OBSTRUCTION SYNDROME POSTTUBERCULOSIS

Created by
Andre Prasetyo Mahesya

1018011109

Perceptor:
dr. Dedy Zairus, Sp.P

CLINICAL WORK OF INTERNAL MEDICINE

SMF PULMONOLOGY
PERIOD DECEMBER 2014 TO MARCH 2015
ABDUL MOELOEK HOSPITAL
BANDAR LAMPUNG

PATIENT STATUS

PATIENT IDENTITY
Initial Name : Ms. E
Sex : Female
Age : 44 years old
Nationally : Indonesia (javanese)
Marital Status : married
Religion : Islam
Occupation : Unemployed
Educational Background : Senior High School
Address : Teluk Betung, Lampung

ANAMNESIS
Taken from: Autoanamnesis
Date
: December, 30st, 2014
Time
: 11.00

Chief Complain
: Out of breath since a week ago
Additional Complaint
: Cough with phlegm, since 1 weeks ago,
nausea; Emesis; loss
of wheight.
History of The Present Illness :
One weeks ago, patients felt cough with phlegm heavely in debt, and
become a shortness of breath 7 mounth later, the symptom is
intermitten. The pleghm was transparant, thick, and has no blood
appearance (-). She has approximately 10 times entered the hospital the
same complaints since last 7 mounts. Another sypmtoms are loss of
apetite and loss of wheight (from 40 kg to 34 kg). Patiens also often
nausea, vomiting, and frequent belching. Vomiting is not much, just like a
little fluid out of the stomach, the symptoms is felt afer teh patient eats.
She could have had tuberculosis treatment for 6 months and decleared by
doctors completed in 4 years ago. Patient deny have previous high blood
preassure, diabetes melitus, and asthma. But the Patient was ever

The History of Illness :

Small pox
(-)
(-) Chicken pox

(-) Malaria

(-) Kidney stone

(-) Disentri

Hernia
(-)

(-) Difthery

(-) Hepatitis

Prostat
(-)

(-) Pertusis

(-) TifusAbdomina

(-) Measles
(-) Influenza

lis
(-) Skirofula
(-) Siphilis

Melena
(-)
(-) Diabetic
Alergy
(-)

(-) Tonsilitis
Kholera

(-) Gonore

(-)
(-) Hipertension.
(-) Vaskular

(-)
Pneumonia

Tumor

(-) Duodeni Ulcer

Disease
(+) Tuberculosis

Familys diseases History :

Father still alive, Hipertension.
Mother still alive, Tuberculosis.
Seven siblings still alive, healthy.
Children are still alive, healthy.

Is there any family who suffer :

Her mother suffer with the same symptoms or
had been diagnose with tuberculosis.
Her father had been diganose with hipertensian.

(+)

+
+

(-)

Anestesi

(-)

Hard to bite

(-)

Parestesi

(-)

Ataksia

(-)

Weak muscle

(-)

Hipo/hiper-estesi

(-)

Afasia

(-)

Tick

(-)

Amnesis

(-)

Vertigo

(-) Others
(-)
Weight
(-) (kg)
Convultion : 40 kg
(-)
Average weight
Height (cm)
: 166 cm
Present Weight
: 34 kg

(-) steady
(+) down
(-) up

Disartri
Syncope

THE HISTORY OF LIFE

Birth place
(-) in home
(-) matrinity
(+) matrinity
hospital

Helped by:
(-) Traditional matrinity(+) Doctor (-) Nurse
(-)
Others

Imunitation History (Unknown)

(-) Hepatitis (-) BCG (-) Campak (-) DPT (-) Polio
Tetanus

Food History
Frequency/day : 3x/day
Amount/day
: 1 place/eat (health)

Educational
(-) SD (-) SMP (+) SMA (-)SMK(-) Course
Academy

Problem
Financial : low
Works: not working
Family : normal
Others : -

Body Check Up
General Check Up

Height : 166 cm
Weight : 34 kg
Blood Pressure : 110/70mmHg
Pulse : 80 x/minute, regular, tense and feeling enough
Temperature : 36.7 0C
Breath (Frequence&type) :28x/minute, regular, thorakoabdominal
Nutrition Condition : low
Consciousness : Compos Mentis
Cyanotic : (-)
General Edema : normal
The way of walk : normal
Mobility : Active
The age predicyion based on check up : 50 years old

Mentality Aspects
Behavior: Normal
Nature of Feeling : Sad
The thinking of process : Normal

Skin
Color : Brown
Keloid : (-)
Pigmentasi: (-)
Hair Growth : Normal, Black, Simetris
Arteries : Touchable
Touch temperature : Afrebris
Humid/dry : Dry
Sweat : Normal
Turgor : Normal
Icterus : An icterus
Fat Layers : Thin
Efloresensi : (-)
Edema : (-)
Others: (-)

Lymphatic Gland
Submandibula : no enlargement
Neck : no enlargement
Supraclavicula : no enlargement
Armpit: no enlargement

Head
Face Expression : Sad
Face Symmetric : Symmetric
Hair : Black
Temporal artery : Normal
Eye
Exopthalmus : (-)
Enopthalmus : (-)
Palpebra : edema (-)/(-)
Lens : Clear/Clear
Conjunctiva : Anemis -/ Visus : Normal
Sklera : Icteric -/-

Ear
Deafnes
: (-)
Foramen : (-)
Membrane tymphani
Obstruction : (-)
Serumen : (-)
Bleeding
: (-)
Liquid
: (-)
Mouth
Lip
:
Tonsil
: (-)
Palatal
:
Halibsts
:
Teeth
: (-)
Trismus
:
Farings
:
Liquid Layers :
Tongue
:

: intact

(-)
Normal
No
(-)
Unhiperemis
(-)
Normal

Lung
Inspection : Left : good breath, no lession
Right: breath left behind, no lession
Palpation : Left : vokal fremitus normal, pain (-)
Right: vokal fremitus decrease, pain (-)
Percussion : Left : resonance
Right: dim
Auscultation : Left : bronkial, wheezing (+), ronkhi (+)
Right: bronkial, wheezing (+), ronkhi (+), decreased breath
sounds
Cor
Inspection : Ictus cordis not visible
Palpation : Ictus Cordis no palpable
Percussion : top: difficult to determinate
Right: difficult to determinate
Left: difficult to determinate
Auscultation : Heart Sound 1 & 2 Regular, murmur (-), gallop (-).
The cor is on the right.

Artery
Temporalic artery : No aberration
Caritic artery : No aberration
Brachial artery : No aberration
Radial artery : No aberration
Femoral artery : No aberration
Poplitea artery : No aberration
Posterior tibialis artery : No aberration

Stomach
Inspection : flat
Palpation : Stomach Wall : undulation (-), pain (-)
Heart : Hepatomegali (-)
Limfe : Splenomegali (-)
Kidney : Ballotement (-)
Percussion : Shifting Dullness (-)
Auscultation : Intestine Sounds (+)

Genital (based on indication)
Male : no indication
Penis : no indication
Testis : no indication

Movement Joint
Arm
Right
Left
Muscle
Normal
Normal
Tones
(+)
(+)
Mass
(-)
(-)
Joint
Normal
Normal
Movement
Active
Active
Strength
5
5

Heel and Leg

Wound/injury
: not found
Varices
: (-)
Muscle (tones&mass)
: (+)/(-)
Joint
: Normal
Movement
: Active
Strength/Power
:5
Edema
: (-) (pitting edema)
Others
: (-)

Reflexs
Right

Left
Tendon Reflex
Normal
Normal
Bisep
Normal
Normal
Trisep
Normal
Normal
Pattela
Normal
Normal
Achiles
Normal
Normal
Cremaster
Normal
Normal
Skin Reflex
Normal
Normal
Patologic Reflex
Not Found
Not Found

Laboratory

Hematology (24-12-2014) Normal

Haemoglobin : 12.2 gr/dl 12-16 gr/dl
Leucocyte : 10.600 /ul 4500-10700 / ul
Variety count
Basophils : 0 % 0-1%
Eusinophils : 0 % 1-3%
Bands : 0 % 2-6%
Segmens : 60 % 50-70%
Lymphocytes : 25 % 20-40%
Monocytes : 15 % 2-8%
Trombocyte : 277.000 /ul 150.000-400.000/ul

Radiology
28-5-2014 AP chest radiograph: destroyed lung
dextra, atelektasis, deviasi trachea to the dextra,
cor pushed to the dextra + post TB

Radiology
24-12-2014 AP chest radiograph: destroyed lung
dextra, atelektasis, deviasi trachea to the dextra,
cor pushed to the dextra + post TB

Resume
Patient Ms. ER (44th), One weeks ago, patients felt cough with
phlegm heavely in debt, and become a shortness of breath
7 mounth later, the symptom is intermitten. The pleghm
was transparant, thick, and has no blood appearance (-).
She has approximately 10 times entered the hospital the
same complaints since last 7 mounts. Another sypmtoms
are loss of apetite and loss of wheight (from 40 kg to 34 kg).
Patiens also often nausea, vomiting, and frequent belching.
Vomiting is not much, just like a little fluid out of the
stomach, the symptoms is felt afer ter patient eats. She
could have had tuberculosis treatment for 6 months and
decleared by doctors completed in 4 years ago. Patient
deny have previous high blood preassure, diabetes melitus,
and asthma. But the Patient was ever smoker before illness.

Diagnose
Working Diagnose
Syndrome Obstructive Post Tuberculosis + destroyed lung dextra +
Gastroesofageal Refluks Disease
Basic Diagnose
Anamnesa: shortness of breath, cough with phlegm;
transparant, thick, blood appearance (-), loss of apetite and loss
of wheight (from 40 kg to 34 kg). Post treathment tuberculosis.
The sound of breath is not same, breath sound on the dextra is
decrease.
BTA (-) in hospital earlier
Vomiting is not much, just like a little fluid and felt after patient
eats.
PA chest radiograph: destroyed lung dextra.
Differential Diagnose
Effusion Pleura e.c. Pulmonary TB
Massa pulmo e.c. Carsinoma.

Support Check Up
Spirometri

Treatment Plan
(1) General Treatment
Bed Rest, half sitting.
Nutrition (high calory, high protein)
(2) Special Treatment

IVFD RL gtt 20X/minute

O2 3 liter
Aminophiline 24 mg/12 hours
Combivent 8,5ml/8hours nebulizer
Ambroxol syr 3x1 cth
Sulcarfat syr 3x1 cth
Omeprazole tab 2x1
Aminofluid kolf/day
Ciprofloxacin 2x1 amp

PROGNOSE
Quo ad Vitam
: Dubia ad malam
Quo ad Functonam : Dubia ad
malam
Quo ad Sanationam : Dubia ad
malam

LITERATURE REVIEW
Parenchymal lesions

Complicati
ons of
Pulmonary
Tuberculosi
s

Thin walled cavity (Open negative syndrome)

Aspergilloma
End stage lung destruction
Scar carcinoma
Airway Lesions
Tuberculous Laryngitis
Bronchiectasis
Tracheobronchial stenosis
Anthracofibrosis
Broncholithiasis
Vascular Lesions
Rasmussen aneurysm
Pleural Lesions
Dry pleurisy
Pleural effusion
Empyema & Bronchopleural fistula
Pneumothorax
General Complications
Cor-pulmonale
Secondary amyloidosis
Chronic respiratory failure

Destroyed Lung
Unilateral destruction of the lung due
to tuberculosis has been a
recognized entity.
Analyzed patients with unilateral
lung destruction and found
pulmonary tuberculosis as the cause
in 83.3% of patients.
It may occur after primary disease or
reinfection.

 Reduced lung volume,

cavities, bronchiectasis
and fibrosis are the
predominant findings in
destroyed lungs.
Fibrotic response
manifests as retraction of
the hilum and mediastinal
shift towards the fibrotic
lung.
Opposite lung will show
compensatory
hyperinflation.

Chest X-ray PA and HRCT Thorax showing destroyed lung on left side with compensatory
hyperinflation on the right side.

 Pulmonary arterial flow is reduced or

absent when there is bronchial
obstruction, stasis of secretions, or
parenchymal infection. Ligation of the
pulmonary artery of patients and
experimental animals with pulmonary
tuberculosis is reported to exacerbate the
disease, as does anastomosis of a major
systemic vessel to the pulmonary artery.

 In our patients angiography showed

pulmonary arterial flow to be absent,
bronchial arteries were prominent, and
there was radiological evidence of
systemic flow into the pulmonary arterial
tree.
It seems likely that these factors led to
lymph stasis and a raised oxygen tension,
favouring progression of the disease and
eventual lung destruction.

GASTROESOFAGEAL REFLUKS
DISEASE

Esophageal defense mechanisms

Esophageal clearance must be able to neutralize the
acid refluxed through the lower esophageal sphincter
Abnormal peristalsis can cause inefficient and
delayed acid clearance.
Dysfunction of the lower esophageal sphincter
transient relaxation of the LES (most common
mechanism), permanent LES relaxation, and
transient increase of intra-abdominal pressure that
overcomes the LES pressure.

Delayed gastric emptying

increased intragastric pressure and, ultimately, increased
pressure against the lower esophageal sphincter.
Hiatal hernia
The lower esophageal sphincter may migrate proximally into
the chest and lose its abdominal high-pressure zone (HPZ), or
the length of the HPZ may decrease.
Obesity as contributing factor
Increased intragastric pressure and gastroesophageal
pressure gradient, incompetence of the lower esophageal
sphincter (LES), and increased frequency of transient LES
relaxations may all play a role in the pathophysiology of GERD
in patients who are morbidly obese.

Sign and symtom

Typical esophageal symptoms include the following:
Heartburn
Regurgitation
Dysphagia
Abnormal reflux can cause atypical (extraesophageal)
symptoms, such as the following:
Coughing and/or wheezing
Hoarseness, sore throat
Otitis media
Noncardiac chest pain
Enamel erosion or other dental manifestations

Diagnose
Testing
The following studies are used to evaluate patients with suspected
gastroesophageal reflux disease:
Upper gastrointestinal endoscopy/esophagogastroduodenoscopy:
Mandatory
Esophageal manometry: Mandatory
Ambulatory 24-hour pH monitoring: Criterion standard in establishing
a diagnosis of gastroesophageal reflux disease
Imaging studies
Chest images may also demonstrate a large hiatal hernia, but small
hernias can be easily missed.
Currently, no role exists for computed tomography scanning,
magnetic resonance imaging, or ultrasonography in the routine
evaluation of patients with reflux disease.

Management
Nonpharmacotherapy
Lifestyle modifications used in the management of
gastroesophageal reflux disease include the following:
Losing weight (if overweight)
Avoiding alcohol, chocolate, citrus juice, and tomato-based
products
Avoiding peppermint, coffee, and possibly the onion family
Eating small, frequent meals rather than large meals
Waiting 3 hours after a meal to lie down
Refraining from ingesting food (except liquids) within 3 hours
of bedtime
Elevating the head of the bed 8 inches
Avoiding bending or stooping positions

Pharmacotherapy
The following medications are used in the
management of gastroesophageal reflux disease:
H2 receptor antagonists (eg, ranitidine,
cimetidine, famotidine, nizatidine)
Proton pump inhibitors (eg, omeprazole,
lansoprazole, rabeprazole, esomeprazole,
pantoprazole)
Prokinetic agents (eg, aluminum hydroxide)
Antacids (eg, aluminum hydroxide, magnesium
hydroxide)

 Surgical option
Transthoracic and transabdominal
fundoplications are performed for
gastroesophageal reflux disease,
including partial (anterior or
posterior) and circumferential wraps.
Open and laparoscopic techniques
may be used

REFERENCES
Gayathri D. Complications Of Pulmonary
Tuberculosis. Departement of Respiratory
Medicine M.S. Ramaiah Medical Collage.
India.
http://emedicine.medscape.com/article/1
76595-overview#a0104
view at 6 january 2015
Longo DL, Fauci AS, Kasper DL, Hauser SL,
Jameson JL, and Loscalzo J. 2012. Harrisons
Principles of Internal Medicine 18th Edition.
United States : McGraw-Hill eBooks.

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