lesion.
to determine sleep pattern of the patient, its
severity, and causes; and also provides Mini-Mental State Examination (MMSE) and
educative value to learn more about sleep Geriatric Depression Scale
hygiene • In elderly patients these procedures may be
• Other tools that may be used to assess necessary to identify comorbid conditions
insomnia include—Epworth Sleepiness such as dementia and depression which
Scale ‡ , Sleep disorders questionnaire § , often result in insomnia.
Insomnia Severity Inventory, and the
Drug Toxicology Screen
Pittsburgh Sleep Quality Index**.
• In occult cases of insomnia suspected to be
Polysomnography (Sleep Study) due to substance abuse.
• It involves monitoring and staging sleep, i.e.
by recording brain waves with EEC, eye CLINICAL NOTES
movements with electrooculogram (EOG),
• History—A comprehensive sleep history
and chin movements with EMG; breathing
obtained from both the patient and the
patterns, e.g. airflow, respiratory effort,
patient’s bed partner is an important
pulse oximetry, heart rate; limb movements,
component in the initial evaluation of
e.g. of the legs and occasionally arms with
insomnia (Table 28.1)
EMG, and body position. Most patients are
• History should focus on age, onset and
also monitored with remote audio and video
duration, patient’s perception of sleep
recordings to observe for behaviors and
problem, coping mechanisms, day-time
seizures. Polysomnography is used in
naps, occupation, lifestyle, family and work-
special circumstances, e.g. to exclude
related stress, habits, travel, medications,
primary sleep disorders.
addiction, and any medical illness. This step
helps to eliminate insomnia due to another
†
Available at: http://www.helpguide.org/life/pdfs/ medical, psychiatric, substance abuse or
sleep_diary.pdf; http://content.revolutionhealth.com/ circadian rhythm disorder
contentfiles/media-pdf-hw-form_tm4434.pdf; and • Nocturnal symptoms6—A specific enquiry
http://www.shuteye.com/sleep-solutions/sleep-patterns/
sleep-diary.aspx should be made from the patient as well as
‡
http://www.reliamed.com/Forms/SleepinessScale.pdf bed-partner about ‘nocturnal’ symptoms
§
http://www.tmj-sleep-pain.com/sleep-disorders.htm
giving rise to transient or chronic insomnia.
**http://www.consultgerirn.org/uploads/File/trythis/
issue06_1.pdf These include respiratory distress, snoring,
192 Diagnosis: A Symptom-based Approach in Internal Medicine
SELECTIVE GLOSSARY of the upper airway that occur during sleep and
lead to breathing cessation (defined as a period
Chronic fatigue syndrome (CFS)—It is a clinical
of apnea > 10 sec) despite persistent respiratory
diagnosis characterized by an unexplained,
efforts. Symptoms include restlessness, snoring,
persistent or relapsing chronic fatigue that is of at
recurrent awakening, morning headache, and
least six months’ duration, and characterized by
excessive daytime sleepiness. Anatomic risk
four or more of the following symptoms present
factors include obesity, an oropharynx
concurrently for at least six months, namely-
“crowded” by a short or retracted mandible, a
impairment of memory or concentration; diffuse
prominent tongue base or tonsils, a rounded
pain; sore throat; tender lymph nodes; new
head shape and a short neck, a neck circum-
headaches; and nonrestorative sleep. Infectious,
ference > 43 cm, thick lateral pharyngeal walls,
immunological, neuroendocrine, sleep, and
or lateral parapharyngeal fat pads. Other
psychiatric mechanisms have been proposed as
identified risk factors include postmenopausal
etiological factors; however, a unifying etiology
status, aging, and alcohol or sedative use. A
for CFS has yet to emerge. Clinical evaluation is
family history of sleep apnea is present in 25 to
based upon above standardized guidelines,
40% of cases. Many people with OSA have
including an assessment of functional impair-
disorders such as hypertension, stroke,
ments. Since there are no specific diagnostic tests
diabetes, gastroesophageal reflux disease,
or biological markers for CFS, the diagnosis is nocturnal angina, heart failure, acromegaly,
made by ruling out other causes of fatigue such as and hypothyroidism. OSA can also be
eating disorders, psychotic disorders, bipolar associated with cardiac arrhythmias (e.g.
disorder, melancholic depression, and substance bradycardia, asystole). Diagnosis is based on
abuse within 2 years of the onset of fatigue. Trigger sleep history, and polysomnography.
points, which suggest fibromyalgia, are absent in
patients with CFS and fibromyalgia rarely coexist Periodic limb movement disorder (PLMD)—It is
in the same patient. characterized by bilateral repeated, rhythmic,
small-amplitude jerking or twitching movements
Fatal familial insomnia (FFI)8—Fatal familial in the lower extremities and, less frequently, in
insomnia is a rare inherited autosomal dominant the arms. These movements occur every 20 to 90
disorder characterized by degeneration of the seconds, mainly in nonrapid eye movement sleep,
thalamus and progressive insomnia. It is caused and can lead to arousals, which are usually not
by a mutation in the prion protein. Patients perceived by the patient. Rather, the presenting
present in their 50’s with a progressive sleep complaint is poor sleep and daytime somnolence.
disorder. There may be autonomic dysfunction. Occasionally, a bed partner may provide the
Dementia and death usually occur within one year history of limb movements.
following presentation. Measuring the cerebral Physical and neurological examinations are
metabolic rate of glucose (CMRglc) with 2-[18F] normal. In some cases, excessive somnolence
fluoro-2-deoxy-D-glucose PET in parallel with may be noted. Definitive diagnosis requires
detailed clinical, neuropsychological examinations polysomnography.
and polysomnography with EEG spectral analyses This condition and restless legs syndrome
may help in presymptomatic diagnosis of FFI. are more common in older patients.
Obstructive sleep apnea (OSA)—It is charact- Restless Legs Syndrome (RLS)/Ekbom
erized by episodes of partial or complete closure syndrome—A disorder characterized by: (1) a
194 Diagnosis: A Symptom-based Approach in Internal Medicine
desire to move the limbs, often with pares- lower brainstem lesions, stroke, Parkinson’s
thesias or dysesthesias; (2) symptoms exacer- disease, COPD, CHF, diabetes mellitus, thyroid
bated by rest and relieved by activity; (3) motor disease, medication effect, and other conditions.
restlessness; and (4) nocturnal increase in The most common reported symptoms are
severity of symptoms. Most patients, however, insomnia, frequent awakenings, a nonrestorative
simply relate a vague, nonpainful, indescribable sleep, choking, shortness of breath, and excessive
discomfort in the limbs and use terms, such as daytime sleepiness or fatigue. Sometimes, bed
crawling, creeping, jittery, tingling, burning, partners report witnessed apneas and mild
itching, aching, etc. The unpleasant limb snoring. The laboratory findings are not helpful.
sensations are precipitated by rest or inactivity, Primary central sleep apnea is frequently
especially in bed at night or in the car, airplane, associated with OSA. When both forms are
theater, etc. Motor activity characteristically present the condition is referred to as mixed sleep
relieves the limb discomfort. Most patients apnea, i.e. sleep apnea syndrome.
notice worsening of symptoms in the evening,
usually in bed before sleep or in the middle of REFERENCES
the night, followed by improvement early in 1. Fanfulla F, et al. The relationship of daytime hypo-
the morning. In severe cases, patients experience xemia and nocturnal hypoxia in obstructive sleep
symptoms both in the day and night. Although apnea syndrome. Sleep 2008;31(2):249-55.
[PMID: 18274273: Abstract].
RLS is idiopathic in most cases, it can be 2. Thomas VD, et al. Predictors of nocturnal oxygen
associated with several conditions, particularly desaturation in chronic obstructive pulmonary
iron, folate, and B12 deficiency. The possible disease in a South Indian population. J Postgrad
Med 2002;48:101[Free full text].
secondary causes of RLS include cigarette 3. Carney RM, et al. Insomnia and depression prior
smoking, varicose veins, hypothyroidism or to myocardial infarction. Psychosom Med 1990;
hyperthyroidism, acute intermittent porphyria; 52(6):603-9. [PMID: 2287700: Free full text].
4. Hayashi M. Nocturnal oxygen desaturation as a
myelopathy or myelitis, carcinoma, and drug predictive risk factor for coronary restenosis after
withdrawal from vasodilators, sedatives, coronary intervention. Circ J 2005;69(11): 1320-
imipramine, or opiates. This condition may be 6. [PMID: 16247205: Free full text].
5 . Morgenthaler T, et al. Practice parameters for
associated with uremia, diabetes mellitus, and the use of actigraphy in the assessment of
rheumatoid arthritis. The diagnosis of RLS rests sleep and sleep disorders: An update for 2007.
largely on clinical history. Polysomnography is Sleep 2007;30(4):519-29. [PMID: 17520797:
Abstract].
rarely necessary. 6. Pressman MR, et al. Nocturia. A rarely
recognized symptom of sleep apnea and other
Sleep apnea: central—A condition associated occult sleep disorders. Arch Intern Med 1996;
with multiple episodes of sleep apnea which are 156(5):545-50. [PMID:8604961: Abstract].
distinguished from obstructive sleep apnea (OSA) 7. Budhiraja R, et al. Sleep-disordered breathing and
cardiovascular health. Curr Opin Pulm Med 2005;
by the complete cessation of efforts to breathe. 11(6):501-6. [PMID: 16217175: Abstract].
This disorder is associated with dysfunction of 8. Cortelli P, et al. Presymptomatic diagnosis in
central nervous system centers that regulate fatal familial insomnia: Serial neurophysiological
and 18FDG-PET studies. Brain 2006;129(Pt
respiration or cardiac dysfunction. This condition 3):668-75. Epub 2006 Jan 6. [PMID: 16399807:
may be idiopathic (primary) or associated with Abstract].
CHAPTER
29 Jaundice
normalizes within 12-24 hours after IV Acute Viral Hepatitis Serology Markers (A, B,
administration of 5-10 mg vitamin K. C and D)
Absence of normalization indicates serious • Generally the following viral hepatitis
hepato-cellular damage (e.g. fulminant serology markers are tested:
hepatitis or liver cirrhosis). IgM anti-hepatitis A virus—(anti-HAV).
IgM anti-hepatitis B core antigen—(anti-
Hepatic Transaminase Enzymes
HBcAg).
• Aspartate aminotransferase (AST/SGOT) Hepatitis B surface antigen—(HBsAg).
and alanine aminotransferase (ALT/SGPT) Anti-hepatitis C virus antibodies—(Anti-
are the two enzymes which are sensitive HCV; may need PCR for HCV-RNA).
indicators of parenchymal cell integrity • If HBsAg is present, testing for coexisting
• Although both transaminase enzymes are HDV by anti-HDV is appropriate‡
widely distributed in the body, ALT is • For the diagnosis of presumed chronic viral
predominantly confined to the liver, and hepatitis, HBsAg and Anti-HCV serology,
therefore, more specific for liver disease. Both using an approved enzyme immunoassay
tests are sensitive indicators of hepatocellular (third generation, i.e. EIA-3), is the initial
necrosis step. Again, testing for HDV is appropriate
• In general AST is more specific for chronic if HBsAg is present
liver disease and ALT for acute liver disease • Acute HEV infection can be diagnosed by the
• In acute hepatitis, the transaminases are 10 presence of IgM anti-HEV and, later in the
times above normal. In cholestatic jaundice, course, finding of IgG anti-HEV
they are about 5 times above normal. Very • The interpretations of viral markers for acute
high levels may be seen in drug-induced hepatitis A, B, and C, and chronic hepatitis
hepatitis, especially paracetamol are summarized in Tables 29.2 to 29.4.
• The HCV infection can also produce wide
fluctuations in transaminases enzymes, Ultrasound (US)
ranging from normal to three to four times • This is the most important noninvasive
the normal range. This yo-yo phenomenon is a investigation in the evaluation of obstructive
distinguishing characteristic of HCV (cholestatic) jaundice, e.g. gallstones and
infection; therefore, the patient must undergo choledochal cysts, by detecting dilated bile
serial testing for monitoring three to four ducts. False-negatives are generally due to
times yearly throughout his or her lifetime inability to visualize the biliary tree, often due
• A sudden fall in the transaminases in a sick to interposed bowel gas
jaundiced patient is indicative of a bad • It also detects focal liver and pancreas
prognosis, as it is seen in acute fulminant diseases like tumors, abscesses and cysts,
hepatitis. (more than 2cm in diameter). It can identify
generalized parenchymal disorders like
Serum Alkaline Phosphatase (SAP)
cirrhosis and fatty change. It is also of great
• Useful in detecting early intra- or extrahepatic help in diagnosing small quantities of ascites.
obstruction; high values (5 times normal) favor
obstruction, and a normal SAP virtually ‡
Hepatitis D can only exist in the presence of hepatitis B,
excludes this diagnosis. because it requires hepatitis B enzymes to replicate.
Jaundice 199
• Identify stigmata of chronic liver disease such bleed, ascites, and renal failure indicate
as spider angiomata, palmar erythema, severe fulminant acute hepatitis
gynecomastia, and testicular atrophy • Beware of asymptomatic jaundice, especially
• Identify signs of portal hypertension such as in an elderly, as neoplasm—primary or
dilated collateral abdominal veins, spleno- metastatic—is a common etiology.
megaly, and ascites; and coagulopathy, e.g.
bruising, bleeding, and petechiae SELECTIVE GLOSSARY
• Presence of a greenish-brown corneal deposit
Gilbert disease—It is a chronic, benign,
of copper (Kayser-Fleischer ring), which is
intermittent, and familial (autosomal recessive)
often discernible only with a slit lamp is
condition, occurs predominately in men,
suggestive of Wilson’s disease
characterized by intermittent jaundice in the
• Imaging studies play a limited role, except
absence of hemolysis or underlying liver disease.
in suspected cases of malignancy or biliary
Also known as unconjugated benign bilirubinemia
obstruction
and familial nonhemolytic jaundice, the
• Because clinical signs are of little or no help
unconjugated hyperbilirubinemia in Gilbert
for identifying various causes of viral
syndrome has been recognized as due to
hepatitis, accurate diagnosis can only be
underactivity of the conjugating enzyme system
achieved with serologic and molecular testing
bilirubin - uridine diphosphate glucuronyl
(Table 29.5). Knowledge of the strengths and
transferase (UGT-1)—the enzyme that conjugates
limitations of these tests allows rational use
bilirubin with glucuronic acid. The
and interpretation of results. 3
hyperbilirubinemia is mild and, by definition,
RED FLAGS less than 6 mg/dl. However, most patients exhibit
levels of less than 3 mg/dl. Patients may report
• HCV infection (vide infra ↓↓) must be ruled vague abdominal discomfort and general fatigue
out in an otherwise asymptomatic patient for which no cause is found. Gilbert syndrome
with persistently elevated ALT is usually diagnosed around puberty, possibly
• All drugs, including herbal remedies and because of the inhibition of bilirubin glucur-
illegal drugs, should be suspected as onidation by endogenous steroid hormones. In
potential hepatotoxins. Iatrogenic (drug) older persons, the diagnosis is usually made
jaundice is more dangerous than viral when unconjugated hyperbilirubinemia is noted
hepatitis. This is because, if the diagnosis of on routine blood test results or unmasked by an
drug induced hepatitis is missed and the intercurrent illness or stress. LFTs: with the
drug is continued, the patient can die exception of unconjugated hyperbilirubinemia,
• All patients with HIV infection should be standard liver function test results are normal.
screened for viral hepatitis markers as A diagnosis of Gilbert syndrome can be made in
coinfection of HCV, HBV, and HIV is common the presence of (1) unconjugated hyperbilirubi-
due to shared modes of transmission. These nemia noted on several occasions; (2) normal
coinfections accelerate the course of chronic results from CBC count, reticulocyte count, and
liver disease and facilitate progression to blood smear; (3) normal liver function test
cirrhosis and hepatocellular carcinoma 4, 5 results; and (4) an absence of other disease
• In a jaundiced patient, signs of liver failure, processes or causes of unconjugated hyper-
such as encephalopathy, coagulopathy, GI bilirubinemia. A simple and easily available
Jaundice 203
bedside oral ‘rifampin test’ †† is found to be useful (HCV infection has been called a silent
to primarily distinguish Gilbert’s disease from epidemic).7 Besides, because of the long lag time
other causes of unconjugated hyperbilirubinemic between initial infection and clinically evident
disorders.6 Besides the usual laboratory methods, liver disease (20-25 years), early diagnosis of
genetic analyses of the UDP glucuronyl HCV infection can be missed or delayed
transferase gene can help in the diagnosis. The considerably. Production of antibodies against
major importance of establishing this diagnosis HCV can be delayed by up to 12 weeks, and
is to reassure patients that the disorder is benign about a third of infected individuals might not
and inconsequential, that the prognosis is have detectable antibody at the onset of
excellent, and that further investigations are not symptoms.8 Further, if symptoms do occur, the
essential. most common complaints such as fatigue,
abdominal pain, poor appetite, weight loss, and
Hepatitis C viral infection—HCV infection is
pruritus are nonspecific; most HCV-infected
not usually diagnosed in the acute phase because
patients have no hepatic symptoms. However,
most patients are initially asymptomatic, and
almost 40% of patients infected with HCV
therefore, have not sought medical attention.
develop at least one extrahepatic manifestation9
during the course of the disease such as mixed
††
Rifampin increases total serum bilirubin levels in patients cryoglobulinemia, which is marked by skin
with and without Gilbert’s syndrome. On fasting for 12 to involvement, marked by rashes, purpura,
24 h, an absolute increase of bilirubin to >1.9 mg/dl 2 to 6 h petechiae, urticaria, or necrotic ulcerations in
after the administration of 900 mg of rifampin distinguishes
patients with Gilbert’s syndrome from those without it. In the lower extremities (i.e. leukocytoclastic
the nonfasting state, an increase in total serum bilirubin to vasculitis); rheumatological manifestations
>1.5 mg/dl 4 to 6 h after the administration of rifampin
such as joint and muscle aches, fibromyalgia;
distinguishes persons with Gilbert’s syndrome from those
without it. kidney disease such as membranoproliferative
204 Diagnosis: A Symptom-based Approach in Internal Medicine
30 Myalgia
Endocrine/Metabolic Panel
Electrolytes
• Where indicated, additional tests such as 24-
• Hypokalemia is usually diuretic induced. hour urine cortisol testing to rule out
Cushing’s disease; oral glucose load/growth
Sr Alkaline Phosphate hormone assay to rule out acromegaly; and
• Usually elevated in osteomalacia, hyperpara- vitamin D assay to rule out osteomalacia may
thyroidism, metastatic carcinoma, Paget’s be obtained.
disease.
Muscle Biopsy/Genetic Analysis
TFTs • If the diagnosis is still inconclusive after the
history, physical examination, and laboratory,
• High TSH values may be the only abnormality
radiologic, and electromyographic evalua-
of hypothyroidism; low TSH values with
tions, a muscle biopsy is required for patients
corresponding high T3 and T4 values confirm
who have a suspected myopathy. The
thyrotoxicosis.
pathologic analysis of biopsy specimens
ANA, RF focuses on the histologic, histochemical,
• Likely to be positive in connective tissue electron microscopic, genetic, and biochemical
disorders; if RF/ANA assay is positive, changes that are found in the affected muscle.
additional studies such as double-stranded Molecular analysis of candidate genes is
DNA, or antiphospholipid antibodies (lupus) becoming a major diagnostic tool in many
may be obtained. muscle disorders.
208
• Presence of associated symptoms or signs, involving the quadriceps muscle group, but may
indicating involvement of organs or tissues also affect the hamstring, and triceps surae
other than muscle, such as dyspnea, orthopnea, groups. Up to six hypothesized theories have
respiratory failure, congestive heart failure, been proposed for the mechanism of DOMS,
arrhythmias, cataracts, mental retardation, and namely: lactic acid, muscle spasm, connective
hepatomegaly is valuable in the clinical tissue damage, muscle damage, inflammation
diagnosis of hereditary myopathies (e.g. and the enzyme efflux theories. The mechanisms,
myotonic dystrophy, Duchenne’s or Becker’s treatment strategies, and impact on athletic
muscular dystrophies) performance remain uncertain, despite the high
• Normal findings on a battery of investi- incidence of DOMS. Clinically, DOMS is a self-
gation do not rule out organic disease, but limiting condition that usually requires no
strongly suggest psychogenic disorders. treatment.
• To rule out myocardial ischemia, infarction. • With barium contrast and follow-through—
to detect mucosal lesions (ulcers), obstruc-
Blood Glucose tion, or mass lesion.
including low Na (< 135 mEq/l), high K (> 5 mEq/l), sinusitis, emotional stress, excitement, physical
low HCO3 (< 15 to 20 mEq/l), and high BUN exhaustion, foods such as chocolate or cheese,
(>20 mg/dl). A high index of suspicion is menstruation, hot weather etc. cannot always be
therefore required in patients with unexplained pinpointed as easily as they can in children. Each
fatigue, hyponatremia or hypotension. episode is similar to the previous ones. The
episodes tend to start at about the same time of
Boerhaave syndrome (Pronunciation: bu-r’hah-
day, last the same length of time, and present
ve - )—It denotes esophageal perforation or
the same symptoms at the same level of intensity.
rupture of the esophagus caused by increased
CVS appears to be linked to migraines in some
intraluminal pressure and distension during
cases. Treatment with migraine medications
retching or vomiting. The presence of a hole or
often helps. Because other more common
other type of opening in the esophageal wall
diseases and disorders also cause cycles of
facilitates the passage of esophageal contents into
vomiting, many people with CVS are initially
the mediastinum resulting in mediastinitis. The
misdiagnosed until the other disorders can be
most common cause of esophageal perforation is
ruled out. To be diagnosed with CVS, a person
injury during a medical procedure such as
must have experienced at least two episodes of
esophagoscopy or placement of a nasogastric
intense nausea and unremitting vomiting or
tube, and pathologic process such as neoplasm
retching lasting hours or days. These episodes
or gastric reflux with ulceration. Less common
must be separated by weeks or months of
causes include injuries from penetrating or blunt
symptom-free intervals. There is no specific test
trauma or injury to the esophagus during an
that will confirm the diagnosis of CVS. Other
operation on another organ, mechanical problem
conditions that can produce vomiting, such as,
such as violent retching or vomiting; ingestion of
labyrinthine disease, metabolic disorders, CNS
a foreign body or caustic agents. The condition
often results in infection of the mediastinum and tumors, and pregnancy must be excluded.
mediastinitis. The Mackler triad is the classic Gastroparesis—Literally translated, it means
presentation of spontaneous esophageal rupture stomach paralysis—is a digestive disorder in
is in a middle-aged man with a history of recent which the motility of the stomach is either
vomiting or retching after dietary overindulgence and abnormal or absent. Normally, the stomach
overconsumption of alcohol, with chest pain and contracts to move food down into the small
subcutaneous emphysema. intestine for digestion. The vagus nerve controls
Cyclic vomiting syndrome—CVS causes bouts the movement of food from the stomach through
or cycles of severe nausea and vomiting that last the digestive tract. Gastroparesis occurs when
for hours or even days, and alternate with longer the vagus nerve is damaged, and the muscles of
periods of no symptoms. The disorder which has the stomach and intestines do not work normally.
no known cause typically begins between the Food then moves slowly or stops moving
ages of 3 and 7 years. Children tend to outgrow through the digestive tract (delayed gastric
CVS when they are teenagers. While the disorder emptying). The most common cause of
occurs most often in children, CVS can begin at gastroparesis is diabetes mellitus; other causes
any age. Adult episodes tend to occur less often include hypothyroidism, vagotomy, gastric
than they do in children, but they usually last bypass surgery,viral infections, medications such
longer. Furthermore, the events or situations that as anticholinergics and narcotics, smooth muscle
trigger episodes in adults such as coryza, disorders such as amyloidosis and scleroderma;
Nausea and Vomiting 217
Parkinson’s disease; multiple sclerosis; and lastic disorder is telangiectasis, which can be
idiopathic gastroparesis. Signs and symptoms of caused by breast cancer and lymphomas.
gastroparesis are: heartburn, pain in the upper Lambert-Eaton myasthenic syndrome is a
abdomen, nausea, vomiting of undigested neurologic PNS that can be caused by a variety
food—sometimes several hours after a meal; of tumors including small cell lung cancer,
early feeling of fullness after only a few bites of lymphoma, breast, colon and other cancers.
food; weight loss due to malnutrition; abdominal Syndrome of inappropriate antidiuretic
bloating, lack of appetite, and gastroesophageal hormone (SIADH) is an endocrine PNS, which
reflux. Gastric emptying scintigraphy of a is seen in as many as 40% of patients diagnosed
radiolabeled solid meal for 2 hours confirms the with small cell lung cancer. Symptoms generally
diagnosis of gastroparesis. Performing the test develop (depending on body system affected)
for a longer duration, up to 4 hours, has been over a period of days to weeks and usually occur
proposed to increase the yield in detecting prior to tumor detection, which can complicate
delayed gastric emptying in symptomatic diagnosis. Some paraneoplastic syndromes may
patients. be confused with metastatic disease or spread
Paraneoplastic syndromes—PNS can be defined of the cancer. The presence of the syndrome may
as a group of symptoms that may develop due be the only indication that a patient has a
to indirect and usually remote immune- malignancy or that a malignancy has recurred.
mediated effects produced by tumor cell Specific diagnosis depends on demonstration of
metabolites or other products which disrupt the specific autoantibodies in various tissues of the
normal function of surrounding cells and tissue. body and imaging studies such as MRI, PET, and
Body systems that may be affected by PNS SPECT scans.
include neurological, endocrine, cutaneous,
renal, hematologic, gastrointestinal, and other REFERENCE
systems. The most common manifestations of
1. Quigley EM, et al. AGA technical review on nausea
PNS are cutaneous, neurologic, and endocrine and vomiting. Gastroenterology 2001;120(1):263-
disorders. An example of a cutaneous paraneop- 86. [PMID: 11208736].
CHAPTER
32 Pain—Chronic
CPK NCS/EMG
• Elevated in myopathies (polymyositis, • These two studies, which compliment one
metabolic disorders, drugs, alcohol, and another, can often distinguish between
muscular dystrophy). neurogenic and myogenic disorders
• NCS distinguish between mononeuro-
INVESTIGATIONS—SPECIFIC† pathies (e.g. due to trauma, compression, or
X-ray/CT Scan entrapment) and polyneuropathies (e.g. due
to metabolic, toxic, malignant, nutritional,
• In patients suspected with bony abnormalities, autoimmune, or hereditary disorders)
e.g. cervical, lumbosacral disk lesions; thoracic • In addition, they may also be helpful in
outlet syndrome; compartment syndromes, excluding organic disorders when psycho-
and neoplastic lesions genic pain or functional syndrome is suspected.
• Lytic lesions may be the only finding early
in Paget’s disease. Cancer Screen/Tumor Markers
• Age and gender related cancer screening, e.g.
MRI breast mammography, Pap smear, PSA, etc.;
• To further evaluate CT scan lesions related and tumor markers, e.g. alpha-fetoprotein, beta
to discogenic pain; spinal canal stenosis; chorionic gonadotropin, carcinoembryonic
various bone and joint lesions; avascular antigen, etc. may be helpful in the evaluation
necrosis, etc of patients suspected with cancer pain.
• MRI is extremely helpful in the evaluation
of pain that may be due to intracranial mass CLINICAL NOTES
lesion; bony or soft-tissue lesions, abscess,
• Although most patients have great difficulty
metastatic deposits; facial pain due to
in describing pain sensation, its assessment
posterior fossa lesions; facial nerve lesions;
is important and helpful diagnostically.
orbital pain; abdominal and pelvic pain due
Therefore, evaluation of a patient with
to inflammation or malignancy.
chronic pain should include the following:
Bone Scan Quality (pricking, lancinating, burning,
• Helpful in evaluating pain due to a stress etc., i.e. somatic, visceral, or neuropathic,
fracture, infection (osteomyelitis); and as explained above);
chronic pain in bone cancer patients – Is it bone pain? Bone pain may begin as a
most commonly due to secondary deposits dull, constant ache that grows worse; it feels
in spine, pelvis, extremities, ribs, and skull deep with boring, stabbing, throbbing,
• Bone scanning is the most sensitive test cramping or gnawing sensation; usually
for evaluating the extent of lesions in increases at night and may not subside
the whole skeleton affected by Paget’s when sleeping; mostly due to metastatic
disease. deposits; referred to a different area from
the site of the problem;
Duration (acute, chronic, constant, or
†
Because of heterogenicity of the chronic pain and its intermittent);
presentation, specific laboratory and imaging evaluation
must be targeted to specific condition and to rule out other
Patient’s functional status (i.e. the impact
life-threatening illnesses. of pain on patient’s daily activities such as
222 Diagnosis: A Symptom-based Approach in Internal Medicine
ability to perform household chores, work • Assess patient’s psychosocial status—A good
tasks, leisure in interests, sleep, etc. with psychosocial and psychosexual history is
the help of VAS, i.e. visual analog scale; ‡ needed when organic diseases are excluded or
A review of previous diagnostic studies coexisting psychiatric disorders are suggested.
(careful reviewing of prior test reports is Obtain sufficient history to evaluate depression;
essential to eliminate unnecessary anxiety disorder; somatization; physical or
repetition); sexual abuse; drug abuse/dependence; and
An assessment of coexisting diseases and family, marital, or sexual problems
conditions (i.e. biological causes such as • History of onset—Discord in family dynamics,
musculoskeletal, neurologic, cardiovas- difficult social interactions, stressful work
cular, respiratory, gastrointestinal, and environment, strained marital relationship,
gynecological disease). sexual problems, and history of substance abuse,
• The mnemonic “PQRST” is helpful when domestic violence, and absence of a clear
dealing with painful conditions: pathophysiologic mechanism suggest a primary
“P” refers to precipitating or palliative psychosocial cause
factors; this information may provide • Circumstances associated with the onset of
clues for possible etiologies or associated pain is important; it helps to identify whether
disorders; the patient’s complaints are related to
“Q” refers to quality of the pain (nocicep- biologic process, or is predominantly psyc-
tive, neuropathic, or mixed - as described hological or psychosocial in origin
above); • Physical examination—Its main purpose is
“R” stands for radiation and original to determine the possibility of underlying
location of pain; radiating pain is biologic process. Each system, particularly
characteristic of neuropathic pain; the ones pertaining to the patient’s
“S” stands for severity of pain: many special- presentation, and including complete
ized clinical tools in multiple languages mental state examination (affect, mood,
are available for pain assessment. 10 ideation, and insight) is performed. Any
Examples include unidimentional scales evidence of primary biologic process
such as the visual analog scale (VAS), responsible for chronic pain is subjected to
verbal rating scale (VRS), numerical further appropriate physical examination
rating scale (NRS), and the pain faces and investigations. Table 32.3 illustrates
scale, etc. (use score 1-to-10 rating scales: location-wise classification of common
severe pain is defined as pain that is rated biological causes for chronic pain
as 7 to 10 on a 0 to 10 VAS); • Assess for Waddell’s signs 11 (Table 32.4), and
“T” stands for timing, including onset, inconsistencies in the above examination;
duration, and frequency—daily, paroxys- positive Waddell’s signs generally indicate a
mal, seasonal, nocturnal, or diurnal. nonphysiological etiology of pain.
‡
VAS: A tool used to help a person rate the intensity of RED FLAGS
certain sensations and feelings, such as pain. The VAS for
pain is a straight line with one end meaning no pain and • Any patient with unexplained, persistent
the other end meaning the worst pain imaginable. A patient pain—somatic, visceral, or bone pain—should
marks a point on the line that matches the amount of pain
he or she feels. It can also be used to help choose the right be suspected of having malignant disease and
dose of pain medicine. appropriate investigations performed.
Pain—Chronic 223
either the arms or the legs. CRPS is characterized account for the degree of pain and dysfunction.
by pain, edema, stiffness, and discoloration. Pain A single, reliable, sensitive, and specific
is intense and burning, out of proportion to the diagnostic test for CRPS is not available;
injury, allodynia (perception of pain from a however, the disease is not fatal.
nonpainful stimulus), or hyperalgesia (disprop-
ortionate to the inciting event). Edema is usually REFERENCES
one of the earliest findings. Stiffness may occur. 1. International Association for the Study of Pain. Web
Discoloration may vary from intensely site: http://www.iasp-pain.org/AM/Template.
cfm?Section=General_Resource_Links&emplate=/
erythematous to cyanotic, pale, purple, or gray. CM/HTML Display.cfm & ContentID=3058#Pain.
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Companies, Inc. p. 1050.
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11-08.
hyperthermic or hypothermic, and shows
5. Turk DC, et al. psychological approaches in the
increased nail and hair growth. Physical treatment of chronic pain patients – when pills,
findings may be minimal; radiographs may scalpels, and needles are not enough. Can J
psychiatry 2008; 52(4):213-23.
show early bony changes. 6. Gatchel RJ, et al. The biopsychosocial approach to
chronic pain: Scientific advances and future
Dystrophic phase—Vasomotor instability for several directions. Psychol Bull. 2007;133(4):581-624.
months: Edematous tissue becomes indurated; skin [PMID: 17592957: Abstract].
7. Wooley CF. Where are the diseases of yesteryear?
becomes cool and hyperhidrotic with livedo DaCosta’s syndrome, soldier’s heart, the effort
reticularis or cyanosis; hair may be lost, and nails syndrome, neurocirculatory asthenia—and the
mitral valve prolapse syndrome.Circulation 1976;
become ridged, cracked, and brittle. Hand dryness
53(5):749-51.
becomes prominent, and atrophy of skin and 8. Thomas HV, et al. Pain in veterans of the Gulf War
subcutaneous tissues becomes noticeable. Pain of 1991: A systematic review. BMC Musculoskelet
Disord. 2006; 7:74. [PMID: 16987407: Free full text].
remains the dominant feature. It usually is constant 9. Stimpson NJ, et al. Prevalence of reported pain,
and is increased by any stimulus to the affected area. widespread pain, and pain symmetry in veterans
of the Persian Gulf War (1990-1991): The use of pain
Stiffness develops at this stage. Radiographs may manikins in Persian Gulf War health research. Mil
show diffuse osteoporosis. The 3-phase bone scan Med 2006;171(12):1181-6. [PMID: 17256678:
Abstract].
is usually positive. Duration is 3-12 months from 10. Web sites: http://www.britishpainsociety.org/
onset. pain_scales_eng.pdf; http://www.partnersagainst
pain.com/ professional-tools/pain-assessment-
Atrophic phase—Usually cold extremity with scales.aspx?id=3.
atrophic changes: Pain spreads proximally, may 11. Fishbain DA, et al. A structured evidence-based
review on the meaning of nonorganic physical
diminish in intensity, but persists with occasional signs: Waddell signs. Pain Med 2003;4(2):141-81.
flare-ups. Skin is thin and shiny; edema is absent; [PMID: 12911018 Abstract].
12. Kasper DL, et al (Eds). Harrison’s Prin. of Internal
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marked demineralization. 13. http://www.emedicine.com/pmr/TOPIC123.HTM.
Accessed on 08-11-08.
The diagnosis of CRPS is excluded by the 14. http://www.emedicine.com/emerg/TOPIC497.
existence of any condition that would otherwise HTM. Accessed on 08-11-08.
CHAPTER
33 Palpitation
Table 33.1: The indications for ambulatory ECG Table 33.2: Common indications/contraindications for
monitoring for symptoms of arrhythmia are as follows2: EPS in patients with palpitations
and is capable of pressing the signal button Table 33.3: Recommendations for echocardiography in
promptly. Newer event recorders have patients with arrhythmias and palpitations5
programmable automatic triggers for rapid Class I
and slow heart rates. The advantages over 1. Arrhythmias with clinical suspicion of structural
heart disease
Holter monitoring are that, a symptom
2. Arrhythmia in a patient with a family history of a
dairy is not needed and the higher yield of genetically transmitted cardiac lesion associated
collected data is useful for detecting with arrhythmia, such as tuberous sclerosis,
rhabdomyoma, or hypertrophic cardiomyopathy
arrhythmia associated with palpitation. 3. Evaluation of patients as a component of the work-
up before electrophysiological ablative procedures
Continuous Mobile Cardiac Outpatient
Class IIa
Telemetry (MCOT)4 1. Arrhythmia requiring treatment
• It has several advantages over traditional 2. TEE or intracardiac ultrasound guidance of radiofrequency
ablative procedures
ambulatory monitoring systems in the
Class IIb
diagnostic evaluation of symptoms such as 1. Arrhythmias commonly associated with, but
palpitations, dizziness, and syncope. MCOT without clinical evidence of heart disease
2. Evaluation of patients who have undergone radio-
can detect asymptomatic clinically significant
frequency ablation in the absence of complications
arrhythmias, and was especially useful to (In centers with established ablation programs, a post-
identify the cause of presyncope/syncope, procedural echocardiogram may not be necessary)
3. Postoperative evaluation of patients undergoing the
even in patients with a previous negative Maze procedure to monitor atrial function
workup. This outpatient monitoring system Class III
allows patients to undergo daily medication 1. Palpitation without corresponding arrhythmia or
dose titration in the outpatient setting, thus other cardiac signs or symptoms
2. Isolated premature ventricular contractions for
avoiding hospitalization.
which there is no clinical suspicion of heart disease
Pacemaker Evaluation
arrhythmias and palpitations are given in
• In patients who complain of palpitation with Table 33.3.
pacemaker.
TFTs
Exercise ECG/TMT
• Hyperthyroidism is associated with AF,
• Indicated in patients who are known to have PSVT, and CHF.
or suspected to have CAD.
Echocardiography Urea, Creatinine, Electrolytes
• May be indicated in patients suspected of • Dehydration and hypovolemia may be
valvular heart disease, CHF, or any structural associated with arrhythmias.
abnormality. The ACC/AHA Guidelines for
the Clinical Application of Echocardiography Urine
state that, “Unless there are other indications
• 24 hours urine collection for vanillylmandelic
for testing, echocardiography need not be
acid (VMA) assay.
performed in a subject with palpitation for
which an arrhythmic basis has been ruled
Drug Levels
out. 5 ” The ACC/AHA indications for
echocard-iography in patients with • To assess for drug toxicity, e.g. digitalis.
Palpitation 229
CLINICAL NOTES
Table 33.4: Clues to arrhythmia in clinical disorders
• An important step in the evaluation of Clinical disorder Clues
palpitation is to establish or exclude the • Systemic hypertension • Vasodilators (nitrates,
presence of underlying structural heart calcium channel
disease such as CAD, CHF, valvular stenosis blockers);
pheochromocytoma
or regurgitation, cardiomyopathy, and • Coronary artery • Ventricular arrhythmias;
congenital cardiac disorders, and to detect life- disease heart blocks
threatening cause of palpitation that place • Heart failure • Digitalis toxicity;
hypokalemia of diuretics
patients at risk of sudden death—VT and VF • Diabetes mellitus • Hypoglycemia
• Any evaluation of palpitations must first • Bronchial asthma • Bronchodilators
confirm that the patient is hemodynamically (methylxanthines, beta-
agonists)
stable, and that the symptoms are not life- • Thyrotoxicosis • Sinus tachycardia, Atrial
threatening, which in many cases can often fibrillation
be made from history, physical examination, • Congenital deafness • Congenital long QT
syndrome
and ECG findings, which are sufficient to • Antiarrhythmic or • Acquired long QT
determine the nature of the problem antidepressant drugs disorder
• A patient with palpitation is usually asympt- • Diuretics • Hypokalemia
• Pre-excitation • Reentry tachycardias
omatic at the time of physical examination,
and the diagnosis of arrhythmia may pose a
real problem if the arrhythmia is not present • Associated symptoms such as chest pain (angina,
at the time of examination. One solution is MI); dyspnea (LVF, MI, pulmonary embolism);
to request the patient to present as soon as lightheadedness, dizziness, or sweating (syncope,
possible at the onset of palpitation. However, hypoglycemia, pheochromocytoma); may
if the history and physical evaluation indicate hemodynamic instability and mandate
indicates the possibility of any serious further evaluation
arrhythmia, it is prudent to monitor the • Evidence of anxiety or depression should be
patient (Table 33.4) sought in patients presenting with palpita-
• History—In a study reported by Summerton tions without clinical evidence of cardiov-
N et al, 6 characteristic historical factors ascular disease. Psychological factors may
contributory to new-onset clinically signif- influence the perception of palpitation as
icant palpitations include: unpleasant and abnormal and thereby
Current medical problems, e.g. thyroid prompt consultation. Psychological factors
disease, asthma, anemia, anxiety, should therefore be integrated into the
depression, perimenopause diagnosis of palpitation
Past history of hypertension, CAD,
• A family history of SCD or syncope may
valvular heart disease, congenital heart
suggest an inherited dilated or hypertrophic
disease, cardiomyopathy
cardiomyo-pathy (HCM)‡, congenital LQTS,
Family history of thyroid disease, palpitation
or Brugada syndrome (BrS: vide infra ↓↓). In
Consumptions—Cigarettes, alcohol,
general, first-degree relatives under 40 with
coffee—per day frequency, and duration
a family history of SCD must be investigated
Current medications, e.g. benzodiaze-
pines, ACE-inhibitors, diuretics, OHA, ‡
The apical variant of HCM, also known as ‘Japanese or
insulin, beta-blockers, antianginals, Asian variant’, is rare and often poses a diagnostic
thyroxin, antidepressants. challenge.
230
heart syndrome: vide infra ↓↓) Midsystolic click, often followed MVP
by systolic murmur
• Palpitations due to AF are the most common
arrhythmia in the elderly (secondary to Triple apical impulse, loud S4, HOCM
harsh, holosystolic murmur
hypertension, and CAD) along left sternal border,
• To help characterize the palpitations, increased with Valsalva
maneuver, decreased with
requesting the patient to simulate their rhythm
squatting, associated with
by tapping his finger on a hard surface can be mitral regurgitation, AF, VT
quite informative. The physician can also help Laterally displaced apical Dilated
the patient by tapping out examples of rapid impulse, S3, S4 gallop, CHF, cardiomyopathy
or irregular rhythm that has been experienced associated with AF, VT
231
leads is observed in a variety of clinical settings in patients who usually drink little or no alcohol.
(e.g. acute septal ischemia, pericarditis, Recently, similar reports indicated that
ventricular aneurysm, and in some normal recreational use of marijuana may have similar
variants like early repolarization), and is not effects. Palpitations are the most common
unique or highly specific for the BrS. A clear symptom. These can be intermittent or
distinction cannot be made on the basis of an persistent, depending on the presence or absence
ECG alone. However, ST segment elevation in of sustained arrhythmia and the ventricular
the right precordial leads in the absence of response to atrial fibrillation. Patients with rapid
ischemia, electrolyte or metabolic disorders, ventricular responses can present with near
pulmonary or inflammatory diseases or syncopal symptoms, dyspnea on exertion, and
abnormalities of central or peripheral nervous angina. The most common rhythm disorder is
system may identify the BrS. In such cases, the atrial fibrillation, which usually converts to
term “idiopathic” is appropriate. The ECG normal sinus rhythm within 24 hours. Atrial
manifestations of BrS are often dynamic or flutter, isolated ventricular premature beats,
concealed, and may be unmasked or isolated atrial premature beats, junctional
modulated by sodium channel blockers tachycardia, and various other rhythm distur-
(ajmaline, procainamide and flecainide), a bances may occur with less frequency. The
febrile state, vagotonic agents, α-adrenergic holiday heart syndrome should be considered
agonists, β-adrenergic blockers, tricyclic or particularly as a diagnosis in patients without
tetracyclic antidepressants, a combination of overt heart disease presenting with new onset
glucose and insulin, hypo- and hyperkalemia, atrial fibrillation. Though recurrences occur, the
hypercalcemia, and alcohol and cocaine toxicity. clinical course is benign and specific antiarr-
Imaging techniques, endocardial biopsy and hythmic therapy is usually not warranted.
cardiac catheterization are useful in ruling out Arrhythmia monitoring and observation are
structural cardiac abnormalities. Finally, adequate in many patients.
extension of the testing to family members is also
Pacemaker syndrome—First described in 1969 by
important because of high incidence of familial
Mitsui et al as a collection of symptoms associated
occurrence. Currently, implantable cardiac
with right ventricular pacing. In a general sense,
defibrillator implantation is the only proven
pacemaker syndrome can be defined as the
effective therapy in preventing sudden death in
symptoms associated with atrioventricular
patients with the BrS, and is indicated in
dyssynchrony. The symptoms of pacemaker
symptomatic patients, and should be considered
syndrome included dyspnea on exertion,
in asymptomatic patients in whom VT/VF is
paroxysmal nocturnal dyspnea, orthopnea,
inducible at time of electrophysiologic study.
palpitations, hypotension, pre-syncope, and even
Holiday heart syndrome—The association syncope. Heart failure signs include elevated neck
between alcohol use and rhythm disturbances, veins, rales, and pedal edema. Physical exam can
particularly supraventricular tachyarrhythmias often reveal cannon A-waves. Additional
in apparently healthy people is called “holiday symptoms attributed to pacemaker syndrome
heart syndrome”. The syndrome was first include easy fatigability, malaise, headache, and
described in persons with heavy alcohol the sensation of fullness and pulsations in the
consumption, who typically presented at head and neck. In the era of physiological dual
weekends or after holidays, but it may also occur chamber pacing, the diagnosis is often forgotten,
Palpitation 233
but pacemaker syndrome may still occur. The heart and produce similar signs and symptoms
diagnosis of pacemaker syndrome requires a high such as dehydration, anemia, or hyperthyroidism.
index of suspicion and the correlation of symptoms
or relative hypotension with periods of ventricular REFERENCES
pacing. The electrocardiogram should be 1. Zimetbaum P, et al. Evaluation of patients with
inspected carefully for loss of atrial capture, palpitation. NEJM 1998;338(19),1369-73.
particularly when anti-arrhythmic drugs which 2. Crawford MH, et al. ACC/AHA Guidelines for
Ambulatory Electrophysiology. A report of the
increase the pacing threshold have been American College of Cardiology/American Heart
prescribed. In addition, environmental sources of Association Task Force on Practice Guidelines. J
electromagnetic interference, both within and Am Coll Cardiol 1999;34(3):912-48. [PMID:
10483977]. Website: http://content.onlinejacc.org/
outside the hospital environment can result in cgi/content/short/34/3/912. (Accessed on 22-07-08)
pacemaker malfunction and aggravating 3. Visit http://content.onlinejacc.org/cgi/content/full/
symptoms of pacemaker syndrome. 48/11/2360 for ACC/AHA guidelines for the use of
EPS.
Postural orthostatic tachycardia syndrome 4. Olson JA, et al. Utility of mobile cardiac outpatient
telemetry for the diagnosis of palpitations,
(POTS)—It is an under recognized but persistent presyncope, syncope, and the assessment of
autonomic disorder in young patients, usually therapy efficacy. J Cardiovasc Electrophysiol
2007;18(5):473-7. [PMID: 17343724: Abstract].
females aged 15 to 50 years, with a variety of
5. Cheitlin MD, et al. ACC/AHA Guidelines for the
symptoms and variable outcome. Patients with Clinical Application of Echocardiography. A report
this condition exhibit orthostatic intolerance (OI) of the American College of Cardiology/American
Heart Association Task Force on Practice Guide-
and excessive tachycardia. Excessive tachycardia
lines (Committee on Clinical Application of Echo-
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minutes) increase in heart rate by more than 30 American Society of Echocardiography. Circulation
1997;95(6):1686-744.[ PMID: 9118558]. Web site:
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“http://circ.ahajournals.org/cgi/content/full/95/6/
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experience difficulty with daily routines such as 6. Summerton N, et al. New-onset palpitations in
general practice: Assessing the discriminant value
housework, shopping, eating, and attending work of items within the clinical history. Family Practice
or school. The possibility exists that all forms of 2001;18;383-92.
OI, including POTS, result from central 7. Lessmeier TJ, et al. Unrecognized paroxysmal
supraventricular tachycardia. Potential for misdia-
hypovolemia even without tachycardia. Adults gnosis as panic disorder. Arch Intern Med
with POTS do not have hypotension, whereas 1997;157(5):537-43. [PMID: 9066458: Abstract].
children may exhibit hypotension. Many patients 8. Masuki S, et al. Excessive heart rate response to
orthostatic stress in postural tachycardia syn-
with POTS are intolerant of exercise. “Idiopathic” drome is not caused by anxiety. J Appl Physiol
POTS must be distinguished from other 2007;102(3):896-903. [PMID: 17110507: Free full
conditions that can reduce venous return to the text].
CHAPTER
34 Polyuria
Table 34.1: Solute vs water diuresis—differential Table 34.2: Differential diagnosis of diabetes insipidus
diagnosis Cranial diabetes insipidus Nephrogenic diabetes insipidus
1-A—Solute (osmotic) diuresis: (due to excessive filtration Trauma (head injury) Drugs (lithium, demeclocycline)
of a poorly reabsorbed solute) Vascular Renal disease
• Glucosuria (Diabetes mellitus, DKA) Hemorrhage/thrombosis Renal tubular acidosis
• Urea diuresis (high-protein parental infusions) Aneurysm Pyelonephritis
• Mannitol or glycerol infusion Sheehan’s syndrome Polycystic kidney disease
Infections Metabolic
• Radiographic contrast media
Meningitis Hypercalcemia
• CRF Encephalitis Hypokalemia
• Alcohol abuse Cerebral abscess
1-B—Nitriuretic syndromes: (due to excessive chronic Granulomatous disease Postrenal transplantation
Tuberculosis Sickle cell disease
sodium loss)
Sarcoidosis Genetic defect
• Diuretics Langerhans cell histocytosis Sex-linked recessive
• Hypernatremia (IV saline) Tumors Psychogenic polydipsia
• Addison’s disease Craniopharyngioma Compulsive water drinking
• Salt-wasting nephropathy Metastases (from breast) Schizophrenia
Postsurgical CNS disease
2-A—Water diuresis: (too much water intake)
Removal of pituitary Multiple sclerosis
• Psychogenic polydipsia/water intoxication/over adenoma
hydration Postradiotherapy (cranial) Idiopathic
• Hypothalamic disease (infiltration or infarction Familial
affecting thirst center) DIDMOAD
• Drugs (diuretics) Idiopathic
8
Table 34.3: Classification of causes of diabetes insipidus on basis of water deprivation
• Abrupt onset of polyuria with craving for ice endocrine and autoimmune disease is an
water (due to stimulation of osmoreceptors in important lead to the diagnosis of CDI / NDI
the back of the throat) suggests CDI, e.g. due • Drug history—A significant number of drugs
to pituitary disorders. Nocturia is common precipitate polyuria by various mechanisms.
• The next step, i.e. after confirming true Over-vigorous diuretic therapy in edematous
polyuria is: Is this water diuresis or solute states is a common cause of polyuria.
diuresis? Generally: Anticholinergics produce dryness of mouth;
Urine osmolarity > 350 mOsm/L suggests patients may therefore ingest excessive
solute diuresis, quantity of water, causing polyuria.
Urine osmolarity < 250 mOsm/L suggests Nephrotoxic drugs such as NSAIDs, ACE
water diuresis, and inhibitors, aminoglycosides may precipitate
Urine osmolarity between 250-350 mOsm/L acute tubular necrosis, which can result in
may be due to either water or solute severe polyuria in the recovery phase. Opiates
diuresis. This differentiation can be by inhibit ADH secretion and may produce CDI,
calculating total solute excretion on a 24 whereas lithium and demeclocycline may
hr urine collection (see 24 hr urinalysis produce NDI
above). • Physical examination should include
• Further, water diuresis needs to be evaluation of the following:
differentiated from CDI and NDI. Patient’s Hydration status, i.e. body weight, pulse,
history, investigations, and in selected cases BP, mucous membrane, skin turgor, and
water restriction test/ desmopressin test help urine output.
to achieve this objective Signs of malignancy, e.g. cachexia,
• History of head trauma; transsphenoidal lymphadenopathy, palpable mass.
surgery; CNS disease (e.g. meningitis, Target organ involvement, e.g. retinopathy,
tuberculosis, CVA, multiple sclerosis, parkin- neuropathy with diabetes mellitus.
sonism, pituitary-hypothalamic tumor, Abdomen—for mass and organomegaly.
metastatic deposits); psychiatric illness, Neurologic exam—to evaluate neurologic
diabetes mellitus, renal disease (e.g. chronic deficit associated with mass lesion,
nephritis); malignancy (hypercalcemia); encephalopathy.
Polyuria 239
Genitourinary exam — for penile, scrotal, syndrome is also known as DIDMOAD, the
testicular, prostate, and pelvic masses. acronym for diabetes insipidus, diabetes mellitus,
• NDI—The characteristic features are: optic atrophy and deafness, which summarizes the
An inability to concentrate urine main clinical features in WS patients, although some
adequately with fluid restriction, patients have additional clinical findings including
The occurrence of dilute urine in the ataxia, hypogonadism, hydronephrosis and
presence of normal or increased psychiatric illnesses. The gene associated with the
osmolarity, and syndrome, called WFS1, is located in the 4p16.1
Lack of responsiveness to vasopressin. region. Patients present with diabetes mellitus
• CDI—The characteristic features are:
followed by optic atrophy in the first decade, cranial
Dilute urine,
diabetes insipidus and sensori-neural deafness in
Mild hyperosmolarity, and
the second decade, dilated renal outflow tracts early
Responsiveness to vasopressin.
in the third decade, and multiple neurological
• Psychogenic polydipsia—Typically:
Both the serum and urine osmolarity are abnormalities early in the fourth decade. Other
low, and abnormalities include primary gonadal atrophy.
Lack of responsiveness to vasopressin. Death occurs premat-urely, often from respiratory
failure associated with brainstem atrophy. Most
RED FLAGS patients eventually develop all complications of this
progressive, neurodegenerative disorder. Though
• Think beyond diabetes mellitus in patients
there is no treatment to reverse the underlying
with polyuria with urine negative for
mechanism of neurodegeneration, early diagnosis
glucose, consider DI. Review history; refer
and adequate hormonal replacement could improve
for more detailed investigations as indicated
quality of life and survival.9, 10
• Unexplained polyuria in any patients with
hypercalcemia—investigate for multiple
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endocrine neoplasia (Chapter 14, Page no. 95
“Dyspepsia”. Review family histories in detail 1. Natsume O. A clinical investigation of nocturnal
endocrine tumors (thyroid, parathyroid, polyuria in patients with nocturia: A diurnal
variation in arginine vasopressin secretion and its
pituitary) are often present in other family relevance to mean blood pressure. J Urol 2006;
members 176(2):660-4. [PMID: 16813917: Abstract].
• Beware of complications in patients with 2. Asplund R. The nocturnal polyuria syndrome
(NPS). Gen Pharmacol 1995;26(6):1203-9. [PMID:
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SELECTIVE GLOSSARY 6. Chadha V, et al. Measurement of urinary
concentration: A critical appraisal of metho-
Wolfram syndrome (WS)— It is a rare, autosomal dologies.Pediatr Nephrol. 2001;16(4):374-82.
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240 Diagnosis: A Symptom-based Approach in Internal Medicine
7. Schubert S, et al. Central diabetes insipidus in a 9. Barrett TG, et al. Wolfram (DIDMOAD) syndrome.
patient with malaria tropica. J Endocrinol Invest. J Med Genet 1997;34(10):838-41. [PMID: 9350817:
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10. Viswanathan V, et al. Wolfram syndrome. J Assoc
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Pacific Physicians.2nd edn. p.18, Jaypee; 2004. Abstract].
CHAPTER
35 Pruritus
Table 35.1: Differential diagnosis of localized pruritus Table 35.2: Differential diagnosis of generalized pruritus
• Scalp/neck • Dermatologic disease
– Seborrheic dermatitis – Urticaria
– Lichen simplex – Xerosis (dry skin)
– Psoriasis – Atopic dermatitis
• Trunk – Contact dermatitis
– Urticaria – Bullous pemphigoides
– Contact dermatitis (axillae, waistline) – Dermatitis herpetiformis
– Erythrasma – Mastocytosis
– Psoriasis (periumbilical) • Drugs/food hypersensitivity
– Scabies – Aspirin, NSAIDs
– Seborrheic dermatitis – Antibiotics, chemotherapeutics
• Inguinal region – N i t r a t e s , monosodium glutamate (food
– Candida preservatives, flavoring agents)
– Contact dermatitis • Infective disease
– Erythrasma – Scabies
– Pediculosis – Pediculosis
– Scabies – HIV/AIDS
– Tinea cruris • Parasitic infections
• Genital (i.e. scrotal, anal, or vulval) region – Hookworm, pinworm, ascariasis
– Local irritants (fabrics, tampons, sanitary wear) – Giardiasis
– Intertrigo (excessive perspiration, moisture) – Oncocerciasis
– Contact dermatitis (hygiene products, barrier • Systemic disease
contraceptives, douches) – Chronic renal failure (uremic pruritus)
– Lichen simplex – Intrahepatic cholestatic pruritus (e.g. viral
– Candidiasis hepatitis, drug-induced cholestasis, carcinoma of
– Dermatophytes (Tinea cruris) liver, biliary cirrhosis)
– Parasites (pinworm, scabies, pediculosis, tricho- – Extrahepatic cholestatic pruritus (e.g. common
moniasis) bile-duct calculus, stricture, carcinoma of pancreas)
– Venereal (herpes, gonorrhea, chancroid, LGV, – Pruritus gravidarum
syphilis) • Endocrine disorders
– Bacterial (erythrasma) – Hyper-and hypothyroidism
– Anorectal disease (hemorrhoids, fissure, fistula, – Hyperparathyroidism
rectal prolapse, polyps, warts, malignancy) – Diabetes mellitus
– Dermatologic disease (Psoriasis, seborrheic – Gout
dermatitis, atopic dermatitis) • Hematopoietic disorders
– Valval disease (atrophic vulvovaginitis; VIN, i.e. – IDA
vulva intraepithelial neoplasia; malignancy) – PVR
• Hands • Malignancy
– Contact dermatitis – Hodgkin’s lymphoma
– Scabies – Non-Hodgkin’s lymphoma
– Eczema – Leukemia
– Dermatitis herpetiformis (elbows) – Carcinoid syndrome
• Legs • Psychiatric disease
– Stasis dermatitis (venous eczema) – Delusion of parasitosis
– Atopic dermatitis (popliteal fossa) – Depression
– Dermatitis herpetiformis (knees, buttocks)
– Lichen simplex chronicus (malleoli)
– Neurotic excoriation scabies, and pemphigus. Presence of hepato-
• Feet megaly or jaundice is indicative of obstructive
– Intertrigo
– Contact dermatitis
jaundice, hepatitis, malignancy of liver, or
– Pitted keratolysis biliary cirrhosis. Symptoms of polyuria,
– Tinea pedis polyphagia, and polydipsia would suggest
246 Diagnosis: A Symptom-based Approach in Internal Medicine
36 Red Eye
DIFFERENTIAL DIAGNOSIS
*The most commonly associated serotypes include
Common adenovirus 8, 19, and 37.
†
Corneal abrasions, i.e. superficial or partial trauma to
• Conjunctivitis (viral, bacterial, allergic, and corneal epithelium; often caused by fingernails, makeup
Keyboard conjunctivitis): vide infra (↓↓).2-4 applicators, dust, and vegetative matter.
250
IOP (tonometry)—Elevated in acute persisting red eye, consider other causes such
glaucoma (normal IOP- 10-21 mm Hg). as AACG, occult FB, trauma, and neoplasm.
Slit-lamp examination—To detect corneal • Recurrent subconjunctival hemorrhage with
and ocular FBs. no known cause, a work-up for hematologic
Fluorescein dye test—Every patient with disorder is indicated.
conjunctivitis should have fluorescein • A gritty sensation is common in conjuncti-
staining in each eye to ensure that a vitis, but the presence of FB must be
corneal aberration, ulcer, or herpetic excluded.
dendrites is not missed. • Hyperacute bacterial conjunctivitis needs
Direct ophthalmoscopy—When performed emergent referral to prevent corneal
from a distance of 15 cm, can detect involvement, including perforation and
opacities in the cornea, lens, and vitreous. visual loss, which could also be due to
The fundus and optic disc, looking for therapeutic misadventure with topical
increase in the cup-disc ratio, which may steroid usage. Therefore, it’s prudent to
signify presence of acute glaucoma, can refrain from treating any patients with
also be evaluated. steroids without consultation.
• Periauricular lymph nodes may be palpable • Beware of allergy or toxicity to topical
in viral, chlamydial conjunctivitis, and acute medications, i.e. iatrogenic, (including
gonoccocal infection. cosmetics) as a cause of persisting symptoms.
• Never use mydriatics when examining red
RED FLAGS eye—acute glaucoma may be precipitated;
• All patients with severe eye pain (suggesting they also act as temporary decongestants, and
increased IOP), photophobia, and corneal mask hyperemia.
haziness require immediate ophthalmic • Syphilis—It being a multisystem, multi-
referral. symptom disorder is a great mimic. Therefore,
• In a patient with acute onset, unilateral it is important to always keep this condition
headache, vomiting, acutely painful eye, or in mind when encountering patients with
Red Eye 253
anterior uveitis, chorioretinitis, retinal repeat occurrences. Patient who have had a
vascular occlusion, and chronic anterior CLARE should be educated and fitted with daily
segment inflammation.7 Further manifest- wear lenses.
ations of syphilis can be complicated by Keyboard conjunctivitis—An inconspicuous
concurrent HIV infection; hence, always way of spread of conjunctivitis—by the use of
consider HIV infection, e.g. CMV retinitis and keyboards of shared computers, at places like a
Kaposi’s sarcoma in patients with syphilis. library, internet café, classrooms, etc. Shared
keyboards and mouse are usually the culprits.
SELECTED GLOSSARY
Transmission of conjunctivitis is nearly certain,
Contact lens-induced acute red eye (CLARE)8— if a patient with conjunctivitis/ carrier used the
Contact lenses offer a unique and viable mode same keyboard earlier. Other examples of
of visual correction and are also of therapeutic conjunctivitis (i.e. red eye) due to fomite
value in a range of ocular disorders. However, transmission include objects such as mobile
several reports in the literature have clearly phones, land phones, TV remote tools, fridge or
shown that contact lens wear is not totally door handles, contaminated vehicles, shovels,
compatible with ocular physiology, and is clothing, bowls/buckets, brushes, tack, and
associated with various complications. Evidence clippers. Symptoms of conjunctivitis usually
also suggests that an increased number of these start within a day or two.
complications are seen with hydrogel lenses
used on an over-extended contact lens wearing REFERENCES
time or improperly used contact lenses in a
1. Mahmood AR, et al. Diagnosis and management
closed eye environment (during sleep). Some of of the acute red eye. Emergency medicine clinics
these conditions include inflammatory responses of North America 2008;26(1):35-55.
such as Contact Lens Induced Acute Red Eye 2. Bal SK, et al.10-minute consultation. Red eye.
BMJ 2005;331:438 (20 August), doi:10.1136/
(CLARE), and Culture Negative peripheral bmj.331.7514.438.
Ulcers (CNPU), and sight threatening responses 3. Chauhan R. “Keyboard Conjunctivitis”. Annals
Internal Medicine 7 April 2006. http://
such as infectious keratitis. While the etiology w w w. a n n a l s . o r g / c g i / e l e t t e r s ? l o o k u p = b y _
of a CLARE response is not clearly understood, date&days=7#2899.
it is seen that the condition is distinct and 4. Feingold EK. The outbreak of conjunctivitis at
Dartmouth. N Engl J Med 2003;348(25):2577-8.
typically presents with the patient waking in the [PMID: 12815147].
early hours with discomfort and pain in the 5. Youssef OH, et al. Odontogenic orbital cellulitis.
Ophthal Plast Reconstr Surg. 2008;24(1):29-35.
involved eye. Other symptoms include an [PMID: 18209637].
intolerance to lens wear associated with redness, 6. Hossain GA, et al. High resolution ultrasound of
lid swelling and mild to moderate amount of ophthalmic patients in a tertiary hospital. Mymen-
singh Med J 2007;16(1):50-6. [PMID: 17344780:
photophobia. Clinical signs include severe Abstract].
bulbar and limbal injection, and the presence of 7. Wuepper KD. “Red eye” as the presenting sign of
diffuse subepithelial to anterior stromal syphilis d’emblée. Calif Med 1967;107(6):518-20.
[PMID: 6078899].
infiltration in the periphery of the cornea. Most 8. Sankaridurg PR, et al. Gram-negative bacteria and
often the presentation is unilateral and epithelial contact lens induced acute red eye. Indian J
Ophthalmol [serial online] 1996 [cited 2008 Sep 23];
involvement is usually minimal. Further, patient 44:29-32. Available from: http://www.ijo.in/
who has endured an episode is susceptible to text.asp?1996/44/1/29/24602.
CHAPTER
37 Sexual Dysfunction
Table 37.1: Classification of sexual dysfunction Table 37.2: Common conditions and agents affecting
sexual function
Disorder Male Female
Psychosocial
• Sexual desire • Alibido/low libido/ • Alibido/low libido/
Psychiatric: Anxiety, depression, PTSD
disorder sexual phobia/ sexual phobia/
aversion aversion
Psychosocial: Ignorance, poor relationship, poor
• Sexual arousal • Erectile • Failure of arousal sexual drive, performance anxiety, prior sexual
disorder dysfunction (absence of vaginal failure, negative attitude
lubrication) Medical
• Orgasmic disorder • Premature • Anorgasmia
Cardiovascular: Angina, previous MI
ejaculation /
Retarded Respiratory: Asthma, COPD
ejaculation Endocrine: Diabetes mellitus, hypothyroidism,
• Sexual pain • Painful ejaculation/ • Vaginismus/ hyperthyroidism
disorder Dyspareunia Dyspareunia Metabolic: Atherosclerosis, hepatic failure, renal
failure
Neurological: Stroke, peripheral neuropathy, spinal
partner), generalized (due to complex, deep rooted cord disorders
Gynecological: Vaginitis, PID, endometriosis, fibroid,
causes), or due to combined factors. postmenopausal vaginal atrophy
Since sexual dysfunction is quite common, Arthritic: Arthritis from any cause
but not obvious, it is essential that physicians STD: herpes, gonorrhea
Aging: Andropause, menopause
assume a proactive role. Every effort should be
Surgical
made to differentiate between psychogenic/ Phimosis, hydrocele, episiotomy scarring, prostatectomy,
functional and organic sexual dysfunction, mastectomy (poor body image), oophorectomy,
colostomy, amputation
assessed via standard questionnaires such as
Drugs
the International Index of Erectile Function and Prescribed: Antihypertensives, antidepressants,
Female Sexual Function Index (see below). In an antipsychotics, mood regulators, antihistamines,
hypnotics, sedatives, hormones, anabolic steroids,
obvious psychogenic case, expensive and time- corticosteroids
consuming investigations should be avoided. Substance abuse: Alcohol, opium, cocaine, barbiturates
However, if an organic cause is suspected to be Genetic
Peyronie’s disease
the basis of sexual dysfunction, every effort
should be made to discern that organic cause as • Post-traumatic stress disorder (PTSD: vide
early as possible, and refer to the appropriate infra ↓↓)
specialist for further investigations and • Sexual enactment factors (lack of penile/
management. vaginal stimulation, lubrication; unfavorable
sexual positions)
DIFFERENTIAL DIAGNOSIS (TABLE 37.2) • Genital (phimosis)
• Endocrine (diabetes mellitus, hypothyroi-
Common dism, thyrotoxicosis)
• Psychogenic factors: • Cardiac (hypertension, CAD)
Personal problems (young men-new • Metabolic (atherosclerosis, dyslipidemia,
partner, anxiety, depression) obesity)
• Medications (antihypertensives, antidepres-
Relationship problems (poor communi-
sants, anxiolytics, etc.)
cation, unresolved conflicts, lost trust,
• Substance abuse (alcohol, tobacco, opioids,
Widower’s syndrome: vide infra ↓↓) cocaine)
Psychosexual problems (sexual perfor- • Pregnancy (especially in the first and last
mance anxiety, prior sexual failure, trimester)
negative learning and attitude about sex) • Aging/postmenopausal.
256
Occasional TFTs
• Vaginal/pelvic disorders (infection—vaginitis, • Elevated TSH with diminished FT4 values in
PID; fibroid, tumor; childbirth injury) primary hypothyroidism, and subnormal/
• Neurogenic (stroke) undetected TSH levels with elevated T3 or T4
• Postsurgical (prostatectomy, pelvic adhesive or both in thyrotoxicosis
disease). • TFTs are also useful to discover subclinical
hyperthyroidism (T3, T4 normal, TSH und-
Rare
etected); and subclinical hypothy-roidism
• Neurogenic (brain tumor, spinal injury/ (T4 normal, TSH raised) which may be
compression) responsible for sexual dysfunction.
• Endocrine (prolactinoma, Addison’s disease,
hypogonadism) Chemistry Panel
• Vascular occlusive disease (Leriche’ syn-
drome: vide infra ↓↓) • LFTs, urea, creatinine, and VDRL as indicated.
• Congenital disease/malformation (Peyronie’s
Serum Testosterone-free (AM Sample)
disease: vide infra ↓↓)
• Genital trauma. • Low levels in patients with diminished
libido, or any signs of diminished secondary
INVESTIGATIONS—GENERAL sexual characteristics, i.e. mild or otherwise
Blood Glucose asymptomatic androgen deficiency, or
hypogonadism.
• Diabetes mellitus is a common cause of ED.
Present evidence supports ED as a significant Microscopy/Culture
marker for diabetes, particularly in younger
• Vaginal secretions (vaginitis, gonococcal);
patients. Men 45 years old or younger with
prostate (prostatitis).
ED were more than twice as likely to have
diabetes mellitus as men without ED, and men
INVESTIGATIONS—SPECIFIC
with ED 46 to 65 years old were likely to have
diabetes. Thus, markers of ED may represent Serum Prolactin (PRL)
an early warning for the development of
• If serum testosterone levels are low, serum
diabetes, which is particularly important
PRL should be measured.
considering many diabetic patients remain
High (>20 ng/ml) levels—either due to
undiagnosed for several years. Therefore,
hypothalamic-pituitary lesion (suppressing
fasting, two hour postprandial blood
glucose, and HbA1c estimation should be GnRH) or drug induced—are observed in
patients with low libido, in women with
obtained.1-3
little or no history of menstruation, and
Lipid Profile gynecomastia.
• Hyperlipidemia, along with hypertension and
LH and FSH
diabetes mellitus, is a risk factor for metabolic
syndrome which often coexists with ED; • Serum LH and FSH estimation helps to
therefore its estimation is important.4,5 differentiate the etiology of sexual dysfunction,
Sexual Dysfunction 257
sensitive manner, avoiding jargon. A simple detailed, i.e. in-depth sexual history is
way to do this is by simply asking, “how needed8
are things going for you sexually?”, or, “how • Loss of NPT—At the very beginning a
is your sex life? Is everything all right?”; this carefully taken sexual history helps to rule
type of inquiry should elicit a clear, quick, out organic causes of sexual dysfunction,
and direct response such as “everything is especially treatable ones. An alerting sign is
fine.” Any other answer may suggest a loss of male morning erection, i.e. loss of
potential sexual dysfunction in him or her NPT during REM sleep. A history of erection
which should be followed up (with consent) that occurs nocturnally, during masturbation,
with specific questions to identify problems or during foreplay, or with other sexual
associated with various phases of sexual partners eliminates significantly neurologic,
response cycle (see above). If the patient is vascular, or endocrine cause of ED. For women
part of the couple, the couple should be there can be a similar loss of nocturnal vaginal
interviewed together lubrication
• It is not unusual for some patient to be • Hidden agenda—Although some patients
unaware of an association between their may present directly with a complaint of
medical problem and underlying sexual sexual dysfunction, many will present with
dysfunction. For example, patients with unexpected add-on problem at the end of
obesity, tension headache, chronic backache, consultation as hidden agenda or exit problem
vaginal discharge, pelvic pain, etc. This is an or parting shot. The exit problem or parting shot
opportunity for the physician to recognize is usually the patient’s main reason for
such an association and tactfully include consultation. Examples wherein such situation
inquiry about sexual dysfunction is commonly encountered are:
• A two way approach may be adopted in Sexual inquiry as part of current illness
obtaining sexual dysfunction history: The management
screening method and the in-depth approach. Sexual inquiry as part of health
If the sexual history seems unrelated to the check-up
chief complaint, a few screening questions Premarital sexual concerns
will suffice. Questionnaires have been Important life events, e.g. marriage
developed to collect data regarding ED Exposure to STD
(International Index of Erectile Function — Medication side-effects
IIEF† and female sexual dysfunction (Female Infertility, menopause, andropause.
Sexual Function Index—FSFI‡) to assess the
• Despite a seemingly indirect or ‘by-the-way’
severity and impact of therapy in such
nature of such encounters, the issue must be
patients which may be useful to understand
recognized and treated with considerable
the nature and scope of the patient’s
importance
problem. If the complaints have direct
• History—Includes age, mode of onset,
bearing to the chief complaints, a more
duration, libido (i.e. sex drive), situational
context, foreplay, fantasies, frequency,
†
Web site: <http://www.urologyspecialists.net/print/ erection, orgasm, ejaculation (normal,
iief.html >Accessed on 16-11-08
‡
web site:<http://www.fsfiquestionnaire.com/FSFI%20 premature, delayed, or absent), and pain felt
questionnaire2000.pdf >Accessed on 16-11-08 during intercourse
Sexual Dysfunction 259
The symptoms persist for at least one month intercourse (coitus), usually due to sexual trauma
and significantly disturb the patient’s social (rape, childhood sexual abuse); or as a conseq-
or occupational functioning (or both). Acute uence of dyspareunia, e.g. childbirth, surgery,
PTSD is diagnosed when the symptoms have gynecologic pathology, atrophic vaginitis; and
lasted for 1-3 months as against chronic PTSD, also due to strict religious upbringing; or psych-
where symptoms have lasted for more than 3 ogenic factors.
months. The importance of this distinction lies
in the fact that active treatment in acute PTSD Widower’s syndrome: It refers to a male who
may reduce the high risk of developing chronic experiences erectile dysfunction (with a new sex
PTSD. Although level of exposure to traumatic partner) secondary to guilt feelings relating to
stressor is directly related to the psychological his dead spouse.
impact, other factors contribute to develo-
pment of PTSD. Thus history of previous panic REFERENCES
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untary muscle constrictions of outer third of
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CHAPTER
38 Sweating Abnormalities
Nail Patella Syndrome (NPS)—It is inherited 2. Aoki K, et al. The effect of diurnal variation on the
regional differences in sweating and skin blood
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organs of both ectodermal and mesodermal Physiol 1995;71(2-3):276-80. [PMID: 7588701:
Abstract].
origin. The diagnostic tetrad includes
3. Schestatsky P, et al. Skin autonomic reactivity to
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patellae, the presence of posterior conical iliac 17(6):349-55. Epub 2007 Nov 29. [PMID: 18049833:
Abstract].
horns, and deformation or luxation (i.e. 4. Sato K. Disorders of eccrine sweat gland. In:
hypoplasia) of the radial heads. Patients often Fitzpatrick TB, et al. Dermatology in General
medicine. 4th ed. 1993. P.40-53.
complain of palmoplantar hyperhidrosis. 5. Labar, et al. Unilateral hyperhidrosis after cerebral
Kidney disease and glaucoma are now infarction. Neurology 1988;38:1679-82. [PMID:
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6. Rousseaux M, et al. Late contralateral Hyperhidrosis
serious complication associated with NPS is in Lateral Medullary Infarcts Stroke 27:991-5.
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7. Cheshire WP, et al. Disorders of sweating. Semin
established during childhood because the nail Neurol 2003;23(4):399-406. [PMID: 15088261:
and patella abnormalities may not become Abstract].
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atrophy: A preganglionic sudomotor dysfunction?.
Mov Disord 2008;23(6):885-8. [PMID: 18361470:
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Mot Res. 2007;24(1-2):71-84. [PMID: 17558924: care patients: An OKPRN and TAFP-Net coll-
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CHAPTER
• Is the pedal edema pitting or non-pitting, i.e. the day progresses, then venous insufficiency
solid? (Table 39.2). is most likely.
• A common but under-recognized cause of leg
Table 39.2: Common examples of pitting vs
nonpitting edema edema is pulmonary hypertension, which
Pitting edema Nonpitting is often associated with sleep apnea. Findings
• CHF • Myxedema (deposition
that may increase suspicion of sleep apnea
of mucinous material) include loud snoring or apnea noted by the
• Cirrhosis of the liver • Parasitic, e.g. filariasis sleep partner, daytime somnolence, or a neck
• NS • Allergic, e.g. angio- circumference >17 inches.
• Hypoproteinemia with neurotic edema • Is the patient taking any drugs that could
severe anemia, e.g. • Postoperative, e.g.
protein-losing excision of malignant cause the edema? Among the drugs that
enteropathy, starvation, regional lymph nodes should be considered are corticosteroids;
nutritional edema.
hormones—progesterone, estrogen, andro-
• Pericardial effusion • Neoplastic, e.g. lymphatic
• Constrictive pericarditis blockage by malignant- gens; NSAIDs; antihypertensive drugs—
tissue calcium channel blockers, vasodilators, beta-
• Drugs, e.g. calcium • Post-thrombotic adrenergic blockers; hypoglycemics—
channel blockers syndrome
pioglitazone, rosiglitazone; antidepressants —
• Venous obstruction/ • Idiopathic in women
insufficiency • Scleroderma trazodone, and chemotherapeutic agents.
• Beriberi (epidemic • Congenital, e.g. Milroy’s • Morning and evening chart of patient’s
dropsy) disease weight—Patients should weigh themselves
nude and with an empty bladder before food
• Is it lipedema or lymphedema? Lipedema (a form
or fluids in the morning and at bedtime. A
of fat maldistribution with sparing of feet)
mean weight gain >1 kg is consistent with
exclusively affects women and is a bilateral
idiopathic edema.10
and symmetrical deposition of fat in the
lower extremities, without involving the feet; • Physical examination—Lower limbs should
whereas in lymphedema the swelling starts be examined in the erect and recumbent
in the most distal part of the foot(marked positions for dilated superficial veins and
foot and toe involvement); this differentiates perforators.
the two conditions. • Homans’ sign, if positive (pain on dorsiflexion
• History of recent limb immobilization or of the ankle), indicates DVT.
confinement to bed following surgery, • Signs of systemic illness associated with
pregnancy, or history of cancer favors the swelling of the legs include—Periorbital edema,
diagnosis of DVT. jaundice, spider angioma, peau d’orange skin,
• Associated symptoms—Dyspnea on exertion, gynecomastia, ascites, hepatomegaly, cardio-
orthopnea, or paroxysmal nocturnal dyspnea megaly, distended neck veins, gallop rhythm,
suggests heart failure as the cause of leg tachycardia, lung crepitations, hypertension,
edema. Jaundice, palmar erythema, spider and lymphatic obstruction.
angiomata, and hepatomegaly suggests
cirrhosis of the liver. Generalized edema and RED FLAGS
swelling of the eyelids (peri-orbital) is
typical with NS. If the leg swelling is absent • Patients with unexplained acute lower limb
or minimal after recumbency but develops as swelling should have duplex sonography
Swelling of the Legs 273
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CHAPTER
40 Syncope
INVESTIGATIONS—GENERAL INVESTIGATIONS—SPECIFIC
ECG CXR
• A 12-lead ECG should be ordered for all • Evaluation of a select number of etiologies of
patients with syncope. A rhythm strip syncope may be aided by CXR. Pneumonia,
278 Diagnosis: A Symptom-based Approach in Internal Medicine
myxoma may be asymptomatic and discovered brady syndrome. It consists of a broad range of
as an incidental finding. Signs and symptoms of electro-physiological abnormalities, including
mitral stenosis, endocarditis, mitral inappro-priate sinus bradycardia, sinus arrest,
regurgitation, and collagen vascular disease can sinus node exit block, chronic atrial fibrillation,
simulate those of atrial myxoma. A high index of and bradycardia-tachycardia syndrome. The
suspicion aids in the diagnosis. Although disease is commonly observed in older patients
transesophageal echocar-diography is more with a history of concomitant heart disease, but
sensitive, 2-dimensional echocardiography is may also be observed in any age group,
usually adequate for diagnosis. including adolescents and children. Its clinical
Basilar Migraine (BM)—Described by Bickerstaff manifestations vary widely. In the early stages
in 1961, BM is a rare variant of migraine which of SSS, most patients are asymptomatic. As the
frequently affects young women and girls, disease advances, however, patients often seek
consists of headache accompanied by dizziness, medical attention for bradycardia-related
ataxia, tinnitus, decreased hearing, nausea and symptoms. Syncope, near-syncope, and
vomiting, dysarthria, diplopia, loss of balance, dizziness are the most frequently reported
bilateral paresthesias or paresis, altered complaints, followed by palpitations, angina,
consciousness, syncope, and sometimes loss of or shortness of breath. Thromboembolic
consciousness. Localized vertebrobasilar vaso- complications are a frequent cause of morbidity
constriction leading to transient posterior and mortality. Sudden cardiac death is possible
at any point during the disease. Pacemaker
circulation ischemia may contribute to the
placement is the cornerstone of treatment for
symptomatology of the disorder. Complications
symptomatic SSS.
of basilar migraines include remote possibility
of a basilar artery infarction. Torsade de Pointes—A malignant form of
polymorphic ventricular tachycardia that is
Carney Syndrome—Carney first described an
characterized by heart rate between 200 and
autosomal dominant multiple neoplasia
250 beats per minute, and QRS complexes with
syndrome featuring cardiac, endocrine,
changing amplitude and twisting of the points
cutaneous, and neural tumors, as well as a
(‘turning of the points ‘). The term also describes
variety of pigmented lesions of the skin and
the syndrome of tachycardia with prolonged
mucosae, which includes myxomas in breast,
ventricular repolarization, long QT intervals
skin, thyroid gland, or neural tissue; potty
exceeding 500 milliseconds or bradycardia.
pigmentation of skin and mucous membranes
Torsades de pointes may be self-limited or may
such as lentigines (i.e. flat brown discoloration
progress to ventricular fibrillation. The patient
of skin), pigmented nevi, or both; and endocrine
usually has syncopal attacks without premo-
overactivity such as Cushing syndrome. This
nition that lasts few seconds or seizures. It is
syndrome belongs to a group of genetic
commonly due to electrolyte imbalance or long
disorders, the lentiginoses, which include Peutz-
QT drugs. There may also be history of conge-
Jeghers, LEOPARD, and Laugier-Hunziker nital deafness or family history of sudden death.
syndromes. The most serious manifestation of
the Carney complex is cardiac myxomas. Wolff-Parkinson-White (WPW) syndrome—
WPW (preexcitation) syndrome is the most
Sick Sinus Syndrome (SSS)—It is also known common accessory pathway SVT. WPW is
as Sinus Node Dysfunction (SND), or tachy- mainly idiopathic or congenital, although it is
Syncope 283
more common among patients with hyper- conduct in an antegrade direction; consequently,
trophic or other forms of cardiomyopathy, the above ECG abnormalities do not appear.
transposition of the great vessels, or Epstein’s However, it conducts in a retrograde direction and
anomaly. In classic (or manifest) WPW thus can participate in reentrant tachycardia.
syndrome, antegrade conduction occurs over Symptoms of WPW syndrome may include
both the accessory pathway and the normal palpitations, chest pain, dizziness, dyspnea, or
conducting system during sinus rhythm. The rarely sudden death.
accessory pathway, being faster, depolarizes
some of the ventricle early, resulting in a short PR REFERENCES
interval and a slurred upstroke to the QRS 1. American College of Emergency Physicians
complex (delta wave). The delta wave prolongs Issues Guidelines for Treatment of Syncope. Ann
Emerg Med. 2007;49:431-444; and Barclay L.
QRS duration to >0.1 sec, although the overall
Medscape News. April 30, 2007.
configuration, apart from the delta wave, may 2. Brignole M, et al. Guidelines on management
appear normal. Depending on the orientation of (diagnosis and treatment) of syncope-update 2004.
Executive Summary. Eur heart J. 2004;25
the delta wave, a pseudoinfarction pattern Q-wave
(22):2054-72. [PMID: 15541843]. Web site: http:/
may be present. Because the early depolarized /eurheartj.oxfordjournals.org/cgi/content/full/25/
parts of the ventricle also repolarize early, the T- 22/2054. Accessed on 26-12-08.
3. Khan Gabriel M. Heart Disease Diagnosis and
wave vector may be abnormal. In concealed WPW Therapy-A Practical Approach. Chap.15 Syncope,
syndrome, the accessory pathway does not p. 473. 2nd ed. Humana Press.
CHAPTER
temperature loss, painful dysesthesias, autonomic Table 41.1: Upper and lower extremity compression/
dysfunction (anhydrosis, orthostatic hypotension, entrapment neuropathies
gastroparesis), or a combination. These patients Upper extremity Lower extremity
will have normal motor function and deep tendon
• Cervical radiculopathies • Lumbosacral disc
reflexes. (C5-C6orC7) syndromes (disc
The large fibers, i.e. A fibers are myelinated • Brachial plexus neuritis herniation with nerve root
motor fibers. These fibers are responsible for (C5-T1) compression (L4-L5 and
• Thoracic outlet syndrome L5-S1)
motion control, proprioception and vibration. (C5-T1) • Sciatic nerve syndromes
The clinical presentation in patients with large- • Long thoracic nerve (L4-S3)
fiber neuropathy (LFN) are impaired vibration, compression (winged • Femoral nerve neuropathy
scapula - C5,6) (L2-L3-L4)
gait instability, weakness, numbness, small • Median nerve compression • Lateral femoral cutaneous
muscle wasting, absent tendon jerks, but (carpal tunnel syndrome- nerve compression
C6-T1) (meralgia paresthetica-L2-
preservation of most cutaneous sensation. • Ulnar nerve palsy L3)
Dysesthesias, if present at all, tend to be tingling (tardy ulnar palsy/claw • Posterior tibial nerve
or segmental/band-like. Sensation for touch is hand-C8-T1)) compression
• Radial nerve palsy (wrist (tarsal tunnel syndrome-L5-
carried by both small and large nerve fibers. drop, Saturday night S2)
Although the diverse etiologies can make the palsy, crutch palsy- • Peroneal nerve
diagnosis of PNs quite challenging, a systematic (C5-T1) compression
(foot drop-L4-S1)
approach that classifies PNs on the basis of
clinical features, taking into account the mode of • Renal failure
onset (i.e. acute or chronic), type of peripheral • Herpes zoster (postherpetic neuralgia)
nerve fiber that may be involved (i.e. sensory, • HIV/AIDS.
motor, or autonomic), distribution (area of
innervation of a nerve or central afferent system), Occasional
associated neurologic symptoms and signs; and • Drugs (Table 41.3)
aided by specific laboratory evaluation and • Nutritional deficiencies (B1, B12, folic acid)
electrodiagnostic (EDx) tools will help in the final • Restless legs syndrome
diagnosis of the disorder. • Guillain-Barré syndrome
• Cranial nerve neuropathies (Trigeminal
DIFFERENTIAL DIAGNOSIS neuralgia, facial palsy)
Common • Hypothyroidism
• Leprosy
• Diabetes mellitus - Type 1, 2; including IGT • Syphilis (tabes dorsalis)
• Alcoholism • Sarcoidosis
• Upper extremity neuropathies (Tables 41.1 • Lyme disease
and 41.2) • Metabolic (hypokalemia, hypocalcemia,
• Lower extremity neuropathies (Tables 41.1 tetany).
and 41.2)
• Acute stress disorders Rare
• Hyperventilation • Vasculitis syndromes (Wegener’s granulo-
• Stroke syndromes matosis)
286 Diagnosis: A Symptom-based Approach in Internal Medicine
Table 41.2: Common causes of peripheral neuropathies Table 41.3: Drug induced polyneuropathies
by distribution of involvement Antibiotics
Distribution Causes Chloramphenicol
Chloroquin
A - Transient Dapsone
upper/lower limbs Normal, neurapraxia Ethambutol
Ethionamide
B - Upper limbs
Isoniazid
• Bilateral Linezolid
– glove and stocking Peripheral neuropathies Metronidazole
– along cervical nerve Cervical radiculopathies Nitrofurantoin
roots Brachial nerve neuropathy Lipid-lowering drugs
Thoracic outlet syndrome Statins
• Unilateral Antiretroviral drugs
– peripheral nerve Carpal tunnel syndrome Chemotherapeutics
lesions Leprosy Cisplatin
Thoracic outlet syndrome Cytarabine
Herpes zoster Vinblastine
C - Lower limbs Vincristine
Cardiovascular
• Bilateral
Ace-inhibitors
– glove and stocking Peripheral neuropathies
Amiodarone
– more on exertion Spinal (lumbar) canal
Hydralazine
stenosis
Rheumatologic
• Unilateral Lumbosacral
Allopurinol
radiculopathies (infection,
Colchicine
disc herniation,
Gold
spondylosis,
Miscellaneous
tumor) Meralgia
Disulfiram
paresthetica (lateral
Interferon alfa
femoral cutaneous
Lithium phenytoin
neuropathy) Herpes
Pyridoxin
zoster Statins
Thalidomide
in awkward positions (sleeping with the • The most common causes of PNs are
arms above the head or sitting with the legs diabetes and alcoholism. In the absence of
tightly crossed). This is due to sustained these two risk factors, obtain additional
pressure on the nerve. These paresthesias historical information, including history of
causing temporary physiological paralysis trauma (compression/entrapment neuro-
but not degeneration, followed by complete pathies), recent viral illness (Guillain-Barré
and rapid recovery are called neurapraxia. syndrome), drug and toxin exposure (Table
• There are three types of PNs: 41.2), occupation (exposure to industrial
Mononeuropathy—Characterized by a focal agents, pesticides), special diets (nutritional
abnormality of a single nerve and usually deficiencies), travel (Lyme disease), and risk
results from local nerve trauma or factors for AIDS
compression; • History of cancer, collagen vascular disease
Mononeuropathy multiplexes (multifocal (vasculitis), hypothyroidism, and leprosy
neuropathy)—Characterized by asymmetric can be associated with PNs
abnormalities in more than one nerve
• A detailed family history should include
trunk, which may occur simultaneously
inquiries as to the presence of gait abnormality,
or over days to years; and
muscular dystrophy, hammer toe, high arches,
PN—Characterized by symmetrical abnor-
etc. to rule out inherited disorders such as
malities of sensation, motor strength, or
Charcot-Marie-Tooth Disease (CMT)
both.
• Onset—Generally gradual over months to
• Symptoms—Depend on the nerves
affected; may involve sensory, motor, years as in diabetes, alcoholism, renal failure,
and/or autonomic systems. vasculitis, malignancy, etc. Causes of acute
Sensory—Tingling and numbness (pares- onset PNs include trauma, ischemic
thesia); burning sensation (dysesthesia); neuropathies, compartment syndromes,
decreased sensation (hypoesthesia), loss of Guillain-Barré syndrome, porphyria, and
sensation (anesthesia), exaggerated pain Lyme disease
perception (hyperesthesia), and stoking- • Distribution (Tables 41.4 and 41.5)—Since
glove pattern. sensory nerves innervate particular regions
Motor—Mainly muscular weakness, muscle (dermatome)* of the body, correlating the
cramping and fasciculation causing symptoms to areas of its supply is an
difficulty with activities of daily living. important method to identify the nerves
Distal muscles are affected initially, e.g. involved. For instance, the median nerve
weakness of dorsiflexion of the toes is innervates the thumb, the first two fingers,
common; diminished ankle reflex is often half of the ring finger, and the part of the hand
an early sign. Proximal muscles are to which they connect, i.e. C6-C7 dermatome.
involved later, except for inflammatory The ulnar nerve innervates the other half of
neuropathies such as PAN and SLE. the ring finger, the little finger, and the
Autonomic—Abnormal (i.e. absent or remainder of the hand, i.e. C8 dermatome.
excessive) sweating is an early symptom;
postural hypotension, constipation,
diarrhea, erectile dysfunction, and urinary *Generally sensory loss does not occur in the entire
corresponding dermatome; there is commonly a focus of
retention occur only with advanced paresthesias, dysesthesias, etc. within a wider area of
autonomic involvement. impaired sensation in that dermatome.
Tingling and Numbness 289
Table 41.4: Neuropathies by pattern of involvement • More diffuse involvement of an entire limb
Localization Pattern Most likely may be caused by involvement of the
diagnoses brachial (C5 to T1) or lumbosacral plexus
Mononeuropathy Single nerve, Direct trauma, (L1 to S3).
e.g. ulnar nerve, compression,
median nerve, entrapment(e.g. • Most often, PNs produce symptoms that are
cranial nerve carpal tunnel generalized and relatively symmetric,
syndrome, Tic
conforming to a distal-to-proximal gradient
douloureux)
typical of stocking and glove distribution in
Multiple Simultaneous Infections,
mononeuropathy or sequential granuloma, the hands and feet, e.g. diabetes mellitus
(mononeuropathy involvement vasculitis, • Unilateral involvement is seen in contralateral
multiplex, of several multiple
multifocal nerves, evolving entrapments
disease of the brainstem, thalamus, or cortex,
neuropathy) over days to (e.g. sarcoidosis) e.g. stroke syndromes
years • Multiple sclerosis may cause symptoms in
Polyneuropathy Longest nerves Metabolic, drugs, several, widely separated areas
first (distal, toxic, hereditary
stocking-glove (e.g. diabetes • Physical examination is performed to
pattern) mellitus) evaluate for possible systemic processes that
Radiculopathy One or more Herniated disk, may be contributing to the neuropathic
nerve roots spondylosis, process. Weight loss, fever, skin rash, icterus,
herpes zoster
lymphadenopathy, arthropathy, organo-
Polyradiculo- Proximal and Guillain-Barré
neuropathy distal weakness, syndrome, CIDP,
megaly are significant signs for possible
sometimes paraproteinemias systemic neurologic disorder
asymmetrical • Palpable thickened and/or tender peripheral
Plexopathy Brachial Trauma nerves along with anesthetic skin patches
Idiopathic
Neoplasm are typical of leprosy
Radiation • Motor examination—Distal muscle groups
Lumbosacral Diabetes are affected initially. Loss of muscle power
Neoplasm
Idiopathic progresses from distal to proximal. Deep
Radiation tendon reflxes are diminished or absent
• Sensory examination—Which sensory tests
Table 41.5: Neuropathies by pattern of involvement
(i.e. pain, touch, temperature, and vibration)
Focal Multifocal to include in the physical examination
• Trauma • Diabetes mellitus depends on the clinical setting
• Ischemic lesions • Nutritional deficiencies
– Diabetes mellitus • HIV/AIDS • For patients with sensory complaints, testing
– Polyarthritis nodosa • Leprosy for all the above four sensory modalities is
– Reynolds’s disease • Sarcoidosis
necessary to uncover sensory dissociation, i.e.
• Entrapment neuropathies • Vasculitis
• Compressive – Polyarthritis nodosa preservation of touch and vibration
neuropathies sensation, but loss of pain and temperature
• Leprosy – Systemic lupus
erythematosus sensation, which is an important clue to
• Sarcoidosis • Multiple sclerosis incomplete spinal cord diseases such as in
• Neoplastic infiltration • Chronic inflammatory
syringomyelia, spinal stroke (i.e. infarction
demyelinating
polyradiculo- of the anterior spinal artery), and Brown-
neuropathy (CIDP) Séquard syndrome.
290 Diagnosis: A Symptom-based Approach in Internal Medicine
• For screening diabetic feet and limbs, matosus. Eliciting a full history, though often
Semmes-Weinstein monofilament (5.07/10 difficult in this population, is vital for
gram) is recommended. The typical accurate diagnosis and treatment.
distribution of paresthesia is distal and • Leprosy must always be considered in a patient
symmetric, the feet being affected first in a with a combination of skin and neural disorder.
stocking distribution followed by the hands • In the case of Guillain-Barré syndrome, the
in a glove distribution. intensity of neuropathy may affect the
• The presence of Tinel’s sign is useful to localize a muscles of respiration, necessitating the use
nerve injury. The Tinel’s sign refers to paresthesias of ventilatory support.
elicited by tapping along the course of a nerve. • Paresthesias and dysesthesias involving multiple
• Clinically LFNs can be distinguished from cranial nerves palsies and radiculopathies,
SFNs during sensory testing—Loss of although similar in presentation to PNs, should
vibration and proprioception indicates alert one to the possibility of leptomeningeal
LFNs, while loss of pain and temperature metastasis; nerve biopsy is strongly indicated in
sensation is due to SFNs. Loss of sensation etiologic diagnosis.
for light touch may be due to LBNs or SFNs. • An often dominating arm pain, which mainly
• Autonomic examination—Blood pressure radiates into the ulnar region, is a sign of the
measurement in supine and standing posture infiltration of the plexus and the C8 and T1 roots.
to check for signs of postural hypotension. The possibility of Pancoast lesions, typically
• Fundoscopy and examination of cranial caused by apical adenocarcinoma or squamous
nerves—It is important to detect optic pallor cell carcinoma of the lung should be considered
due to drug toxicity, hereditary demyelinating not only in the presence of brachial plexopathy,
diseases, etc. Diabetes mellitus, leprosy, but also when C8 or T1 radiculopathy is found,
sarcoidosis, malignant lymphomas, myelomas, usually associated with ipsilateral Horner
etc. are known to involve cranial nerves† (V, syndrome, characterized by miosis with a
VII, IX, X, and XII) besides causing PNs. pupil that is slow to dilate, a mild (1-2mm)
ptosis, ipsilateral anhydrosis and apparent
RED FLAGS enophthalmos.
• Although human rabies is rare cause of PNs,
• Upper extremity paresthesias could be the sole clinicians and public health workers should
manifestation of coronary syndrome, especially suspect rabies when a history of possible
in individuals with cardiac risk factors. animal contact is known or when unexplained
• In older patients, PNs is not an uncommon atypical progressive neuropathy or unusual
presentation of many chronic illnesses, febrile encephalitis is observed.1
including neoplasms and inflammatory
processes such as systemic lupus erythe- REFERENCE
1. Human Death Associated with Bat Rabies—
†With the exception of second cranial nerve.
California, 2003 JAMA 2004;291(7):816-7.
CHAPTER
42 Tinnitus
• Cerumen impaction
Rare
• Foreign body
• Ear infection (acute otitis externa; otitis • Severe anemia, leukemia
media: acute and chronic; labyrinthitis : • Temporomandibular joint (TMJ) dysfunc-
viral, herpes zoster—geniculate ganglion) tion (subluxation, arthritis, ankylosis,
• Otosclerosis synovitis)
• Ménière’s disease • Atherosclerotic, vascular disorders (carotid
• Positional vertigo (BPPV) artery aneurysm, arteriovenous malfor-
• Barotrauma/dysbarism.† mation, vascular tumors)
• Neurologic (palatomyoclonus, idiopathic
Nonotologic stapedial muscle spasm)
• CNS diseases (multiple sclerosis)
• Migraine syndromes (migraine equivalent,
• Autoimmune inner ear disease (Cogan’s
acoustic migraine)
disease: vide infra ↓↓).
• Labile blood pressure (hypertension/
hypotension)
INVESTIGATIONS—GENERAL
• Diabetes (hypoglycemia)
• Thyrotoxicosis CBC, ESR
†
Injury following pressure changes; includes injury to • Leukocytosis with infective ear disorders
the eustachian tube, ear drum, lung and stomach. may be seen
Tinnitus 293
INVESTIGATIONS—SPECIFIC CSF
Biochemistry • Helpful in diagnosing multiple sclerosis and
• Urea, creatinine, electrolytes, lipids, VDRL, central nervous system syphilis.
FTA, ABS—if indicated by history and
examination. Brainstem Evoked Potentials
with tinnitus, can be experienced by people such as advanced or very young age, renal
with normal hearing in quiet situations, or hepatic impairment, pregnancy, or
according to a new research.5 history of hearing loss, or excessive and loud
• Evaluation of tinnitus includes, besides noise exposure.
otoaudiological examination, an evaluation • Ongoing audiologic monitoring for possible
of psychosocial wellbeing of the patient, with ototoxicity may be helpful when prolonged
special attention to signs of depression.6 use of ototoxic agents is needed.
• Is it subjective or objective? (see above) • Continued counseling about the risk of
• Objective tinnitus is unusual, but it may indicate hearing loss is warranted if the patient is
glomus tumors, arteriovenous malformations, exposed to damaging sounds.
carotid stenosis, aneurysms, anemia, a patent • Counselling, preferably including general
eustachian tube, or myoclonus. information leaflet, is the cornerstone in the
• If it is subjective, is it unilateral or bilateral? management of tinnitus in the vast majority
In general, pulsatile tinnitus, unilateral of patients. There is no cure for tinnitus in
tinnitus, and tinnitus associated with other the common sense of the word, especially in
unilateral otologic symptoms represent chronic cases. Many learn to live with their
tinnitus when they are convinced of the non-
potentially more serious underlying disease
threatening nature of their problem. Patients
than bilateral tinnitus.7
can obtain relief from the symptom with
• Episodic tinnitus suggests Ménière’s disease.
assistance from clinicians who are familiar
Pulsatile tinnitus suggests a vascular origin.
with tinnitus management strategies.
Auscultation over the neck, periauricular area,
orbits, and mastoid should be performed.
RED FLAGS
Tinnitus of venous origin can be suppressed
by compression of the ipsilateral jugular vein. • Tinnitus plus unilateral hearing loss should
• Acute tinnitus, which can last days or weeks, increase suspicion for acoustic neuroma.
may be caused by ear infection, medications, • The presence of other neurologic signs along
head or neck injury, excessive sound with vertigo and deafness would suggest
exposure, earwax, and changes in blood multiple sclerosis, advanced acoustic
pressure or metabolism. With appropriate neuroma, basilar artery occlusion or
evaluation, such underlying conditions insufficiency, brainstem tumors, and central
usually can be identified and treated, often nervous system syphilis.
with resultant resolution of tinnitus. • The severity of tinnitus varies from
• Chronic tinnitus (persistence for 6 months occasional awareness of a noise to an
or more) can also result from these conditions unbearable sound that drives some persons
and is more likely to occur in people who to contemplate suicide.9,10
have hearing loss.
• Concurrent medical conditions to be
SELECTIVE GLOSSARY
considered include diabetes, hypertension, Cogan’s syndrome— It is a chronic inflammatory
thyroid disorders, hyperlipidemia, infection, disorder that most commonly affects young
anemia, B12 or zinc deficiency.8 adults. Clinical hallmarks are interstitial
• Ototoxic drugs should be used with keratitis and vestibuloauditory dysfunction.
particular caution in patients who have risk Typical Cogan’s syndrome consists of flares of
factors that predispose them to ototoxicity, interstitial keratitis and sudden onset of Ménière-
Tinnitus 295
like attacks (nausea, vomiting, tinnitus, and nerve palsy, hypoglossal nerve palsy, or Horner
vertigo and hearing loss). Life-threatening aortic syndrome. Because of the insidious onset of
insufficiency develops in 10% of reported cases. symptoms, these tumors often go unnoticed,
Atypical Cogan’s syndrome (audiovestibular and delay in diagnosis is frequent. Because of
dysfunction with other types of inflammatory the location and extent of involvement, glomus
eye disease) is associated with vasculitis in 20% jugulare tumors present a significant diagnostic
of cases, and has a less favorable prognosis than and management challenge.
typical Cogan’s syndrome.
Glomus Jugulare Tumor—A relatively rare, REFERENCES
usually benign neoplasm—a paraganglioma 1. Alleva M, et al. Tinnitus. Primary Care
arising from sympathetic or parasympathetic 1990;17(2):289-97. [PMID: 2196610].
paraganglia outside the adrenal gland— 2. Noel CA, et al. Tinnitus. Diagnosis and treatment
of this elusive symptom. Geriatrics 2003;58(2):28-
originating in the chemoreceptor tissue of the 34. [PMID: 12596495].
carotid body, glomus jugulare, glomus 3. Axelsson A, et al. Tinnitus induced by
tympanicum, and aortic bodies. Glomus tumors occupational and leisure noise. Noise Health
2000;2(8):47-54. [PMID: 12689461].
are encapsulated, slowly growing, highly 4. Cochran JH Jr, et al. Tinnitus as a presenting
vascular, and locally invasive tumors. Although symptom in pernicious anemia. Ann Otol
most paragangliomas are sporadic, they can be Rhinol Laryngol 1979;88(2 Pt 1):297. [PMID:
443725].
familial. Glomus jugulare tumors occur 5. American Academy of Otolaryngology, Head
predominantly in women in the fifth and sixth and Neck Surgery (2008, January 4). Silence
decades of life. The most common symptoms May Lead To Phantom Noises Misinterpreted As
Tinnitus. ScienceDaily Retrieved September 21,
are conductive hearing loss and pulsatile 2008, from http://www.sciencedaily.com- /
tinnitus. Other aural signs and symptoms are releases/2008/01/080101093825.htm
6. Zoger, et al. Relationship between tinnitus severity
ear fullness, otorrhea, hemorrhage, bruit, and
and psychiatric disorders. Psychosomatics 2006
the presence of a middle ear mass. Significant 47:282-8 [PMID: 16844885: Free full text].
ear pain is uncommon. Involvement of the inner 7. Waldvogel D, et al. Pulsatile tinnitus—a review
of 84 patients.J Neurol 1998;245(3):137-42.
ear produces vertigo and sensorineural hearing [PMID: 9553842].
loss. Cranial nerve involvement produces 8. Ochi K, et al. Zinc deficiency and tinnitus. Auris
hoarseness and dysphagia. The presence of Nasus Larynx 2003;30 Suppl:S25-8. [PMID:
12543156].
jugular foramen syndrome (paresis of cranial 9. Frankenburg FR, et al. Tinnitus, psychosis, and
nerves IX-XI) is pathognomonic for this tumor, suicide. Arch Intern Med 1994;154(20):2371,
but it usually follows one year after the initial 2375. [PMID: 7944860].
10. Lewis JE, et al. Tinnitus and suicide. Clin
symptoms of hearing loss and pulsatile tinnitus. Otolaryngol Allied Sci 1994;19(1):50-4. [PMID:
Less commonly, glomus tumors produce facial 8174302: Abstract].
CHAPTER
43 Tiredness
*Tiredness, fatigue, and weakness, though used • Physiological (overbusy lifestyle, sedentary
interchangeably, convey different meanings. Tiredness is a lifestyle)
state of subjective feeling of listlessness or lethargy which • Psychological (depression, anxiety, fibro-
can occur at rest; whereas fatigue is an excessive tiredness
on mental or bodily activity, lack of energy, which occurs myalgia: vide infra ↓↓)
in tasks requiring sustained effort. Weakness denotes a • Acute postinfection syndromes (mostly
demonstrable reduction or loss of the strength or force of
muscle contraction or power. Exhaustion is extreme fatigue,
postviral syndromes)
a marked loss of strength. • Chronic infections (TB, hepatitis, HIV, AIDS)
297
CBC INVESTIGATIONS—SPECIFIC
• To assess the type and severity of anemia— CXR
generally IDA due to nutritional deficiency,
chronic disease, or chronic blood loss. • In patients with history of TB, tobacco CHF,
• Leukocytosis in pyogenic infection. smokers, and infection.
• Marked leukocytosis with atypical WBCs in
Chronic Infection Screening
leukemia.
• TB, malaria, brucellosis, infective endocarditis,
† Ref. Chapter 37 ‘Sexual dysfunction’. p 254 hepatitis serology (HBsAg, HCV antibodies),
‡ and viral markers (CMV, EBM).
Ref. Chapter 28 ‘Insomnia’. p 189
298 Diagnosis: A Symptom-based Approach in Internal Medicine
associated with family or social stressors, mood Table 43.1: Tiredness: Historical symptoms and
disturbances, and associated with either possible etiologies
insomnia or early morning awakening Symptoms Etiologies
(depression) is more likely to be psychogenic. The
Weight loss Neoplasm; endocrine
patient presents with multiple and non-specific disorders (diabetes
symptoms with a normal physical examination. mellitus,
• Organic—Tiredness from organic causes is hyperparathyroidism,
thyrotoxicosis, Addison’s
acute in onset and shows a progressive disease); chronic infection
course; stressors are often absent; family (TB, infective endocarditis,
dynamics is sound and supportive. Sleep HIV)
disturbances may be present, but is often Weight gain Obesity, hypothyroidism,
Cushing’s syndrome
related to the underlying disease process.
Prolonged fever Infective disease (TB,
Tiredness is less in the morning and worsens brucellosis, infectious
with activity. The patient presents with mononucleosis,
associated symptoms (Table 43.1), and the endocarditis,
toxoplasmosis)
physical examination usually suggests
Alcohol, drug abuse, Cirrhosis of the liver,
potential underlying cause tobacco smoking systemic toxic effect,
• A mixed category of tiredness is more COPD, lung malignancy
common which involves any of the above Polyuria Diabetes mellitus, diabetes
entries occurring in combination. One insipidus,
hyperparathyroidism,
abnormality discovered may be treated and chronic renal failure,
resolved without changing the patient’s hypercalcemia, Cushing’s
symptoms of tiredness (e.g. hypothyroidism syndrome
or malignancy with depression). A balanced Intermittent tiredness Myasthenia gravis, familial
periodic paralysis
approach is essential to solve such problems
Tiredness precipitated Periodic paralysis
• In patients with tiredness, recognition of the on carbohydrate meal, syndrome
symptoms of sleep deprivation is essential, after exercise
as many such patients do not have a clear Female, tiredness after Fibromyalgia
awareness of their own sleepiness. Therefore, minimal exertion,
hyperalgesic aches
a detailed ‘sleep history’ (Ref. Table 28.1, page and pains, insomnia
no.192) is mandatory, because sleep disorders TATT, with no weight loss Psychogenic disorder
are often associated with excessive daytime or abnormal work-up
sleepiness which can be misunderstood by Dyspnea, palpitation, Anemia (nutritional
the individual as tired feeling6, 7 increased sweating deficiency of iron, folic
acid, malabsorption
• Physical examination— May reveal depressed
syndrome); CAD; cardiac
patient with characteristic sad facial expre- valvular disease, COPD;
ssion; skin pallor, petechiae, ecchymoses, thyrotoxicosis
purpura (anemia, leukemia); skin pigmen-
tation (Addison’s disease); lymphadenopathy (hypothyroidism, hyperthyroidism). Cardiac
(infection, leukemia, metastasis ); hepatosp- and lung examination may reveal the presence
lenomegaly(infections, cirrhosis, malignancy, of S3 gallop, wheezing, or rales suggesting a
leukemia); stigmata of alcohol or drug abuse cardiopulmonary etiology. A neurologic
(gynecomastia, palmar erythema, needle examination may identify neuromuscular
tracks, infected skin lesions); and thyromegaly disease as the cause (e.g. diplopia, ptosis,
300 Diagnosis: A Symptom-based Approach in Internal Medicine
dysphagia, dysarthria, limb weakness in energy conservation stage the person typically
myasthenia gravis). tries to compensate for stress with behaviors like
procrastination, decreased sexual desire, social
RED FLAGS withdrawal, cynicism, apathy, resentment, and
substance abuse. However, it’s typically not until
• A person may present his symptoms of
the final exhaustion stage that the person realizes
tiredness as a hidden agenda or a ticket of entry:
that something is very wrong; symptoms include
i.e. to discuss symptoms related to some
sadness, extreme fatigue, severe headache, and
personal beliefs, e.g. sexual dysfunction or HIV
even suicidal ideation. Underlying depression or
infection, and psychological symptoms. Such
anxiety is common in such people—especially if
factors may be more important to the
there’s suicidal ideation. A short-term psycho-
individual than fatigue or tiredness itself.
therapy or psychopharmacotherapy may be
Eliciting detail emphatic history usually
indicated for stabilization, although taking a
uncovers these hidden agendas which
simple break can cure some burnout.
reassures individual’s help-seeking behavior.8
• Avoid exhaustive, unfocussed work up; they Fibromyalgia—It is a poorly defined, complex,
are not likely to be rewarding and in fact may chronic, and disabling disorder that causes
be counterproductive, reinforcing the widespread pain and stiffness in the muscles,
patient’s belief in an existence of an insidious tendons, and ligaments with multiple tender points
unidentified medical illness. (trigger points); most frequent in women aged 20-50.
• Chronic tiredness, lasting over six months, for Symptoms include generalized fatigue or tiredness,
which diagnosis is elusive, should not be reduced physical endurance, pain in specific areas
confused with CFS; however, the criteria for of the body, especially neck, shoulders, chest, back
CFS may be considered for further evaluation. (upper and lower), hips and thighs, insomnia or
• Chronic tiredness with depression or anxiety, poor sleep, sensations of numbness or swelling
suicidal ideation, and psychomotor retardation (although swelling is not actually present), chronic
demands careful attention.9 headaches, morning stiffness, worst on first arising,
along with unrefreshing sleep and fatigue. It is
SELECTIVE GLOSSARY commonly associated with conditions such as
depression, anxiety, viral infection, CFS, eating
Burnout Syndrome—It is a popular term rather
disorders, physical or sexual abuse, IBS, tension
than a scientific diagnosis denoting a severe state
headache, migraine, and hypothyroidism. Physical
of exhaustion and cynicism that occurs frequently
examination is normal except for trigger points; there
among individuals who do ‘people-work’ of some
are no specific tests for fibromyalgia; lab work up is
kind. Heavy workload, long hours, prolonged
normal.
stress, poor coping mechanisms, low self-esteem
are all associated with burnout syndrome. Some Myasthenia Gravis— It is an autoimmune condition
experts think the condition progresses through in which autoantibodies are developed against the
stages—alarm (stress arousal), resistance (energy acetylcholine receptors of neuromuscular junctions.
conservation), and exhaustion. During the first The disease presents as fluctuating weakness and
stage, the person is irritable, forgetful, anxious, fatigability of voluntary muscles. The muscles of
and unable to concentrate. Physical symptoms the eyes, head and neck are most commonly
may include hypertension, palpitations, bruxism, affected. Diplopia or unilateral ptosis is the initial
insomnia, headaches, and GI problems. In the symptoms in the majority. In severe cases, limb
Tiredness 301
and trunk muscles are involved and respiratory and swallowing difficulties are extre-
function may be compromised. Myasthenia gravis mely rare.
may be life-threatening when respiratory muscles Between attacks, patients often expe-
are affected (myasthenic crisis). Initial symptoms rience muscle spasms or difficulty
may be subtle and only apparent at the end of the relaxing their muscles, a condition known
day or when the patient is fatigued. Exacerbations as myotonia.
of myasthenia gravis may be precipitated by the Attacks usually begin in early childhood
use of anesthesia, narcotics or sedatives. Other
Giving oral glucose or glucose and subcutaneous
autoimmune conditions, such as thyroid diseases
insulin may trigger a hypokalemic attack,
and rheumatoid arthritis, are more common in
myasthenia gravis patients and their families. The whereas giving potassium may trigger a
diagnosis is confirmed by the Tensilon test, hyperkalemic attack. Because this primarily is
electromyographic studies, and the finding of an inherited condition, the most important
elevated acetylcholine receptor antibodies. aspect of diagnosis is obtaining a family history.
44 Urinary Frequency
†
According to the International Continence Society, urinary
‡
incontinence is defined as a condition of involuntary urine Symptoms suggestive of cystitis and urethritis, usually in
loss that is objectively demonstrable and is a social or post-menopausal women with atrophic vaginitis, and post-
hygienic problem. coital sexual trauma.
304
for distended bladder due to retention or predominantly with eosinophils, associated with
urethral obstruction. In women, pelvic fibrosis with or without muscle necrosis. The
examination, and in men digital rectal cause of EC remains unclear, although it has been
examination should be performed. Abnormal associated with various etiological factors, such
neurological findings such as deep tendon as allergy, bladder tumor, bladder trauma,
hyperreflexia or absence of the bulbocaver- parasitic infections and chemotherapeutic
nosus reflex suggest the possibility of agents. EC is, probably, caused by the antigen-
underlying neurologic lesion. antibody reaction. This leads to the production
of various immunoglobulins, which, in turn,
RED FLAGS cause the activation of eosinophils and initiates the
• UTI in male—In every male who has even inflammatory process. The most common
symptom complex consists of frequency,
one episode of UTI, a careful search must be
hematuria, dysuria and suprapubic pain.
made for possible cause; history of sexual
Cystoscopy and biopsy are the gold standard for
exposure may need direct inquiry
diagnosis. Additional laboratory evidence
• In all women of childbearing age, exclude
supporting the diagnosis includes proteinuria,
pregnancy by doing a pregnancy test if a
microscopic hematuria and peripheral eosinophilia,
period has been missed. The chances of an
the last one occurring in few patients. There is no
unrecognized pregnancy presenting with
curative treatment for this condition. Current
polyuria can thus be minimized
treatment modalities include transurethral resection
• Urinary tract TB is a common masquerade;
of the bladder lesion along with nonspecific
presenting in various systemic and genito-
medical therapy, such as nonsteroidal
urinary symptoms. Diagnosis depends on
antiinflammatory agents or steroids. Because the
constant awareness, especially in patients
lesion tends to recur in spite of the above therapy,
with sterile pyuria
long-term follow-up is mandatory’. 10, 11
• In patients with irritative voiding symptoms
associated with neurologic signs such as REFERENCES
diplopia, blurred vision, paresthesia, consider
1. Latini JM, et al. Voiding frequency in a sample of
neurogenic bladder—multiple sclerosis is a
asymptomatic. American Men. J Urol
strong possibility 2004;172(3):980-4. [PMID: 15311017: Abstract].
• Not all prostate hyperplasia is benign; 2. van Haarst EP, et al. The 24-h frequency-volume
chart in adults reporting no voiding complaints:
periodic prostate cancer screening is indicated Defining reference values and analyzing
in select cases. Prostate cancer often is variables. BJU Int 2004;93(9):1257-61. [PMID:
asymptomatic despite extensive spread 15180618: Abstract].
3. Fitzqerald MP, et al. Urinary habits among
• Interpret elevated prostate specific antigen asymptomatic women. Am J Obstet Gynecol
(PSA) with caution, as it may be elevated in 2002;187(5):1384-8. [PMID: 12439535: Abstract].
4. Clemens JQ, et al. Overlap of voiding symptoms,
both BPH and prostate cancer.
storage symptoms and pain in men and women. J
Urol 2007;178(4 Pt 1):1354-8. [PMID: 17706719:
SELECTIVE GLOSSARY Abstract].
5. Barry MJ, et al. Overlap of different urological
Eosinophilic Cystitis(EC)—It is a ‘rare symptom complexes in a racially and ethnically
clinicopathological condition characterized by diverse, community-based population of men and
women. BJU Int 2008;101(1):45-51. [PMID:
transmural inflammation of the bladder 17868419: Abstract].
307
45 Urticaria and
Angioedema
• IgM anti-HAV; IgM anti-HBc; HBsAg, i.e. • Complement determinations are not indicated
Hepatitis B surface antigen may be present for patients who have urticaria alone (since
Urticaria and Angioedema 311
have been described—an acquired form of this with or without treatment. Sweet’s syndrome
disorder may also be observed, sometimes in does not appear to be as rare as it seems though a
association with an underlying lymphoma. It is full blown classical picture may not be observed
important to consider this disorder in the in each case. Raised, erythematous and painful
differential diagnosis of unexplained, episodic plaques, particularly if they are asymmetrical,
cutaneous angioedema or abdominal pain. especially in females, should arouse the suspicion
Quantitative and functional analyses of C1 of this entity. This is more likely in patients who
esterase inhibitor and complement components have underlying malignancy.
C4 and C1q should be performed when HAE is
Urticarial vasculitis—It is thought to be due to
suspected.
immune complex mediated inflammation (i.e.
Sweet’s syndrome (Acute febrile neutrophilic hypersensitivity vasculitis). Although the
dermatosis or acute neutrophilic dermatosis)— prevalence of urticarial vasculitis is low, it is
Named after Dr Sweet from Plymouth, England, nevertheless important to recognize because this
who first described this condition in 1964, is a disease can be associated with other systemic
reactive process to an internal condition such as conditions (e.g. SLE, Henoch-Schönlein syndrome)
URTI, vaccination, pregnancy, IBD, RA, leukemia, and is amenable to effective treatment. It is more
internal malignancy, and drugs, e.g. NSAIDs, common in women than in men, and it usually
cotrimoxazole. It may also occur as a result of presents in the fourth decade of life. If skin lesions
external triggers such as needle prick, biopsy or have an urticarial appearance and last longer than
insect bite. In some patients they arise only in sun 24 hours in the same location, urticarial vasculitis
exposed areas, but in others no underlying should be considered. Typically these urticarial-
condition is found. It is characterized by the like lesions are:
abrupt onset of tender, red-to-purple papules, and • Less pruritic and more painful than observed
nodules that coalesce to form plaques. The with true chronic urticaria
plaques usually occur on the upper extremities, • More prominent on lower extremities
face, or neck and are typically accompanied by • May be palpable and purpuric
fever and peripheral neutrophilia. It most often • Following resolution may leave pigmented
occurs in middle-aged women, but men, children changes in the skin.
and the elderly may also be affected. Common Angioedema may accompany urticarial
symptoms include high or moderate fever; vasculitis. In addition, urticarial vasculitis may
arthralgia; and one or more tender red papules be associated with systemic signs and symptoms
or plaques which enlarge and persist for several such as fever, arthralgia, arthritis, uveitis,
weeks, they may have blisters, pustules or ulcers, episcleritis, hematuria, wheezing, chest pain,
and sometimes they appear to clear in the center. and diarrhea. Histopathologic findings include
Sometimes other organs are affected including swelling of endothelial cells, neutrophilic
bones, nervous system, kidneys, intestines, liver, perivascular infiltration, extravasation of
heart, lungs, muscles and spleen. Investigations erythrocytes, leukocyto-clasis (nuclear dust), and
may reveal: raised ESR or CRP, indicating fibrinoid deposits around blood vessels.
systemic inflammatory disease; raised WBC count Hemorrhage and edema of the dermis may also
(neutrophil leukocytosis); and numerous occur. The clinical course is usually benign, on
neutrophil inflammatory cells on skin biopsy, average lasting 3 years. The prognosis varies,
without leukocytoclastic activity. Sweet’s lesions depending on whether the diagnosis is
resolve eventually without leaving a mark or scar, normocomplementemic urticarial vasculitis
314 Diagnosis: A Symptom-based Approach in Internal Medicine
46 Vaginal Bleeding—
Abnormal
likely play an even larger role in pelvic imaging Serum Testosterone, Free Testosterone,
in future”5 17-Hydroxyprogesterone
• Further, three-dimensional saline infusion
• In women with hyperandrogenic symptoms
sonography (3D SIS) is found to be valid and
and signs – serum testosterone > 60 ng/dl
reliable in women suspected of having
supports the diagnosis of PCOS
intrauterine abnormalities, and may indeed
• If serum testosterone > 150 ng/dl, then 17-
have relevant clinical value in addition to
hydroxyprogesterone estimation is indi-
conventional SIS.6
cated to rule out functional adrenal or
Hysteroscopy ovarian neoplasm.
Table 46.4: Differential diagnosis of abnormal resulting in irregular, heavy menses and
vaginal bleeding (AVB) probably dysmenorrhea. Once ovulation
Ovulatory bleeding Physiologic: and menstruation are regularly esta-
Midcycle ovulation
(Mittelschmerz) blished, the cycle follows a predictable
Anatomic lesion: pattern (Table 46.1) and any deviation can
Fibroids; PID; be considered as AUB.
cervical-infection, polyp,
cancer; IUD Menstrual history—The first day of last
Systemic disease: menstrual period should be included in
Bleeding diathesis; hepato- all adult female patients, i.e. the date that
renal disorder
Local disorders:
the menstrual flow began. Many patients
Foreign body; trauma; assume that occurrence of any bleeding
infection; urethral prolapse; is a ‘period’. Also, for many women,
growth
monthly may mean once every calendar
Anovulatory bleeding Hypothalamic dysfunction:
Premenarcheal month, so that a period on day 1 and day
perimenopausal; stress, 27 of the same month, while normal, may
weight loss, heavy strike her as having periods twice a
exercise
Excess androgen, prolactin, month. Failure to make this distinction
cortisol can result in misleading information. A
Hypothyroidism menstrual calender^ (over three or more
PCOS
Oral contraceptive use: months) can be a very useful guide. The
Inadequate estrogen quantity (the passage of ‘clots’ or inability
dose to control bleeding with tampons is
Postmenopausal Endocrine pathology:
Fibroid; polyp; cancer
significant and indicates heavy bleeding),
Cervical pathology: duration, and frequency of bleeding‡
Erosion; polyp; cancer with respect to previous menstrual cycles
Vaginal pathology: are recorded. Any significant deviation
Atrophic vaginitis
Pregnancy Early pregnancy: from normal should be noted and
Abortion: patient’s cycles are categorized as in
Complete; incomplete; Table 46.2.
inevitable; missed
Late pregnancy: Postcoital bleeding (any bleeding after
Placenta previa; abruptio intercourse or in association with
placenta; douching) is suggestive of cervical
Retained products of
dysplasia, or endocervical polyps.
gestation
Ectopic pregnancy Postmenopausal bleeding (any bleeding
occurring in a postmenopausal woman
• The history should determine the following at least 1 year after cessation of cycles)
information: should be evaluated for endometrial
Age of onset of bleeding, age of onset of puberty. hyperplasia and carcinoma.
Though premenarchal bleeding may be
^
associated with precocious puberty, local Visit web site -http://www.americanpregnancy.org/
gettingpregnant/ovulationcalendar.html
pathology, as well as adrenal and ovarian
‡
tumors must be ruled out. In adolescence, It is not uncommon for women to change their sanitary
products frequently for hygienic reasons or because of
AUB is common in the first 2-3 years after personal preference or concern for toxic shock syndrome
menarche due to many anovulatory cycles, than because of heavy flow.
Vaginal Bleeding—Abnormal 321
• Associated symptoms—Pain, discharge, fever, Pap smear and biopsy of any lesion in
nausea, vomiting, dysuria; symptoms of the genital tract.
hyperthyroidism (fatigue, weight loss,
sweating, palpitation); hypothyroidism Digital Rectal Examination (DRE) and
(fatigue, cold intolerance, constipation); Proctoscopy
symptoms of hyperprolactinemia (headache,
nipple discharge, galactorrhea); symptoms • May be warranted to identify alternative
of virilization (excess hair growth); bleeding sources of bleeding such as rectal or urethral.
diathesis (easy bruisability, petechiae, epi-
staxis, gingival bleeding); etc. should be RED FLAGS
addressed
• In a woman of reproductive age, pregnancy
• Sexual history—Sexual abuse and activity,
including high risk behavior, and domestic should always be ruled out despite a nega-
violence screening is recommended tive history of sexual activity
• Personal and family history—Marital status, • AUB in a woman of reproductive age must
parity, infertility, epilepsy, and blood dys- be considered a complication of pregnancy
crasia. Smokers have higher incidence of until proved otherwise
menstrual dysfunction • Vaginal bleeding in a postmenopausal
• Medications§—Oral contraceptives, anticoa- woman must be considered a malignancy
gulants antidepressants, antiepileptics, anti- until proved otherwise
psychotics, opiates, Tamoxifen, and herbal • Reevaluate patients diagnosed with hyper-
preparations (ginseng, ginkoba, soya supple- plasia with atypia for persistent or
ments) worsening hyperplasia within 3-6 months of
• Physical examination—Evidence of puberty
treatment
(breast development, axillary and pubic
• Vaginal bleeding that occurs before
hair growth); virilization, hirsutism;
pubertal development or normal menarche
hypothyroidism (dry skin, coarse hair,
bradycardia, delayed reflexes); hypert- should raise suspicion of nonendocrine
hyroidism (sweating, weight loss, palpit- causes; rule out adrenal and ovarian tumor,
ation); abdominal distension, tenderness, including rhabdomyosarcoma (sarcoma
hepatomegaly, splenomegaly; skin pete- botryoides)
chiae; etc. • AUB during adolescence should be attri-
buted to a coagulation disorder until proven
Pelvic Examination
otherwise
Inspection of genitalia—Anatomy, dis- • AUB before menarche may warrant pelvic
charge, foreign body, evidence of trauma,
examination under general anesthesia to
and source of bleeding—uterine or extra-
exclude focal lesions such as trauma, sexual
uterine.
abuse or assault, and malignancy
Other lesions—Polyps, fibroids, pelvic
• Any AVB/AUB should be investigated in
mass.
women taking Tamoxifen or Raloxifene
§ because the resulting side effects of these
Common medications, which increase the cytochrome
P450 enzymatic processes in the liver, may induce more drugs (indicated in breast cancer) include
rapid metabolism of steroid hormones, thereby decreasing
an increase in the risk of endometrial cancer
their bioavailability and result in AUB that is secondary to
a relative insufficiency of estrogen or progesterone. and thrombosis.
322 Diagnosis: A Symptom-based Approach in Internal Medicine
47 Vertigo
Common Occasional
• Ototoxic drugs (aminoglycoside antibiotics,
• Physiological (motion sickness)
aspirin, frusemide, phenytoin, quinine)
• Positional vertigo (vertebrobasilar ischemia,
• Epilepsy (aura in temporal lobe epilepsy)
cervical spine dysfunction, or benign paro-
• Physical (barotrauma, noise trauma)
xysmal positional vertigo, i.e. BPPV)
• Head injury (posttraumatic labyrinthine
• Vestibulopathy (vestibular neuronitis, laby-
concussion, perilymph fistula).
rinthitis, herpes zoster)
• Vascular (subarachnoid hemorrhage, verte-
brobasilar ischemia, brainstem infarct, cere- ‡
This term usually refers to elderly persons who often
bellar infract, lateral medullary syndrome, have altered sensory inputs or premature aging of the
i.e. PICA syndrome: vide infra ↓↓) vestibular nuclei.
325
for papilledema or optic atrophy (II), ocular outweigh vestibular causes. Therefore, in
movements (III, IV, and VI), corneal reflex** the elderly, it is more sensible to consider
(V), and facial movements (VII) vertigo (along with other conditions which
• Otoscopy can detect otitis media, serous otitis frequently accompany it) as part of a more
or cholesteatoma general syndrome2
• Onset and duration—Generally, central • In an elderly sudden onset of severe vertigo,
vestibular disorders, i.e. central vertigo, are headache, nausea and vomiting, usually
characterized by gradual and insidious associated with other neurological symp-
onset of continuous imbalance, whereas a toms, such as diplopia, dysphasia, hemi-
peripheral vestibular disorder, i.e. peripheral paresis—but without hearing loss or
vertigo, is classically characterized by tinnitus—is strongly suggestive of verte-
sudden, short lived (of few hours) episodes brobasilar insufficiency
of vertigo (Table 47.2). • Sudden, episodic vertigo, associated with
Table 47.2: Vertigo: Causes and onset of attack progressive unilateral hearing loss and
Acute tinnitus, lasting from hours to days is
• CVA, TIA: vertebrobasilar event; subarachnoid suggestive of Ménière’s disease
hemorrhage; cerebellar infarct • Vertigo precipitated by positional factors,
• Head trauma, concussion
• Infections – otological – vestibular neuronitis i.e. vertigo on arising from supine to sitting
• Tumor or standing position; vertigo with sudden
• Seizure
neck movements, accompanied by nystag-
Recurrent
• CVA, TIA
mus, but without hearing loss, is suggestive
• Ménière’s disease of cervical spine dysfunction, vascular
• Tumor ischemia, or BPPV
• Migraine
• Seizure • Mild vertigo (vague sensation of motion)
• Toxic – drugs, substance abuse with prominent tinnitus, progressive
• Multiple sclerosis unilateral sensorineural hearing loss, and
• Syphilis
• Surgery/otological/ENT procedures loss of corneal reflex strongly suggests
• Psychogenic cerebellopontine angle tumor—usually
Positionally provoked vertigo acoustic neuroma
• Benign passional vertigo
• Vertigo with multiple neurological signs
• Cervical sprain, OA, whiplash injury
• Vascular—Anterior vestibular artery occlusion, and symptoms, such as blurring or loss of
verte-brobasilar artery insufficiency vision, diplopia, dysarthria, paresthesia,
• Postsurgical (head/neck/ENT) status
and ataxia is suggestive of multiple sclerosis
• Central cause
(vide infra ↓↓)
• Age—In young adults psychological causes • Vertigo that is increased by a loud noise
predominate, whereas vestibular disorders (Tullio phenomenon, i.e. vestibular hyper-
do in the middle age. In the elderly, sensitivity to sound) and Valsalva maneuver
cerebrovascular and cardiac disorders, suggests perilymphatic fistula
combined with multiple sensory deficits • Organic vertigo is accompanied by nystag-
mus; a psychogenic etiology is almost cer-
**
Abnormal or absence of corneal reflex on the affected tain when nystagmus is absent during a
side may be the first signs of CP angle tumors. vertiginous episode.
328 Diagnosis: A Symptom-based Approach in Internal Medicine
Multiple Sclerosis (MS)—An idiopathic inflamm- resulting in difficulty with activities of daily
atory demyelinating disease of the CNS, mainly living and even falls. Medication is usually
affecting young adults, and characterized by not helpful unless there is clear vertigo due
destruction of myelin in the central nervous to inner ear dysfunction. However, Patients
system. Patients with MS commonly present with can be helped by increasing their sensory
an individual mix of neuropsychological input by using a cane, not to support a weak
dysfunction, which tends to progress over years leg, but by dragging it along the ground,
to decades. Clinical manifestations include visual which increases sensory input through the
loss, extraocular movement disorders, and arm where the cane is held. The individual
paresthesias, loss of sensation, weakness, has a better sense of stability and ‘where the
dysarthria, spasticity, ataxia, and bladder ground is’, and many times can walk more
dysfunction. The usual pattern is one of recurrent steadily and safely.
attacks followed by partial recovery. The diagnosis
PICA (Posterior inferior cerebellar artery) Syn-
of MS is based on a classic presentation (i.e. optic
drome—The PICA syndrome, also known as
neuritis, transverse myelitis, internuclear
lateral medullary syndrome, or Wallenberg’s syndrome,
ophthalmoplegia, paresthesias), and on the
is the most common brainstem stroke. It is
identification of other neurologic abnormalities, typified by vertigo, ipsilateral hemiataxia,
which may be indicated by the patient’s history dysarthria, ptosis and miosis. Patients often
and examination. Typical findings on an MRI also have Horner’s syndrome (unilateral ptosis,
help to establish the diagnosis of MS. Patients miosis and facial anhidrosis). There also may
with atypical pre-sentations and/or a normal or be saccadic dysmetria (overshoot), saccadic
atypical MRI may require evoked potential pulsion (pulling of the eye during vertical
studies, to uncover subclinical neurologic saccades toward the side of lesion). Diagnosis is
abnormalities, or cerebral spinal fluid (CSF) generally via MRI. Prognosis is generally good
analysis, which also serves to exclude treatable with full or near full recovery expected at
disorders and document MS-like immune 6 months.
activity in the CNS.
REFERENCES
Multiple Sensory Deficit Syndrome—This
term usually refers to elderly persons who 1. Neubauser H, et al. The interrelations of migraine,
vertigo, and migrainous vertigo. Neurology.
often experience dizziness as a result of 2001;56(4):436-41. [PMID: 11222783: Abstract].
altered sensory inputs or premature aging 2. Tinetti ME, et al. Dizziness among older adults:
of the vestibular nuclei. Visual impairment A possible geriatric syndrome. Ann Intern Med
2000;337-44. [PMID: 10691583: Free full text].
(cata-racts), deafness (presbycusis), 3. Mackle T, et al. Atypical clinical presentations of
decreased ability to feel their legs (peripheral vestibular schwannomas. Otol Neurotol 2007;
neuropathy), painful or disabling orthopedic 28(4):526-8. [PMID: 17414179: Abstract].
4. Penido Nde O, et al. Vestibular Schwannoma:
disorders, and muscle weakness collectively Spontaneous tumor involution. Rev Bras Oto-
alter the patient’s perception of space, rhinolaryngology (Engl Ed) 2007;73(6):867-71.
fluidity of motion, and confidence in walking, [PMID: 18278239: Free full text].
CHAPTER
48 Vision Loss—Gradual
Lipid Profile
Occasional
• To evaluate hyperlipidemia, including serum
• Optic nerve compression (mass lesion)
homocysteine levels.
• Intracranial tumors
• Intraorbital tumors
Coagulation Screen
• Retinitis pigmentosa
• Complications of cataract surgery (inflam- • PT, PPT, lupus anticoagulant, Factor V Leiden,
mation, retinal detachment, posterior cap- antithrombin III, protein C, protein S, etc. are
sular fibrosis). indicated in patients with hypercoagulable
states, e.g. retinal vascular occlusions.
Rare
TFTs
• Toxic amblyopia (drugs/toxins – alcohol,
anticholinergic agents, amiodarone, cortico- • In severe hyperthyroidism extraocular
steroids, chloroquin, digoxin, ethambutol, muscle entrapment (thyroid oculopathy)
isoniazid, lithium, streptomycin, sildenafil, may cause progressive loss of visual acuity
and tobacco) and visual field.
IOP (Tonometry)
* In children common causes of visual failure are congenital • Elevated in acute glaucoma; greater than
cataract, retinitis pigmentosa and retinoblastoma. 30 mm of Hg is highly suspicious.
332 Diagnosis: A Symptom-based Approach in Internal Medicine
Colored halos around lights, i.e. Table 48.2: Visual field defects with localization of lesion
whenever patient looks at white light, he
Vision defect Localization/examples
sees it as if white light is split into its
Tunnel vision Concentric diminution of field, e.g.
component colors, red being outermost, glaucoma, late papilledema.
seen in prodromal stage of angle closure Enlarged blind Early papilledema (optic nerve
glaucoma, and cataract. spot head enlargement)
• Current medications:4 Systemically administered Central scotoma, Optic nerve head to chiasmal
i.e. loss of central lesion, e.g. demyelination,
drugs produce a wide variety of adverse effects
mecular vision vascular, toxic, nutritional.
on the visual system; e.g. amiodarone, Unilateral field Optic nerve lesion, e.g. tumor,
ethambutol, linezolid, sildenafil, long-term use loss, i.e. monocular vascular.
of glucocorticoids, phenothiazine, adrenergic field defect
agents, certain β2-adrenergic agonists, and Bitemporal Optic chiasma lesion, e.g. pituitary
hemianopia tumor
anticholinergic agents.
Hemonymous Lesion behind optic chiasma, i.e.
• Associated disorders, e.g. tuberculosis, hemianopia optic tract to occipital cortex
diabetes mellitus, hypertension, hyperlipi- Upper quadrant Optic radiation (Temporal), e.g.
demia, thyroid disease, autoimmune disease, homonymous tumor, vascular
and malignancy. hemianopia
Lower quadrant Optic radiation (Parietal)
• Past history of ocular disease or surgery, e.g.
homonymous
orbital trauma, FB, corneal ulcer. hemianopia
• Family history, e.g. developmental cataracts, Homonymous Occipital cortex
corneal dystrophies, retinitis pigmentosa, hemianopia with
central vision
Leber’s hereditary neuropathy. (macula) sparing
• Physical examination includes tests for—
Visual acuity for distance and near, with
and without glasses (Snellen chart) in all • Systemic examination for any collaborative
instances (except in chemical trauma†). evidence for loss of vision is important. For
Visual field: (Table 48.2). example:
Analysis of central visual field with an Stenotic vascular disease (carotid or
Amsler grid (to locate macular blind spots vertebral artery atherosclerotic disease,
and areas of distortion and wavy lines) arteritis, dissection)
used in daily self-monitoring for the Cardiac disease (hypertension, endo-
progression of macular degeneration. carditis, atrial myxoma, valvular dis-
Pupillary reaction: (ref. swinging flashlight orders)
test, chapter 49: Vision Loss Sudden.) Autoimmune disease (RA, ankylosing
Fundus examination (ophthalmoscope) spondylitis, giant cell arthritis, SLE)
with dilated pupil to assess the red reflex, Granulomatous disease (sarcoidosis)
optic disk for papilledema, and retina for Hematological (anemia, hypercoagulable
presence of hemorrhage, cotton wool spots. states, antiphospholipid syndrome)
Neurological (head injury, mass lesion,
†
seizures, MS)
In chemical exposure, the dictum is ‘treat first, examine
later’; copious irrigation should be initiated before Psychological (conversion syndromes,
attempting a visual acuity examination. malingering).
334
49 Vision Loss—Sudden
Sudden vision loss (SVL) or acute visual loss is Sudden: less than 1 hour
• Amaurosis fugax
an ophthalmic emergency requiring immediate
• Central retinal artery occlusion
medical attention to avert permanent visual • Acute angle closed glaucoma
impairment. • Vitreous hemorrhage
SVL means anything from instantaneously • Migraine
DIFFERENTIAL DIAGNOSIS
• Central retinal venous occasion (CRVO)
Common
• Cerebrovascular accidents
• Acute angle closure glaucoma (AACG) • Transient ischemic attack (anterior circulation)
• Vitreous hemorrhage • Migraine (ophthalmoplegic).
336
Table 49.2: Bilateral vision loss of sudden onset • Due care must also be taken not to diagnose
• Migraine with usual aura seemingly inappropriate behavior (due to
• Vertebral artery spasm/embolism vision loss) as of psychogenic in origin
• Bilateral optic nerve damage • Beware of acute presentation of vision loss
• Occipital lobe infarction
• Occipital lobe trauma that is actually of chronic (gradual) onset,
but suddenly noticed by the patient.
50 Weakness in the
Arms and Legs
• For specific bacterial, viral, fungal organisms MRI—Cervical and Lumbosacral Spine
causing meningitis, encephalitis.
• Useful in obtaining more information about
Creatine Kinase (Total)—(CK) lesions already seen on CT scans and in
• Markedly elevated, 10 to 200 times normal, diagnosing white matter lesions, e.g.
in muscular dystrophy, and inflammatory multiple sclerosis, and lesions in the posterior
myopathies fossa.
342
Table 50.1: Common causes of fatigue and athenia to occlusion of anterior spinal artery
• Anemia
(common in patients with aortic athero-
• Anxiety sclerosis, aortic aneurysm)
• Addiction—abuse-alcohol, narcotics • Subacute onset weakness in the limbs, i.e.
• Cardiac disease CHF
• Chronic fatigue syndrome evolving over a few days or weeks, is usually
• Depression seen in diseases such as meningitis,
• Dehydration and electrolyte disorders encephalitis, neoplasms, multiple sclerosis,
• Deconditioning/sedentary lifestyle
• Drugs — adverse effects myasthenia gravis, and dermatomyositis
• Diabetes • Chronic limb weakness, which evolve over
• Fibromyalgia
• Hypothyroidism
weeks or months (some overlap with
• Infection — chronic-TB, hepatitis, HIV disorders mentioned above), include motor
• Pain—chronic neuron disease, most neuropathies, and
• Pregnancy/postpartum
• Pulmonary – COPD
many genetic muscular diseases
• Renal – ESRD • The combination of UMN and LMN signs in
• Sleep disorders a patient is an important clue to the diagnosis
of motor neuron disease, e.g. ALS
1. Distribution:
• The combination of distal muscle weakness
a few muscles
and sensory loss is commonly due to
a limb (monoparesis)
peripheral neuropathy
both lower limbs (paraparesis)
• The combination of proximal muscle
both limbs on one side (hemiparesis)
weakness without sensory loss is commonly
all four limbs (quadriparesis).
2. Type of weakness: due to myopathy
upper motor neuron lesion • History should be focused to elicit infor-
lower motor neuron lesion mation that will provide clues to the cause
both UMN and LMN, or neither. of weakness: (Table 50.2)
3. Evolution of weakness: Onset—to establish if acute or chronic
sudden and improving Alteration of consciousness, headache,
gradually worsening over days or weeks visual disturbances
evolving over months or years Gait—disturbances of equilibrium
The time course of the onset of weakness, What muscles are affected by the
i.e. (evolution) is usually helpful in deter- weakness? e.g. foot, lower leg, thigh,
mining the possible etiology. upper arm, lower arm, facial, or back
• Generally the rate of onset of limb weakness Are both sides of the body affected by
may be divided into acute, subacute, and weakness and is it symmetrical? This
chronic information helps determine which
• Acute onset limb weakness is typical vascular joints, muscles and /or nerves may be
events, affecting contralateral UMN path- affected, e.g. peripheral muscle weakness
ways, resulting in either hemiparesis or due to peripheral neuropathy is sym-
hemiplegia metrical compared with individual nerve
• Sudden onset weakness in all four limbs or nerve root disease which should be
(tetraparesis) or in both legs (paraparesis) is suspected if weakness is asymmetrical or
seen with spinal cord infarction, usually due confined to one limb
344
Table 50.2 : Historical clues for neuromuscular weakness History of trauma—It can determine
possible cause of muscle weakness
Findings Probable diagnosis
Exercise history—Muscle overuse may
Acute weakness with Stroke; spinal cord injury
neurologic deficit(s) cause muscle weakness.
Intermittent neurologic TIA • Past medical history—Diabetes and chronic
deficit renal failure can cause peripheral neuropathy
Fever, coryza, headache Viral meningitis, encephalitis which may result in muscle weakness; diabetes,
Fever, otitis, sinusitis Bacterial meningitis, cerebral
hypertension and high cholesterol are risk
abscess
Risky sexual exposure, Gonococcal, syphilis, HIV factors for cerebrovascular disease (stroke)
Urethral discharge which may result in muscle weakness;
Symptoms of raised Mass lesion pernicious anemia may cause subacute
intracranial pressure
combined degeneration of the cord and muscle
Exercise-provoked Myasthenia gravis
weakness weakness. History of TB, malignancy may
Heat-induced symptoms Multiple sclerosis suggest infection or mass lesion
(hot sun, hot shower, • Dietary history—Vit. B12 deficiency can cause
fever); double vision-
peripheral neuropathy which may result in
blurring; multiple
neurologic deficit, muscle weakness
exacerbations and • Medications—Some medications can cause
remissions
peripheral neuropathy, e.g. amiodarone,
Neck / back pain with or Cervical spondylosis,
without radiation degenerative disk disease phenytoin, nitrofurantoin; some medi-
Rash around eyelids, Dermatomyositis, cations may increase risk of thrombotic
difficulty arising from polymyositis cerebrovascular disease (stroke), e.g. oral
a chair
contraceptive pill, hormone replacement
Positive medication Drug-induced myopathy
history (statins, steroids, anti- therapy; some medications can increase the
retrovirals) risk of hemorrhagic stroke, e.g. warfarin
Positive family history Muscular dystrophy, • Cigarette smoking—It is a major risk factor
autoimmune disorder
for cerebrovascular disease
• Alcohol history—It can be a cause of
If there is limb weakness, are the facial muscles
peripheral neuropathy
also affected by weakness?—weakness of the
• Family history—Strokes, diabetes, high
muscles of the face associated with weakness
cholesterol, hypertension, hereditary motor
of the limbs would suggest a diagnosis of and sensory neuropathy, Duchenne muscular
cerebrovascular disease, a mass in the brain dystrophy
or spinal cord • Physical examination includes:
Aggravating factors—They help to Gait, neck stiffness
determine the cause of muscle weakness, Glasgow coma scale , (GCS) i.e. level of
e.g. muscle power decreases with use in consciousness
myasthenia gravis Blood pressure, palpation of all peripheral
Recent viral infection—May suggest a viral pulses including carotids for bruits;
illness itself as the cause of muscle cardiac examination for arrhythmias,
weakness, e.g. influenza or Guillain- Barré murmur
syndrome (symptoms begin 7-10 days Optic fundi for papilledema, diabetes and
after the infective illness) hypertensive retinal lesions.
Weakness in the Arms and Legs 345
51 Weight Loss
Occasional HIV
• Nonmalignant GI disorders (chronic panc- • In patients with any sexual risk factor.
reatitis, gastroparesis)
• Hyperthyroidism Urea, Creatinine, Electrolytes
• Organ failure (advanced CHF, COPD,
• Progressively increasing levels in renal
hepatic, and renal disease)
failure
• Social stressful events (economic hardship,
• Hyponatremia with hyperkalemia in
isolation).
Addison’s disease.
Rare
Tuberculin or PPD Test
• Substance misuse (diuretics, laxatives,
• A positive reaction (≥10 mm of induration)
cocaine, amphetamine)
indicates TB infection; may be negative in
• Nonmalignant GI disorders (IBD, mala-
patients with severe weight loss and AIDS.
bsorption, celiac disease)
348
RED FLAGS
†
Web site: www.mna-elderly.com; for Mini Nutritional • A high index of suspicion is essential to
Assessment tool.
‡ diagnose eating disorders; patients can be
Refer to Mini-Mental State Examination (MMSE) and
Yesavage’s Geriatric Depression Scale in standard text- very manipulative, critical, and secretive, and
books. commonly lie about food intake
350
• Consider depression in most patients with any specific eating disorder, and therefore
weight loss. It may be the primary cause or present with subsyndromal cases of anorexia
may coexist with any secondary illness nervosa or bulimia nervosa. Examples include:
• UWL, when accompanied with anorexia, • A female of anorexia nervosa, except that she
may be the only sign of malignancy has regular menses
• Occult malignancy must be regarded as the • A female of anorexia nervosa, without weight
most common cause of weight loss in the loss
• A female frequently indulging in self-
absence of major symptoms and signs
induced vomiting after eating even a small
• Continued weight loss should be monitored
food intake
even if the initial evaluation is nondiagnostic
• A female repeatedly chewing and spitting
• Weight loss may be the initial presentation
out, but not swallowing large amounts of
of diabetic ketoacidosis food.
• Beware of the potential for associated
substance abuse. REFERENCES
SELECTIVE GLOSSARY 1. Rakel TB of Fam Med 7th edn. Part IV: Nutrition
and Family Medicine; p.1097.
Eating Disorder-Not Otherwise Specified— 2. Metalidis C, et al. Involuntary weight loss. Does a
negative baseline evaluation provide adequate
ED-NOS(DSM IV TR-307.50) is an emerging reassurance? Eur J Intern Med 2008;19(5):345-9.
issues in Eating Disorders; this diagnosis is given Epub 2007 Nov 26.[PMID: 18549937: Abstract].
3. Kondo DG, Sokol MS. Eating disorders in primary
to patients who have significant eating disorder
care: A guide to identification and treatment.
symptoms, but do not meet the full criteria for Postgrad Med 2003; 114: Nov (online article).
NOTE
INDEX
A Age Aortic
of menarche 45 dissection 50
Abdominal related macular degeneration stenosis 49
angina 10 331 Aortoduodenal fistula 147
CT scan 318 Agnosia 73 Aphasia 73
distension 1 Airway obstruction 111 Appendicitis 9, 10
pain 7, 8 Albuminuria in renal disorders 2 Apraxia 73
wall pain 10 Alcoholic Arrhythmias 226
Abnormal vaginal bleeding 315, hepatitis 3 Arterial blood gases 110
320 liver disease 196 Arthralgia 29
Acid fast stain 69 Alkaline phosphatase 2, 220 Arthritis 29
Acoustic neuroma 165, 328 Allergic rhinitis 69 Ascariasis 84
Acute Alport’s syndrome 174 Ascites 2
abdomen 9 Alzheimer’s disease 74, 79 Aseptic abortion 9
abdominal Ambulatory Asherman’s syndrome 19
conditions 14 ECG 226 Aspergillosis 177
pain 9 EEG 65 Aspiration 69
angle closure glaucoma 249, Amenorrhea 18, 315 Asteotic dermatitis 242
335 Aminotransferases 2 Asthma 114
backache 37 Amyotrophic lateral sclerosis 104, exacerbation 69
bacterial gastroenteritis 10 340 Atrial myxomas 281
bronchitis 69 Anal disease 148 Atrophy of vulva and vaginal skin
chest pain 53 Analgesic 23
cholecystitis 9 nephropathy 235 Atypical chest pain 54
closed angle glaucoma 212 rebound headache 156 Autoantibody tests 200
coronary syndrome 48 Anaphylactic laryngeal edema 111 Autoimmune
exacerbation of COPD 108 Ancylostoma duodenale 84 disease 19, 75, 333
hydramnios 9 Anemia 115, 197 disorders 128
intermittent porphyria 215 Angioedema 127, 308 Autologous serum skin test 310
laryngotracheobronchitis 109 Angioneurotic edema 109 Autonomic neuropathy 60
leukemia 132 Angiotensin-converting enzyme
narrow angle glaucoma 156 122 B
pancreatitis 9 Anhidrosis 264 Back pain 36
porphyria 340 Anorectal Bacterial infection 10
postinfection syndromes 296 and pelvic floor function tests Balloon expulsion test 59
respiratory distress syndrome 59 Barotrauma 165
109 manometry 59 Barrett’s esophagus 104
stress Anorexia nervosa 19, 58 Basilar migraine 282
disorders 285 Antalgic gait 139 Bell’s palsy 121
reaction 26 Anterior uveitis 249 Bence Jones protein 38
systemic illness 26 Antiacetylcholine antibodies 101 Benign
urinary retention 9 Antibiotic-related diarrhea 60 breast disorders 42
viral hepatitis 196, 199 Antigliadin antibodies 348 disorders 316
Adams-Stokes attacks 281 Antimitochondrial antibodies 200 hematuria 170
Addison’s disease 10, 297 Antiphospholipid syndrome 273 intracranial hypertension 156
Adenocarcinoma 148 Anti-Smith antibody 32 neoplasm 99
Adrenal crisis 215 Anxiety 25, 220 prostatic hypertrophy 303
352
Berger disease 175 Carcinoid tumor 148, 181 Choroidal melanoma 331
Biliary Carcinoma of Chromosomal abnormalities 19
ascites 3 anus 60 Chronic
colic 10 bronchus 43 active hepatitis 132
Biopsy 265, 271 colon 58, 60 anovulation 318
Bladder incontinence 63 rectum 60 backache 37
Bleeding 146 Cardiac bronchitis 114
diathesis 171 and bronchial asthma 112 daily headache 156
disorders 316 arrhythmias 49, 115 dyspnea 118
Blepharitis 249 causalgia 49 fatigue syndrome 193, 206, 220
Blind ending vagina 23 disease 333 glaucoma 331
Body enzymes 50, 278 illness 19
spasm 63 ischemia 212 infections 75, 148, 296
twitching 63 murmurs 230 low back pain 219
Boerhaave syndrome 216 syndrome X 49, 55 neck pain 219
Bone Cardiopulmonary exercise testing oral steroids 38
marrow aspirate and biopsy 117 overuse syndromes 220
244 Carney syndrome 282 pain 219
scan 221 Carotid syndromes 223
Bowel incontinence 63 Doppler papilledema 331
Brain scan 332 renal failure 235
and meningeal biopsy 77 ultrasound 325 subdural hematoma 156
natriuretic peptide 271 sinus hypersensitivity 277 Churg-Strauss syndrome 181
tumors 64 Casino’s test 3 Cirrhosis 3
Brainstem Cataract surgery 331 Clitoromegaly 23
auditory evoked responses Cauda equina syndrome 38 Clostridium difficile 60
166 Cavernous Cluster headache 156, 249
evoked potentials 293 hemangiomas 250 CMV retinitis 331
Breakthrough bleeding 316 sinus thrombosis 128 CNS
Breast 44 Celiac sprue 60 diseases 292
abscess 43 Central disorders 212
cancer 44, 45 post-stroke pain 220 infections 121
lump 42, 42, 45 retinal venous occasion 335 tumors 121
Bronchiectasis 69, 70, 115, 177 Cerebellar gait 139 Cocaine lung 177, 182
Bronchitis 49, 177 Cerebral Coccydynia 38
Bronchogenic carcinoma 69, 70, malaria 121 Cogan’s syndrome 294
177 venous thrombosis 156 Cold
Bronchoscopy 71, 110, 117, 187 Cerebrovascular accidents 121, abscess 43
Brown-Séquard syndrome 143 335 weather 303
Brucellosis 132 Cervical Collagen disease 30
Brugada syndrome 231 and lumbosacral spine 341 Colon malignancy 84
B-type natriuretic peptide 116 culture 317 Colonic
Budd-Chiari syndrome 3 spondylosis 156 arteriovenous 148
Burkitt’s lymphoma 128 Chair test 143 neoplasm 148
Burnout syndrome 297, 300 Charcot-Marie-Tooth syndrome 286 Common gait disorders 142
Chest Complex regional pain syndromes
C pain 48 220, 223
wall Concealed accidental hemorrhage
Calcium 207 bruising 49 9
channel blockers 156 syndrome 49 Congenital heart disease 226
Cancer of Cholecystitis 10 Connective tissue disease 132, 297
esophagus 147 Cholelithiasis 10 Constipation 57
stomach 147 Cholestatic Constrictive pericarditis 2
Cancer pain syndromes 220 jaundice 197 Contact lens
Capsule endoscopy 149 pruritus 242 induced acute red eye 253
Carbohydrate malabsorption 91 Cholestatoma 165 use 251
Carbon monoxide poisoning 111 Choriocarcinoma 316 Conversion disorder 10
Index 353
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