Dr.

Cemara, dr Dini, dr Himawan, dr Yusuf, dr Agung

PEMBAHASAN TUTORIAL 1
BATCH 4 2012
ILMU PENYAKIT DALAM
 1. ASTHMA: DEFINITION

Definition:
 a chronic inflammatory disorder
of the airways causes airway
hyperresponsiveness that
usually associated with variable
airflow obstruction that is often
reversible.
reversible

 Airway hyperresponsiveness
leads to recurrent episodes of:
 wheezing,

 breathlessness,

 chest tightness, and

 coughing

GINA 2005
1. ASTHMA: RISK FACTORS

Risk factors for asthma

may be classified as:
 Host factors that
predispose or protect
them from developing
asthma,

 Environmental factors that

influence:
 the susceptibility to the
development of asthma,
 precipitate asthma
exacerbations, and/or
 cause symptoms to persist.

GINA 2005
1. ASTHMA: CLASSIFICATION

Measurements of lung function enhance

diagnostic confidence.

Spirometry:
 Airway obstruction:
FEV1/FVC <75% or FEV 1 <80%
 Reversibility: improvement of FEV1 ≥15%
after bronchodilator inhalation.
 Classification of asthma severity

Peak expiratory flow meter:

 Reversibility: improvement of PEF ≥15%
after bronchodilator inhalation
 Variability: daily PEF measured at night
after bronchodilator & morning before
bronchodilator >20%.

GINA 2005
PDPI. Asma: pedoman diagnosis & penatalaksanaan di Indonesia. 2004
1. ASTHMA: CLASSIFICATION ON
TREATMENT
 1. ASTHMA: THERAPY

Asthma
management has
six interrelated
parts:
1. Education
2. Assess &
monitor severity
3. Avoid exposure
to risk factors
4. individual
medication
plans
5. plans for
managing
exacerbations
6. regular followup

GINA 2005
2. DIABETES MELLITUS:
DEFINITION

DM:
 a group of common
metabolic disorders that
share the phenotype of
hyperglycemia.

Depending on the etiology,

factors contributing to
hyperglycemia include:
 ↓insulin secretion,
 ↓ glucose utilization, &
 ↑ glucose production.

Harrison’s principles of internal medicine. 18th ed. McGraw-Hill; 2011.

2. DIABETES MELLITUS:
PATHOPHYSIOLOGY

Acute complication:
 Diabetic ketoacidosis
 Hyperosmolar nonketotic

Chronic complication:
 Microangiopathy:
 Polyneuropathy
 Retinopathy
 Nephropathy
 Macroangiopathy:
 Stroke
 Coronary heart disease
 Peripheral artery disease

Basic & clinical endocrinology

Color atlas of pathophysiology
3. MANAGEMENT OF TYPE 2 DM

Harrison’s principles of internal medicine. 18th ed. McGraw-Hill; 2011.

Diagnosisi & tatalaksana DM tipe 2 di Indonesia. PERKENI
3. MANAGEMENT OF TYPE 1 DM

Harrison’s principles of interal medicine. 18th ed. McGraw-Hill; 2011.

4. TYPHOID FEVER
4. TYPHOID FEVER

Widal test:
• Antibody detection to somatic antigen O & flagel antigen H from salmonella.
• Diagnostic result: the titer increase by >4 x after 5-10 days from the first result.
• Titer for antibody O increase at 6-8 days after the first symptoms, while antibody H
increase at 10-12 days.
4. TYPHOID FEVER

Blood cultures: often (+) in the 1st week.

Stools cultures: yield (+) from the 2nd or 3rd week on.
Urine cultures: may be (+) after the 2nd week.
(+) culture of duodenal drainage: presence of Salmonella in carriers.
Jawetz medical microbiology.
5. HEART FAILURE

Heart failure is
present when:
 the heart is unable to
pump blood forward at a
sufficient rate to meet the
metabolic demands of the
body (forward failure), or

 Is able to do so only if the

cardiac filling pressures are
abnormally high (backward
failure),

 or both.

Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott Williams & Wilkins; 2011.
5. HEART FAILURE

Lilly LS. Pathophysiology of heart disease. 5th ed. LWW; 2011.

5. HEART FAILURE

Lilly LS. Pathophysiology of heart disease. 5th ed. LWW; 2011.

5. HEART FAILURE

Framingham criteria:
criteria:
 ≥ 2 major or 1 major + 2 minor
 Minor criteria are acceptable only if they cannot be
attributed to another medical condition (e.g., pulmonary
hypertension, chronic lung disease, cirrhosis, ascites,
nephrotic syndrome).
 6. ARTHRITIS

Osteoarthritis:
steoarthritis:  Gout arthritis:
arthritis:
 space narrowing (white arrow),
Acute gouty arthritis: soft tissue
swelling.
 osteophytes/spur (arrowhead),
Advanced gout: the erosion are slightly
 subchondral cysts, removed from the joint space, have a
rounded or oval shape, & are
 subchondral characterized by a hypertrophic
sclerosis/eburnation (black calcified "overhanging edge." The joint
arrow). space may be preserved or show
Current diagnosis & treatment in rheumatology. 2nd ed. McGraw-Hill; 2007.
osteoarthritic type narrowing.
Harrison’s principles of internal medicine. 18th ed. McGraw-Hill; 2011.
6. ARTHRITIS

Current diagnosis & treatment in rheumatology. 2nd ed. McGraw-Hill; 2007.

Harrison’s principles of internal medicine. 18th ed. McGraw-Hill; 2011.
7. ARTHRITIS
 Ciri OA RA Gout SA

Awitan
ARTHRITIS
Inflamasi
gradual

-
gradual

+
akut

+
Variabel

Patologi Degenerasi Pannus Mikrotophi Enthesitis

Jumlah Sendi Poli Poli Mono-poli Oligo/poli

Tipe Sendi Kecil/besar Kecil Kecil-besar Besar

Predileksi 1st CMC, DIP, PIP MCP, PIP, MTP, kaki, Sacroiliac
pergelangan pergelangan kaki Spine
tangan/kaki, kaki & tangan Perifer besar
Temuan Sendi Bouchard’s nodes Ulnar dev, Swan Kristal urat En bloc spine
Heberden’s nodes neck, Boutonniere enthesopathy
Perubahan Osteofit Osteopenia erosi Erosi
tulang erosi ankilosis

Temuan - Nodul SK, Tophi, Uveitis,

Extraartikular pulmonari cardiac olecranon bursitis, konjungtivitis,
splenomegaly batu ginjal insuf aorta,
psoriasis, IBD
Lab Normal RF +, anti CCP Asam urat
7. ARTHRITIS

Tuberculous arthritis:
 The classic presentation: monarthritis with pain, stiffness, &
gradual loss of function over weeks to months.
 15% have an acute presentation that mimics septic arthritis
or microcrystalline disease.
 fever, night sweats, & weight loss are present in only 50% of
patients.
 Most patients do not have active TB elsewhere, and the
chest radiograph may be normal.
 Smears of synovial fluid reveal acid-fast bacilli in only 20%
of cases, but 80% of cultures of synovial fluid grow M
tuberculosis

Current diagnosis & treatment in rheumatology. 2nd ed. McGraw-Hill; 2007.

7. ARTHRITIS

Osteoarthritis
Rheumatoid artrhitis

Harrison’s principles of internal medicine. 18th ed. McGraw-Hill; 2011.

Acute gout arthritis Current diagnosis & treatment in rheumatology. 2nd ed. McGraw-Hill; 2007.
Kumar & Clark clinical medicine. Saunders; 2005.
 7. ARTHRITIS

Gout:
 transient attacks of
acute arthritis
initiated by
crystallization of
urates within & about
joints,
 leading eventually to
chronic gouty arthritis
& the appearance of
tophi.
 Tophi: large
aggregates of urate
crystals & the
surrounding
inflammatory reaction.

Harrison’s principles of internal medicine. 18th ed.

McGraw-Hill; 2011.
Robbins’ pathologic basis of disease. 2007.
7. ARTHRITIS

Current diagnosis & treatment in rheumatology. 2nd ed. McGraw-Hill; 2007.

8. ARTHRITIS

The management of acute

gout is to provide rapid &
safe pain relief.
 NSAID,
 Colchicine.
 Corticosteroid if NSAID is
contraindicated.

Preventing further attacks by

uric acid lowering agent:
 Allopurinol
 Probenecid

Uric acid lowering agent

shouldn’t be given on acute
attack, unless the patient has
consumed it since 2 weeks
before.
Current diagnosis & treatment in rheumatology. 2nd ed. McGraw-Hill; 2007.
9. TUBERCULOSIS

International Standard fo Tuberculosis Care-WHO
9. TUBERCULOSIS

International Standard fo Tuberculosis Care-WHO
10. CHEST PAIN

Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott Williams & Wilkins; 2011.
10. CHEST PAIN

Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott Williams & Wilkins; 2011.
10. CHEST PAIN
10. CHEST PAIN

Lilly LS. Pathophysiology of heart

disease. 5th ed. Lipincott Williams
& Wilkins; 2011.
11. ANAEMIA

Wintrobe clinical hematology.

11. ANAEMIA

Hoffbrand essential hematology.

11. ANAEMIA
 12. HEPATITIS B

HBsAg (the virus coat, s= surface)
 the earliest serological marker in the serum.

HBeAg
 Degradation product of HBcAg.

 It is a marker for replicating HBV.

HBcAg (c = core)
 found in the nuclei of the hepatocytes.

 not present in the serum in its free form.

Anti-
Anti-HBs
 Sufficiently high titres of antibodies ensure
imunity.

Anti-
nti-Hbe
 suggests cessation of infectivity.

Anti-
Anti-HBc
 the earliest immunological response to HBV

 detectable even during serological gap. Principle & practice of hepatology.

13. OBSTRUCTIVE LUNG DISEASE

a working definition of
COPD:
 a disease state
characterized by airflow
limitation that is not fully
reversible.

 The airflow limitation is

usually both progressive
& associated with an
abnormal inflammatory
response of the lungs to
noxious particles or
gases.

GOLD. WHO.
13. OBSTRUCTIVE LUNG DISEASE
 13. OBSTRUCTIVE LUNG DISEASE

The choice of bronchodilator drugs (ß2-agonists, anticholinergics, &

methylxanthines) depends on the availability of medication and the patient’s
response.
13. OBSTRUCTIVE LUNG DISEASE

Exacerbation symptoms:
 Worsening dyspneu
 Increased sputum production
 Changed color of sputum (become
purulent)

Acute exacerbation is divided into:

 Severe: has all of the above
 Moderate: 2/3 of the above
 Mild: 1 of the above with upper
respiratory tract infection for 5 days,
fever with no other cause, worsening
cough/wheezing, increased breathing
frequency/heart beat >20% baseline.

GOLD. WHO.
PPOK diagnosis & penatalaksanaan di Indonesia.
13. OBSTRUCTIVE LUNG DISEASE
14. ASTHMA EXACERBATION
14. ASTHMA EXACERBATION
14. ASTHMA EXACERBATION
Moderate Episode Severe Episode
14. ASTHMA EXACERBATION

Criteria for Admission to
Intensive Care Unit,
Unit, with
consultation of an asthma
specialist or a critical care
specialist, is indicated in:
 Severe asthma with a lack of
response to initial therapy in the
emergency department or
worsening asthma despite
adequate therapy
 Presence of confusion,
drowsiness, other signs of
impending respiratory arrest, or
loss of consciousness
 Impending respiratory arrest:
hypoxemia despite supplemental
oxygen (PaO2 <60 mm Hg
and/or PaCO2 >45 mm Hg.
GINA 2005
 Hospitalization
 pretreatment FEV1 or PEF < 25%
of the predicted or personal best
value
 posttreatment FEV1 or PEF < 40%
of predicted or personal best,
usually require hospitalization.
 Discharge
 Patients with posttreatment lung
function in the range of 40 to 60
percent predicted can potentially
be discharged, assuming adequate
followup is available.
15. MALIGNANCY

Multiple myeloma represents a
malignant proliferation of plasma cells
derived from a single clone.

The classic triad of myeloma:
 marrow plasmacytosis (>10%), "punched out" lesions
 lytic bone lesions, represents a purely osteolytic
 serum and/or urine M component. lesion with little or no
osteoblastic activity
15. MALIGNANCY

Protein electrophoresis:
16. HEMATEMESIS
DIagnosis Clinical Finding
Mallory-Weiss tear Vomiting, retching, or coughing preceding
hematemesis. Especially in an alcoholic patient.
May also occur in hyperemesis gravidarum.

Esophageal varices Patient with portal hypertension (e.g. cirrhosis) will

cause varices around the sites of portosystemic
perforation anastomoses.

GERD History of recurrent heartburn after meal.

Peptic ulcer perforation Patient with history of recurrent gastritis or long

term use of NSAID.
16. HEMATEMESIS
16. HEMATEMESIS

Cirrhosis
 the development of fibrosis to the
point that there is architectural
distortion with the formation of
regenerative nodules.
 This results in a decrease in
hepatocellular mass, and thus
function, & an alteration of blood
flow.
 16. HEMATEMESIS

Portal hypertension caused by:
 ↑ intrahepatic resistance to
the passage of blood flow
through the liver due to
cirrhosis & regenerative
nodules
 ↑ splanchnic blood flow
secondary to vasodilation
within the splanchnic vascular
bed.

Portal hypertension cause

varices around the sites of
portosystemic anastomoses:
 hemorrhoids at the anorectal
junction;
 esophageal varices at the
gastroesophageal junction;
 caput medusae at the
umbilicus.
17. TROPIC INFECTION
18. ACUTE HEPATITIS
19. ADVERSE DRUG REACTION
Antibioics Adverse Effect
Aminoglycosides Ototoxicity & nephrotoxicity
Tetracyclines Tetracycline-calciumextravasation complex: inhibits bone
growth in neonates & produces teeth staining
Chloramphenicol Direct toxicity of nitroso-chloramphenicol on DNA
Cephalosporin Anaphylaxis. Hypersensitivity reactions may be compound
specific (eg, cefaclor)
Co-trimoxazole Erythema multiforme major (Stevens-Johnson syndrome) &
toxic epidermal necrolysis.
Quinolones Diarrhea and skin rashes occur in 4-8% of patients.
The studies with beagle puppies who got the quinolones
whose bones didn't seem to grow very well and the cartilage
didn't seem to develop.
Macrolides Gastrointestinal discomfort and nausea are common
Reversible cholestatic jaundice can occur 10-14 days after
initiation of therapy
20. HYPERTENSION
20.
HYPERTENSION

If a drug is not
tolerated or is
contraindicated, then
one of the other
classes proven to
reduce
cardiovascular events
should be used
instead.

Treating SBP and
DBP to targets that
are <140/90 mmHg
is associated with a
decrease in CVD
complications.

In patients with
hypertension and
diabetes or renal
disease, the BP goal
is <130/80 mmHg.
21. AUTOIMMUNE DISEASE

Systemic lupus
erythematosus:
 an autoimmune
disease
 organs & cells
undergo damage
 initially mediated by
tissue-binding
autoantibodies &
immune complexes.
21. AUTOIMMUNE DISEASE
 21. Autoimmune Disease
Rheumatoid arthritis (RA)
• Chronic inflammatory disease of unknown etiology
marked by a symmetric, peripheral polyarthritis.
• RA is a systemic disease  extraarticular
manifestations.
• 10% of RA have secondary Sjögren's syndrome
(keratoconjunctivitis sicca or xerostomia).
• a score of 6: definite RA.
22. MURMUR & HEART SOUNDS
22. MURMUR & HEART SOUND

Lilly LS. Pathophysiology of heart disease.

22. MURMUR & HEART SOUND
23. POLYURIA

If polyuria is shown to be dilute, pathophysiologic
mechanisms include:
1. Hypothalamic or central diabetes insipidus with inability
to synthesize and secrete vasopressin;

2. Nephrogenic diabetes insipidus with an inadequate

renal response to vasopressin;

3. Transient diabetes insipidus of pregnancy produced by

accelerated metabolism of vasopressin;

4. Primary polydipsia, in which the initiating event is

ingestion of excess fluid and the subsequent hypotonic
polyuria is an appropriate physiologic response.
23. POLYURIA

During the dehydration or water deprivation
test:
 primary polydipsia: concentrate his urine
without becoming hyperosmolar
 diabetes insipidus: become hyperosmolar
without concentrating the urine.

After the patient is given desmopressin:

 Hypothalamic DI has minimal
concentration of the urine & an additional
↑ in urine osmolality of at least 50%.
 partial hypothalamic DI concentrate their
urine minimally with dehydration, but the
maximum urinary concentration is not
achieved, and there is an additional boost
with administered desmopressin
 Nephrogenic DI do not concentrate their
urine & no further increase in urine
osmolality after the administration of  Harrison’s principles of internal medicine. 18th ed.
 Greenspan’s clinical endocrinology.
desmopressin.
24. ALTITUDE ILLNESS

Acent to high altitude
Normal physiologic

changes during
acclimation include:
↓ PO2 in the inspired gas
 ↑ sympathetic tone;
 ↑erythropoietin, leading to
Less pressure driving O2
diffusion ↑Hb & erythrocyte;
 ↑ tissue capillary density &
mitochondrial numbers;
hyperventilation
 ↑ levels of 2,3-bpg,
enhancing O2 utilization.
Respiratoric alkalosis &
dehydration
24. ALTITUDE ILLNESS

AMS is a neurologic syndrome characterized by nonspecific symptoms
(headache, nausea, fatigue, and dizziness) with a paucity of physical
findings developing 6–12 h after ascent to a high altitude.

HACE (but not AMS) is an encephalopathy whose hallmarks are ataxia

and altered consciousness with diffuse cerebral involvement but
generally without focal neurologic deficits.

The exact mechanisms causing these syndromes are unknown. MRI

studies have suggested that vasogenic (interstitial) cerebral edema is a
component of the pathophysiology of HACE.

Impaired cerebral autoregulation in the presence of hypoxic cerebral

vasodilatation and altered permeability of the blood-brain barrier due to
hypoxia-induced chemical mediators like histamine, arachidonic acid,
and vascular endothelial growth factor (VEGF) may all contribute to
brain edema.
25. URINARY TRACT INFECTION
25. URINARY TRACT INFECTION
25. URINARY TRACT INFECTION

 Cystitis: dysuria, frequency, urgency, suprapubic

discomfort, foul odor & greyish urine.

 Pyelonefritis: fever, chilling, nausea, vomit, flank pain,

diarrhe, leukocyte silinder.

 Urethritis: dysuria, frequency, pyuria.

Harrison’s principles of internal medicine. 18th ed. McGraw-Hill; 2011.
26. THYROTOXIC CRISIS

It may occur in a patient with a
history of Graves' disease who
has discontinued antithyroid
medication or in a patient with
previously undiagnosed
hyperthyroidism

Clinical picture:
 acute onset of hyperpyrexia (with
temperature > 40 °C),
 sweating,
 marked tachycardia often with
atrial fibrillation,
 nausea, vomiting,
 diarrhea,
 agitation,
 tremulousness, &
 delirium
BEDAH
25. BASIC LIFE
SUPPORT
http://en.wikipedia.org/wiki/Burn

26. BURN INJURY

• Berat luka bakar:
• Ringan: derajat 1 luas
< 15% a/ derajat II <
2%
• Sedang: derajat II 10-
15% a/ derajat III 5-
10%
• Berat:
Berat derajat II > 20%
atau derajat III > 10%
atau mengenai wajah,
tangan-kaki, kelamin,
persendian,
pernapasan
 To estimate scattered burns: patient's
palm surface = 1% total body surface TOTAL BODY
area
SURFACE AREA

Kedalaman Luka Bakar: IIB

Luas luka bakar: 10%
BB: 50 kg
Rumus Baxter:
4 x50 x10 =2000ml
Parkland formula = baxter formula ½ dlm 8 jam1000ml
Tetes/menit: 1000/8=125cc/jam
http://www.traumaburn.org/referring/fluid.shtml 125x20/60= 41.667 tetes/
tetes/menit
http://emedicine.medscape.com/article/2047916

27. CHEST TRAUMA

Disorders Etiology Clinical

Hemothorax lacerated blood Anxiety/Restlessness,Tachypnea

Tachypnea,Signs
Tachypnea of
vessel in thorax Shock,Tachycardia
Tachycardia
Frothy, Bloody Sputum
Diminished Breath Sounds on Affected
Side,Flat
Side, Neck Veins, Dullness to
percussion
Simple/Closed Blunt trauma Opening in lung tissue that leaks air into
Pneumothorax spontaneous chest cavity, Chest
Pain,Dyspnea,Tachypnea
Decreased Breath Sounds on Affected
Side,hipersonor
Open Pneumothorx Penetrating Opening in chest cavity that allows air to
chest wound enter pleural cavity, Dyspnea,Sudden sharp
pain,Subcutaneous Emphysema
Decreased lung sounds on affected side
Red Bubbles on Exhalation from wound
(Sucking chest wound)
Disorders Etiology Clinical
Tension Anxiety/Restlessness, Severe ,Poor Color
Penumothorax Dyspnea,Tachypnea,Tachycardia
Absent Breath sounds on affected side,
Accessory Muscle Use, JV Distention
Narrowing Pulse Pressures,Hypotension
Tracheal Deviation, hypersonor

Flail Chest Trauma a segment of the rib cage breaks becomes

detached from the rest of the chest wall, 3 ribs
broken in 2 or more places,painful when
breathing,Paradoxical breathing

Pleural Efusion congestive heart Dyspnea, cough, chest pain, which results from
failure, pleural irritation, Dullness to percussion,
pneumonia, decreased tactile fremitus, and asymmetrical
malignancy, or chest expansion, with diminished or delayed
pulmonary expansion on the side of the effusion,
embolism decreased tactile fremitus, and asymmetrical
infection chest expansion, diminished or delayed
expansion on the side of the effusion

Pneumonia Infection, Fever,dysnea,cough,rales in ausultation

inflammation
http://emedicine.medscape.com/ As blood increases, it puts pressure on heart
pleural space fills with blood and other vessels in chest cavity

TREATMENT FOR
HEMOTHORAX
• ABC’s with c-spine control as indicated
• Secure Airway assist ventilation if
necessary
• General Shock Care due to Blood loss
• Consider Left Lateral Recumbent
position if not contraindicated
• RAPID TRANSPORT
• Contact Hospital and ALS Unit as soon
as possible Upright chest radiograph:
• needle decompressionif indicated blunting at the costophrenic angle or
• Chest tubeas soon as patient stable an air-fluid interface
http://emedicine.medscape.com/

SIMPLE/CLOSED PNEUMOTHORAX
Th/
• ABC’s with C-spine control
• Airway Assistance as
needed
• If not contraindicated
transport in semi-sitting
position
• Provide supportive care
• Contact Hospital and/or
ALS unit as soon as
possible
• Usually self correcting
http://emedicine.medscape.com/

OPEN PNEUMOTHORAX
Th/ :
• ABC’s with c-spine
control as indicated
• High Flow oxygen
Inhale • Listen for decreased
Inhale breath sounds on
affected side
• Apply occlusive dressing
to wound
• Notify Hospital and ALS
unit as soon as possible
Causes the lung to collapse due to increased
pressure in pleural cavity
Can be life threatening and can deteriorate
rapidly
 http://www.cssolutions.biz
OCCLUSIVE
DRESSING
 http://www.cssolutions.biz

TENSION
PNEUMOTHORAX
 TREATMENT

ABC’s with c-spine as
indicated

Needle Decompression of
Affected Side

High Flow oxygen including
BVM
• Air builds in pleural
Treat for S/S of Shock
space with no where
Notify Hospital and ALS
for the air to escape unit as soon as possible
• collapse of lung on
If Open Pneumothorax and
occlusive dressing present
affected side BURP occlusive dressing
• increased pressure
on mediastium,the
other lung, and
great vessels
http://www.trauma.org/index.php/main/article/199/
http://emedicine.medscape.com/article/424547

NEEDLE DECOMPRESSION

Locate 2-3 Intercostal space

midclavicular line

Cleanse area using aseptic
technique

Insert catheter ( 14g or larger)
at least 3” in length over the top
of the 3rd rib( nerve, artery, vein
lie along bottom of rib)

Remove Stylette and listen for
rush of air

Place Flutter valve over catheter

Reassess for Improvement
http://emedicine.medscape.com/article/4337
79
FLAIL CHEST
multiple adjacent ribs are broken in multiple
places, separating a segment, so a part of
the chest wall moves independently
The first rib is often fractured
posteriorly (black arrows). If multiple
rib fractures occur along the
midlateral (red arrows) or anterior
chest wall (blue arrows), a flail chest
(dotted black lines) may result.
http://emedicine.medscape.com/

TREATMENT
ABC’s with c-spine control as indicated
Good analgesia
intercostal blocks
avoiding narcotic analgesics
better ventilationimproved tidal volume, increased
blood oxygenation
Positive pressure ventilation
avoid pulmonary barotrauma
Chest tubes as required.
Adjustment of position
make the patient most comfortable and provide relief of
pain
Aggressive pulmonary toilet
Surgical fixation
PLEURAL EFFUSION

Excess of pleural fluid in the pleural
cavity
 fluid formation from parietal pleura,
Interstitial spaces of lungs, or peritoneal
cavity
 decreased fluid removal by the
lymphatics

THERAPY
• Bed rest
• Treat the cause
– Heart failure : diuretics
– TB : OAT + Steroids should be
added to treatment for 4-6 weeks
– etc
• Therapeutic aspiration
– Large effusion
– Cardiac or respiratory embarasment
– Secondary infection of effusion
– Failure of medical management
28. LYMPHADENOPATHY

Enlargement of the lymph nodes

Types
 Localized lymphadenopathy
 localized spot of infection
 Generalized lymphadenopathy
 generalized infection all over the body e.g., influenza
 Persistent generalized lymphadenopathy (PGL)
 persisting for a long time, possibly without an apparent cause
 Dermatopathic lymphadenopathy
 associated with skin disease
CAUSE

Reactive
 acute infection (e.g., bacterial, or viral)
 chronic infections (tuberculous lymphadenitis, cat-scratch disease).

Tumoral:
 Primary: Hodgkin lymphoma and non-Hodgkin lymphoma give
lymphadenopathy in all or a few lymph nodes. [4]
 Secondary: metastasis, Virchow's Node, Neuroblastoma, and Chronic
Lymphocytic Leukemia.

Autoimmune etiology
 systemic lupus erythematosus, rheumatoid arthritis all giving a
generalized lymphadenopathy.

Immunocompromised etiology:
 AIDS. Generalized lymphadenopathy early sign
 "Lymphadenopathy syndrome“first symptomatic stage of HIV
progression, preceding a diagnosis of AIDS.[5]

Bites from certain venomous snakes

Unknown etiology:
 sarcoidosisKawasaki disease
http://www.aafp.org/afp/1998/1015/p1313.ht
ml
 v

http://en.wikipedia.org/wiki/File:Tuberculosis_symptoms.svg
29. Vascular Disorders

http://5_autoimmune_vasculitis.php.htm
Disorder Onset Etiology Clinical Feat.
Buerger Disease chronic Segmental Intermitten claudicatio,Smoking
vascular
inflammation
Polyarteritis nodosa acute immune complex– Fever,Malaise,Fatigue,Anorexia,
induced disease weight loss,Myalgia,Arthralgia in
necrotizing large joints,polyneuropathy, cerebral
inflammatory lesions ischemia, rash, purpura, gangrene,
small and medium- Abdominal pain, does not involve the
sized arteries lungs

Vasculitis Acute/ Circulating a small vessel vasculitis,usually

hypersensitif chronic immune affect skin, but can also affect
complexesdrugsf joints, gastrointestinal tract, and the
ood,other kidneysitching, a burning
unknown cause sensation, or pain, purpura
Wegener chronic autoimmune tissue destruction of upper
granulomatosis respiratory tract (sinuses, nose,
ears, and trachea [the “windpipe”]),
the lungs, and the kidneys
Takayasu arteritis chronic unknown of systolic blood pressure difference
inflammatory (>10 mm Hg) between arms,
proscess pulselessness,bruit a.carotid
 http://www.wegenersgranulomatosis.net/5_autoimmune_vasculitis.php

BUERGER DISEASE
 IIB

Branches of the aortic arch

IIA

Abdominal aorta,
renal arteries, or
both
Ascending aorta,
aortic arch, and uvahealth.com
Type IIa region Thoracic
its branches
plus thoracic descending aorta,
descending abdominal aorta,
aorta renal arteries, or a
combination

intechopen.com http://www.ispub.com/journal/the-internet-journal-of-cardiology/volume-7-number-2/
BUERGER’S DISEASE (THROMBANGIITIS
OBLITERANS)

Exclusively associated with cigarette smoking

Occlusive lesions seen in muscular arteries, with a
predilection for tibial vessels

Presentation
 rest pain
 Gangrene
 Ulceration

Recurrent superficial thrombophlebitis (“phlebitis
migrans”)

Young adults, heavy smokers, no other atherosclerotic
risk factors

Angiography - diffuse occlusion of distal extremity
vessels

Progression - distal to proximal

Clinical remission with smoking cessation
30. MULTIPLE MIELOMA

Proliferation of malignant plasma cells
and a subsequent overabundance of
monoclonal paraprotein (M protein)

Sign & symptoms
 Haemathologicleukopenia, anemia, and
thrombocytopenia
 weakness
 The cells cause
 soft-tissue masses (plasmacytomas)
 lytic lesions in the skeleton

Complications
 bone pain
 Hypercalcemia
 renal failure
 spinal cord compression
 pathologic fracturesanemia
 Infection (often pneumococcal)

http://emedicine.medscape.com/article/204369
GUIDELINES FOR STANDARD INVESTIGATIVE
WORKUP PATIENTS

Complete blood count (CBC)
 anemia, thrombocytopenia, or leukopenia
 increased erythrocyte sedimentation rate (ESR)
 Rouleau formation

Serum and urine assessment f
 monoclonal protein
 Bence Jones protein

Serum-free light chain assay (in all patients with newly diagnosed plasma
cell dyscrasias)

Bone marrow aspiration and/or biopsy

Serum beta(2)-microglobulin, albumin, and lactate dehydrogenase
measurement

Standard metaphase cytogenetics

Fluorescent in situ hybridization

Skeletal survey (X-Rays)
 punched-out areas skull, vertebral column, ribs, pelvis
multiple, rounded, punched-

MRI
http://emedicine.medscape.com/article/204369
31. ABDOMINAL COLIC
Disorders Etiology Clinical
Nephrolithiasis Hypercalciuria, severe flank pain radiating to the groin,
groin gross
Urolithiasis infection, or microscopic hematuria, nausea, and
hyperuricemia vomiting. IVP could directly visualized stone
formation
Hepatolithiasis Bile Stasis, Calculi or concretions located proximal to the
infection confluence of the right and left hepatic ducts,
parasites,bacter RUQ Pain. Fever, Dx: USG, MRCP
y
Hepatic Amoeba right upper quadrant pain, fever and jaundice.
AbscesS Chronic infection Anorexia, malaise and weight loss.
Calsification Calsification rare,only in chronic condition
Cholelithiasis Bile stasis, Episodic abdominal pain (increases when
cholesterol consuming fat), pain resolves over 30 to 90
minutes.localizes the pain to the epigastrium
or right upper quadrant radiation to the right
scapular tip (Collins
sign).Dyspepsia,Gallstones on
cholecystography or ultrasound scan
4F: Female, Forty, Fertile, Fat. Dx:USG, MRCP
http://emedicine.medscape.com/
 Nephrolithiasis

Hepatolithiasis

Cholelithiais

http://www.downstatesurgery.org/files/cases/hepatolithiasis.pdf
 32. CONGENITAL MALFORMATION
Disorder Definition Radiologic Findings

Hirschprung Congenital Barium Enema: a transition zone that

aganglionic separates the small- to normal-diameter
megacolon aganglionic bowel from the dilated bowel
above
Intussusception A part of the Intussusception found in air or barium
intestine has enema
invaginated into
another section of
intestine
Duodenal Dueodenum Plain X-ray: Double Bubble sign
atresia
Anal Atresia birth defects in Knee chest position: to determined the
which the rectum is distance of rectum stump to the skin
malformed (anal dimple)

http://emedicine.medscape.com/
 Intussusception Hirschprung

Classifcation:

A low lesion
 colon remains close to the skin
 stenosis (narrowing) of the anus
 anus may be missing altogether,
with the rectum ending in a blind
pouch

A high lesion
 the colon is higher up in the pelvis
 fistula connecting the rectum and
the bladder, urethra or the vagina

A persistent cloaca
 rectum, vagina and urinary tract are
joined into a single channel

http://emedicine.medscape.com/ Learningradiology.om Duodenal atresia

 33.LABIOGNATOPALATOSHISIS

Celah pada bibir, gusi dan langitan

RULE OF TEN :
 Berat badan 10 lb (5 kg)
 Usia 10 minggu

 Kadar hemoglobin darah

10 g/dL

http://en.wikipedia.org/wiki/Cleft_lip_and_palate
http://www.scribd.com/doc/55885689/labio-gnato-palatoschisis
• Cleft palate
• the two plates of the skull that form the hard
palate (roof of the mouth) are not completely
joined
• The soft palate is in these cases cleft as well

• Cleft lip
• formed in the top of the lip
• a small gap or an indentation in the
lip (partial or incomplete cleft)
• continues into the nose (complete
cleft)
• due to the failure of fusion of the
maxillary and medial nasal processes
(formation of the primary palate)
 34.Gastroskisis vs Omphalocele

Gastroschisis
 Defect in the anterior abdominal wall through which the
abdominal contents freely protrude
 No overlying sac and the size of the defect is usually
less than 4 cm
 The abdominal wall defect the junction of the
umbilicus and normal skin
 Almost always to the right of the umbilicus
 The intestines can undergone inflammation, edema 
determines whether reduction of the extruded intestine
and closure of the abdominal wall can be accomplished
primarily or in stages

http://www.chop.edu/service/fetal-diagnosis-and-treatment/fetal-diagnoses/gastroschisis.html
Treatment: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1514688/

Pimary Closure
 The intestine is returned to the abdominal cavity and the
abdominal wall is closed during one procedure
 Depend on:
 degree of visceral abdominal disproportion
 Condition of the baby
 Complicationforce to primary closure
 Infection
 abdominal compartment syndrome
 respiratory compromise
 hemodynamic compromise of intra- organshypoxia
intra-abdominal organs
 Structural or functional damage to the bowel

Staged Closure
 staged approach to repair the defectaverage of five to 10 days
 a spring-loaded silastic (silicone plastic) pouch placed around
the herniated bowel
 The bowel is slowly and gently pushed back down
into the abdomen over the course of a few days
 Surgical facial repair
http://neoreviews.aappublications.org/content/7/8/e419.full
 TREATMENT

Semua kasus anak wajib
memperhatikan
 Jaga stabilitas air dan
elektrolit,
 asam basa
 dan suhu

http://neoreviews.aappublications.org/content/7/8/e419.full

Omphalocele
 type of abdominal wall defect intestines, liver, and
occasionally other organs remain outside of the
abdomen in a sac because of a defect in the
development of the muscles of the abdominal wall
 involves the umbilical cord

Treatment:
 Surgery must be delayed until the baby is stable if
the omphalocele sac is intact.
 Small omphaloceles  repaired immediately
 Larger omphaloceles  require gradual reduction
by enlarging the abdominal cavity to accommodate
the intestinal contents
http://en.wikipedia.org/wiki
35. THE BREAST LUMP
Tumors Onset Feature
Breast cancer 30-
30-menopause Invasive Ductal Carcinoma , Paget’s disease (Ca Insitu),
Peau d’orange , hard, Painful, not clear border,
infiltrative, discharge/blood, Retraction of the
nipple,Axillary mass
Fibroadenoma < 30 years They are solid, round, rubbery lumps that move freely in
mammae the breast when pushed upon and are usually painless.
Fibrocystic 20 to 40 years lumps in both breasts that increase in size and
mammae tenderness just prior to menstrual
bleeding.occasionally have nipple discharge
Mastitis 18-50 years Localized breast erythema, warmth, and pain. May be
lactating and may have recently missed feedings.fever.
Philloides 30-55 years intralobular stroma . “leaf-like”configuration.Firm,
Tumors smooth-sided, bumpy (not spiky). Breast skin over the
tumor may become reddish and warm to the touch.
Grow fast.
Duct Papilloma 45-50 years occurs mainly in large ducts, present with a serous or
bloody nipple discharge
PROGNOSIS
 Staging systems inc.TNM
 Tumour size and axillary node
status are important
parameters
 10-year survival rate for
lymph node neg disease is
80% vs 35% for tumours with
positive nodes
TREATMENT OPTIONS
 Surgery
 Mastectomy
 Breast conservation
 +/- Axillary dissection
 Radiation therapy (local
control)
 Chemotherapy (systemic
control)
 Hormonal Rx (systemic
control)
 http://emedicine.medscape.com/article/ http://en.wikipedia.org/wiki/

36. MALE GENITAL DISORDERS

Disorders Etiology Clinical
Testicular Intra/extra-vaginal Sudden onset of severe testicular pain followed by
torsion torsion inguinal and/or scrotal swelling. Gastrointestinal
upset with nausea and vomiting.
Hidrocele Congenital anomaly, accumulation of fluids around a testicle, swollen
blood blockage in testicle,Transillumination +
the spermatic cord
Inflammation or
injury

Varicocoele Vein insufficiency Scrotal pain or heaviness, swelling. Varicocele is

often described as feeling like a bag of worms
Hernia skrotalis persistent patency of Mass in scrotum when coughing or crying
the processus
vaginalis
Chriptorchimus Congenital anomaly Hypoplastic hemiscrotum, testis is found in other
area, hidden or palpated as a mass in
inguinal.Complication:esticular neoplasm,
subfertility,
subfertility, testicular torsion and inguinal hernia
 HERNIA SKROTALIS

http://www.medscape.org/viewarticle/420354_8
37. PHIMOSIS
Phimosis Paraphimosis

Inability to retract the
Entrapment of a
distal foreskin over the retracted foreskin
glans penis behind the coronal

Physiologic in newborn
sulcus

Emergency

Complications
 Superficial vein
 Balanitis obstruction  edema
 Postitis and pain  penile
 Balanopostitis glands necrosis

Treatment
Treatment
 Dexamethasone 0.1%  Manual reposition
(6 weeks) for  Dorsum incision
spontaneous retraction
38.
 TREATMENT

ABC’s with c-spine as
indicated

Needle Decompression of
Affected Side

High Flow oxygen including
BVM
• Air builds in pleural
space with no where
Treat for S/S of Shock
for the air to escape
Notify Hospital and ALS
unit as soon as possible
• collapse of lung on
If Open Pneumothorax and
affected side occlusive dressing present
• increased pressure BURP occlusive dressing
on mediastium,the
other lung, and
great vessels

http://www.trauma.org/index.php/main/article/199/
http://emedicine.medscape.com/article/424547

NEEDLE DECOMPRESSION

Locate 2-3 Intercostal space

midclavicular line

Cleanse area using aseptic
technique

Insert catheter ( 14g or larger)
at least 3” in length over the top
of the 3rd rib( nerve, artery, vein
lie along bottom of rib)

Remove Stylette and listen for
rush of air

Place Flutter valve over catheter

Reassess for Improvement
39. INHALATION INJURY

Anticipate respiratory problems:
 Head, Face, Neck or Chest burned
 Nasal or eyebrow hairs are singed
 Hoarseness, tachypnea, drooling present
 Loss of consciousness in burned area
 Nasal/Oral mucosa red or dry
 Soot in mouth or nose
 Coughing up black sputum
 In enclosed burning area (e.g. small apartment)
INHALATION INJURY

Supraglottic Injury • Subglottic Injury

 Susceptible to injury – Rare injury
from high – Injury to Lung
temperatures parenchyma
– Usually due to
 May result in superheated steam,
immediate edema of aspiration of scalding
pharynx and larynx liquid, or inhalation of
 Brassy cough toxic chemicals
 Stridor – May be immediate but
 Hoarseness usually delayed
 Carbonaceous sputum • Wheezing or Crackles
 Facial burns • Productive cough
• Bronchospasm
INHALATION INJURY

Other Considerations
 Toxicgas inhalation
 Smoke inhalation

 Carbon Monoxide poisoning

 Thiocyanate poisoning

 Thermal burns

 Chemical burns
INHALATION INJURY MANAGEMENT

Airway, Oxygenation and Ventilation
 Assess for airway edema early and often
 Consider early intubation,
intubation RSI
 When in doubt oxygenate and ventilate
 High flow oxygen
 Bronchodilators may be considered if
bronchospasm present
 Diuretics not appropriate for pulmonary edema

Circulation
 Treat for Shock (rare)
 IV Access
 LR/NS large bore, multiple IVs
 Titrate fluids to maintain systolic BP and perfusion
 Avoid MAST/PASG
INHALATION INJURY MANAGEMENT

Other Considerations
 Assess for other Burns and Injuries
 Treat burn soft tissue injury
 Treat associated inhalation injury/poisoning
 Cyanide poisoning antidote kit
 Positive pressure ventilation
 Hyperbaric chamber (carbon monoxide poisoning)

Transport considerations
 Burn Center
 Hyperbaric chamber
40. The Breast Lump
http://en.wikipedia.org/wiki/Burn

41. BURN INJURY

prick test (+)

To estimate scattered burns:
patient's palm surface = 1%
total body surface area
 42. Hypovolemic Shock

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1065003
/
 http://www.nlm.nih.gov/medlineplus/ency/article

43.BILIARY SYSTEM
Disorder Clinical Feature
Pancreatitis Chronic Abdominal pain, normal or mildly elevated pancreatic enzyme
levels, malabsorbsion (steatorrhea), diabetes mellitus (CHRONIC)
sudden in onset abdominal pain radiates the back, worse in supine
position,Profuse vomiting, fever(ACUTE)
(ACUTE)
Acute Acute right upper quadrant pain and tenderness, radiates to back or below
cholesistis the right shoulder blade,Fever and leukocytosis, Clay-colored stools,
jaundice, Nausea and vomiting,Palpable gallbladder/fullness of the RUQ
,Murphy sign
Cholelithiasis Episodic abdominal pain (increases when consuming fat), pain resolves
over 30 to 90 minutes.localizes the pain to the epigastrium or right upper
quadrant radiation to the right scapular tip (Collins
sign).Dyspepsia,Gallstones on cholecystography or ultrasound scan,4F.
Dx:USG, MRCP
Choledocholithiasis  at least one gallstone in the common bile duct
Pancreatic >50 years,abdominal
years pain, lower back pain,jaundice, Dark urine and clay-
Tumor colored stools,Fatigue and weakness, Painless Jaundice, palpable
gallbladder (ie,
ie, Courvoisier sign),
sign),Loss
),Loss of appetite and weight loss,Nausea
loss,
and vomiting, Trousseau sign, in which blood clots form spontaneously in
the portal blood vessels, the deep veins of the extremities, or the
superficial veins anywhere on the body, Diabetes mellitus, Tumor marker
http://www.top5plus5.com http://www.charlestongi.com/cms/images/conditions/pancreatitis.jpg
44. FLUID THERAPY
http://emedicine.medscape.com/article/120034

45. THYROID ENLARGEMENT (GOITER)

Abnormal enlargement of the thyroid gland
and can occur for a number of different
reasons
http://emedicine.medscape.com/article/120034

Toxic goiter
CLASSIFICATION

associated with hyperthyroidism

Examples:
 diffuse toxic goiter (Graves disease)
 toxic multinodular goiter
 toxic adenoma
Nontoxic goiter

Without hyperthyroidism or hypothyroidism

It may be diffuse or multinodular

Examples:
 goiter identified in early Graves disease
 endemic goiter
 chronic lymphocytic thyroiditis (Hashimoto disease)
Underactive (hypothyroid goiter)
 Disease Clinical Feature
Tiroiditis the inflammation of the thyroid gland,acute or
subacute, fatigue, malaise, and myalgia, Fever, pain
hyperthyroidismhypothyroidism

Adenoma folikuler most common, asymptomatic thyroid mass/nodule,

Toksik goiter
Struma Noduler non toksik
firm and nontender nodule,obstruction sign, no
thyroid disease symptoms
Lab: TSH N, fT4 N, T3 N
Thyrotoxic symptoms.
Lab: TSH ↓, fT4↑/N, T3↑
not associated with abnormal thyroid function.
Lab: TSH ↑/↓, Ft4 N, T3 N

http://emedicine.medscape.com/article
46.SALIVARY
46.SALIVARY ENLARGEMENT
Unilateral Salivary enlargement
• Salivary Gland Tumor
Parotid Tumor
• Bacterial Sialadenitis • Painless, asymptomatic
• Chronic Sialadenitis mass posterior cheek
• Sialolithiasis region.
Bilateral Salivary enlargement with
• Pain indicates perineural
hypofunction invasion
• Viral Sialadenitis • facial nerve weakness or paralysis
• Sjogren's Syndrome
• Human Immunodeficiency Virus
(HIV Infection or AIDS)
• Chronic granulomatous disease
• Sarcoidosis
• Tuberculosis
• Leprosy
Classification of parotid tumours:
1. Adenoma
A) Pleomorphic

Any age(>60years), no gender predilection 75% of all parotid tumours
B) Warthin's tumour

Over 60 years Male to female ratio is 4:1
2. Carcinomas

Acinic cell Carcinoma: Low grade malignancy
 Overall 5-year survival is 82%, and 10-year survival is 68%

Adenoid Cystic carcinoma
 may remain quiescent for a long time fatal due to perineural spread,
pulmonary metastasis
 Overall 5-year survival is 35%, and 10-year survival is approximately 20%

Malignant mixed tumors
 Overall 5-year survival is 56%, and 10-year survival is 31%

Adenocarcinoma and Squamous Cell Carcinoma
 Both have poor prognosis5 year survival is 25%

Mucoepidermoid carcinoma
 most common malignant tumor Low grade and high grade
47. URINARY TRACT STONE
melihat lokasi batu
besar batu
terjadi bendungan/ tidak
 48.WILMS’ TUMOR
• Survival

Epidemiology
– One of the real successes of
 Second most common modern medicine
pediatric solid • 1930s – 30% survival
abdominal tumor, most • 2010s – >90% survival
common renal – Multidisciplinary,
malignancy multimodality approach
 Ethnic variability – • Surgery is a critical component
AA>Caucasian>Asian • The role of the surgeon is
central
 Presents between age 1-
• The model for treatment of
5; most commonly age 3 Wilms tumor has become a
 66% before age 5 paradigm for successful cancer
therapy
 95% before age 10
– Research now focused on
reducing toxicity, i.e. the
amount of chemotherapy and
radiation neccessary
CLINICAL PRESENTATION

No tumor-specific symptoms
 1/3rdpatients may have anorexia, vomiting,
malaise

Painless abdominal massmost common

Physical Exam
 Smooth, palpable large abdominal mass
 Hematuria – 30%
 Associated congenital abnormalities – 25%

Renal ultrasonography the initial study

 49. NIPPLE DISCHARGE

1. Galactorrhea
2. Intraductal
papilloma
3. Duct ectasia
4. Carcinoma
THE BREAST
Tumors Onset Feature
Breast cancer 30-menopause Invasive Ductal Carcinoma , Paget’s disease (Ca Insitu),
Peau d’orange , hard, Painful, not clear border,
infiltrative, discharge/blood, Retraction of the
nipple,Axillary mass
Fibroadenoma < 30 years They are solid, round, rubbery lumps that move freely in
mammae the breast when pushed upon and are usually painless.
Fibrocystic 20 to 40 years lumps in both breasts that increase in size and
mammae tenderness just prior to menstrual
bleeding.occasionally have nipple discharge
Mastitis 18-50 years Localized breast erythema, warmth, and pain. May be
lactating and may have recently missed feedings.fever.
Philloides 30-55 years intralobular stroma . “leaf-like”configuration.Firm,
Tumors smooth-sided, bumpy (not spiky). Breast skin over the
tumor may become reddish and warm to the touch.
Grow fast.
Duct Papilloma 45-50 years occurs mainly in large ducts, present with a serous or
bloody nipple discharge
50. COLONIC CARCINOMA
Time Course Symptoms Findings
Early None None
Occult blood in stool
Mid Rectal bleeding Rectal mass
Change in bowel Blood in stool
habits
Late Fatigue Weight loss
Anemia Abdominal mass
Abdominal pain Bowel obstruction
PATHOGENESIS

Janne PA, Mayer RJ. N Engl J Med 2000;342:1960.

SITE DISTRIBUTION
STAGING OF COLORECTAL CANCER
 SCREENING FOR COLON CANCER SAVES
LIVES!!!
Mortality
Test Reduction
Fecal occult blood testing (FOBT ) 33%
33%
Flexible sigmoidoscopy 66%
(in portion of colon examined)

FOBT + flexible sigmoidoscopy 43%

(compared to sigmoidoscopy alone)

Colonoscopy ~76-
~76-90%
(after initial screening and polypectomy)
COLORECTAL CANCER SCREENING
FIRST ASSESS RISK

AVERAGE RISK INDIVIDUAL

All patients age 50 years and older, the
asymptomatic general population

HIGH RISK

Personal history – polyp or cancer

Family history – polyp or cancer in first
degree relatives
 DOUBLE-CONTRAST BARIUM ENEMA

Advantage
 Examines entire colon
 Relatively low cost

Disadvantge
 Never studied as a screening test
 Missed 50% of polyps > 1cm
in one study
 Detects 50-75% of cancers in those with
positive FOBT
 Interval between exams unknown

Winawer et al. Gastroenterology 1997; 112:599

Rex, Endoscopy 1995; 27:200
Lieberman et al. N Engl J Med 2000; 343:163
FLEXIBLE SIGMOIDOSCOPY

Pros
 May be done in office
 Inexpensive, cost-effective
 Reduces deaths from rectal cancer
 Easier bowel preparation, usually done without
sedation

Cons
 Detects only half of polyps
 Misses 40-50% of cancers located beyond the view
of the sigmoidoscope
 Often limited by discomfort, poor bowel preparation

Selby et al N Engl J Med 1992; 336:653 Stewart et al Aust NZ J Surg 1999; 69:2
Newcomb et al. JNCI 1992; 84:1572 Painter et al Endoscopy 1999; 3:269
Rex et al. Gastrointest Endosc 1999; 99:727
COLONOSCOPY

Advantage
 Examines entire colon
 Removal of polyps performed at time of exam
 Well-tolerated with sedation
 Easier bowel preparation, usually done without sedation

Disadvantage
 Expensive
 Risk of perforation, bleeding low but not negligible
 Requires high level of training to perform
 Miss rate of polyps < 1 cm ~25%, > 1 cm ~5%

Rex et al. Gastroenterology 1997; 112:24-8

Postic et al. Am J Gastroenterol 2002; 97:3182-5