TUBERCULOUS PLEURAL EFFUSION DISEASE

Created by:

Dessy Eva Dermawaty, S. Ked.

Gita Augesti, S. Ked.

PATIENT STATUS

PATIENT IDENTITY

• Initial Name : Mr. S• Sex : Male• Age : 42 years old• Nationality : Indonesia (Javanese)• Marital Status : Married• Religion : Islam• Occupation : Freelance Workers• Educational Background : Elementary School• Address : Kangkung

ANAMNESIS Taken from : Autoanamnesis Date : June 8th, 2015 Time : 16.15

Chief Complain : Dyspnea Additional Complaint : Productive cough, chills,

fever, decrease appetite, colic pain.

HISTORY OF THE PRESENT ILLNESS :

• Patient came to hospital and told that he has gotten a dyspneu since one week ago, and it was getting worse on the seventh day. Dyspneu felt worst when the patient was doing his activities and in lying position. Tightness will be reduced if the patient is in the down position or sitting position. Patient also felt difficulty to throw the greeny mucus when he was coughing up. The patient also felt colic pain, chills at night, fever, and decrease apppetite.

Patient felt dyspneu and productive cough since 3 weeks ago. He said that he has treated in a hospital 3 times. History of bleeded cough was denied. History of taking 6 months drug package was denied. History of family disease is hypertention in his father. History of Asthma was denied. He had been a smoker since 40 years ago (1packs/day). The patient works as a freelance worker and often affected by dust.

Family’s diseases History :Family’s Disease History is hypertention in his father.

Is there any family who suffer :Patient didn’t know

Weight Average weight (kg) : - kg Height (cm) : 165cm Present Weight : 80 kg (if the patient doesn’t know certainly)

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

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 HistoryFrequency/day : 3x/dayAmount/day : 1 place/eat (health)Variation/day : Rice, vegetables, fishAppetite : Decrease

Educational

(+) Elementary school (-) SMP (-) SMA (-)SMK (-) Course Academy

Problem

Financial : low

Works : -

Family : Bad Relation

Others : -

 

Body Check Up

General Check Up

Height : 165 cm

Weight : 80 kg

Blood Pressure : 120/80 mmHg

Pulse : 88x/minute

Temperature : 36,60C

Breath (Frequence&type) : 20x/minute Nutrition Condition : Fat, IMT 29,38 Consciousness : Compos Mentis Cyanotic : (-) General Edema : (-) The way of walk : Normal Mobility : Active The age predicyion based on check up : 42 years old

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

Skin

Color : Olive Keloid : (-) Pigmentasi : (-) Hair Growth : Normal Arteries : Touchable Touch temperature : Afrebris Humid/dry : Dry Sweat : Normal Turgor : Normal Icterus : Anicteric Fat Layers : Enough Efloresensi : (-) Edema : (-) Others : (-)

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

Head Face Expression : looked moderate illness Face Symmetric : Symmetric Hair : Black Temporal artery : Normal

Eye Exopthalmus : (-) Enopthalmus : (-) Palpebra : edema (-)/(-) Lens : Clear/Clear Conjunctiva : Anemis +/+ Visus : Normal Sklera : Anicteric

Ear Deafnes : (-) Foramen : (-) Membrane tymphani : normal Obstruction : (-) Serumen : (-) Bleeding : (-) Liquid : (-)

Mouth Lip : (-) Tonsil : (-) Palatal : Normal Halibsts : No Teeth : (-)

Trismus : (-) Farings : Unhiperemis Liquid Layers : (-) Tongue : Clean

Neck JVP : Normal Tiroid Gland : no enlargement Limfe Gland : no enlargement

Chest Shape : Simetric Artery : Normal Breast : Normal

Lung Inspection : Left : simetric, normal

Right: simetric, normal Palpation : Left : vocal fremitus decreased, pain

(-) Right : vocal fremitus normal,

pain (-) Percussion : Left : redup

Right: redup Auscultation : Left : vesicular decrease

Right: vesicular normal

Cor Inspection : Ictus cordis invisible. Palpation : Ictus Cordis feel in ICS V left

midclavicula Percussion : difficult to essess Auscultation : Heart Sound 1 & 2 Regular

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 : distended , Symetrics Palpation : Stomach Wall: undulation (-), pain (-)

Heart : Hepatomegali (-)

Limfe : Splenomegali (-)

Kidney : Ballotement (-) Percussion : Shifting Dullness (-) Auscultation : Intestine Sounds (+)

Movement Joint Arm Right Left Muscle Normal Normal Tones Normal Normal Mass Normal Normal Joint Normal Normal Movement Normal Normal Strength Normal Normal

Heel and Leg Wound/injury : not found Varices : (-) Muscle (tones&mass): Normal Joint : Normal Movement : Normal Strength/Power : Normal 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

Routine Blood Hb : 12,8 gr/dl Leukosit : 11.080/ mikroliter LED : 58 mm/jam Trombosit : 555.000 Diff. Count

Basofil : 0%Eosinofil : 0%Stem : 0%Segment : 77%Limfosit : 12%Monosit : 11%

Blood Chemistry Test. SGOT : 48 SGPT : 108 GDS : 113 Ureum : 26 mg/dl Creatinine : 1 mg/dl

BTA Test One Time : (-) Morning : (-) One Time : (-)

Pleural AnalysisMacroscopic.

Color : Yellow and cloudy

Microscopic. Cell count : >1000 cell/Ul Normal: 0-5 cell/Ul Glucose : 138 mg/dl Normal: 50-80

mg/dL Protein : 5,4gr/Ul PMN : 16% MN : 84% Rivalta Test: Positive PH :7,7

Anatomic Patology Test There is no malignancy detected, and the

morphology found was consistent with Tuberculous pathology anatomy

CHEST X-RAY

PULMO: HIPERLUSENT, INTERCOSTAL SPACE INCREASE, FLATTER DIAFRAGHM

RESUME

Patient came to hospital and told that he has gotten a dyspneu since one week ago, and it was getting worse on the seventh day. Dyspneu felt worst when the patient was doing his activities and in lying position. Tightness will be reduced if the patient is in the down position or sitting position. Patient also felt difficulty to throw the greeny mucus when he was coughing up. The patient also felt colic pain, chills at night, fever, and decrease apppetite.

Patient felt dyspneu and productive cough since 3 weeks ago. He said that he has treated in a hospital 3 times. History of bleeded cough was denied. History of taking 6 months drug package was denied. History of family disease is hypertention in his father. History of Asthma was denied. He had been a smoker since 40 years ago (1packs/day). The patient works as a freelance worker and often affected by dust.

 

Working DiagnoseTuberculous Pleural Effusion

Basic Diagnosea. Anamnesis

Recurrent cough with or without sputum greenist white. Dyspneu with smooth wet crackles Chills Sweat Fever Malaise

b. Physics Examination Vocal Fremitus decrease Dim percussion Smooth wet crackles.

Support Examination

Leucocyte increase : 11.080 SGOT and SGPT increase : 48 & 108 Chest X-Ray : : hiperlusent in left lung Pathology Anatomi test : Positif (+) Tuberculosa Rivalta Test : Positif (+)

Differential Diagnose Destroyed Lung Pneumonia Ca Paru Bronchitis Cor abnormality

Basic Differential Diagnose

Anamnesis Chronic Productive Cough Dyspneu with smooth wet crackles Chills Sweat Fever

Physics Examination Vocal Fremitus decrease Dim percussion Smooth wet crackles. Support Examination Leucocyte increase : 11.080 SGOT and SGPT increase : 48 & 108

Support Check Up

Check sputum smear (culture and resistance) Check smear of pleural fluid (culture and resistance) Re-check your blood sugar after correction Laboratory

Ureum Creatinin Electrolite GDS Lipid Profile Uric Acid Albumin

TREATMENT PLAN

(1) General Treatment Bed Rest Nutrition (high calory, high protein)(2) Special Treatment Non Medicamentosa

Stop Tobacco Avoid Tobacco Smoke Activity adjustment Go to doctor immedietly if appear any symptoms

Medicamentosa O2 3-4L/minute IVFD RL gtt XX/minute Rifampicin 600mg INH 300 mg Pirazinamide 1000mg Etambutol 1000mg Ceftriaxone inj 1 gram/12 hour Aminophilin 1 amp/ drip Salbutamol tab 0,5 mg / GGI / Cetirizine ½ / Metil

Prednisolon 2mg → 3 caps 1 Paracetamol 3 x 500 mg tab Ranitidine inj 1amp / 12 hour Mucogard 3xCII Metil Prednisolon 3 x 16mg Tapp off Curcuma 2x1

Prognose

Quo ad Vitam : Dubia ad bonam Quo ad Functonam : Dubia ad bonam Quo ad Sanationam : Dubia ad bonam

REFERENCE

Pleural Effusion et cause TuberculosaTuberculous pleural effusions occur in up to 30% of patients with tuberculosis. Tuberculosis (TB) is a major public health problem in developing countries. Although the majority of patients with TB have pulmonary TB, extrapulmonary TB affecting mainly the lymph nodes and pleura serves as the initial presentation in about 25% of adults. TB is the leading cause of pleural effusions in some countries. It is important to consider the possibility of tuber- culous pleuritis in all patients with an undiagnosed pleural effusion. A pleural effusion as an isolated manifestation of TB has been likened to a primary chancre as a manifestation of syphilis. Both are self-limited and of little immediate concern, but both may lead to serious disease many years later. Tuberculous pleuritis is thought to represent primarily a hypersensitivity reaction to tuberculous protein and the bacillary burden in the pleural space is low.

INCIDENCE

The percentage of patients with TB who have pleural effusions has varied markedly from county to country. In Burundi more than 25% of patient with TB have tuberculous pleural effusions while in South Africa 20% of TB patients have tuberculous pleural effusions. In contrast only 3–5% of patients in the USA are reported to have tuberculous pleural effusions.The lower percentage in the USA is probably in part due to under reporting of the disease in the USA because the pleural fluid cultures are frequently negative.

PATHOGENESIS

The current hypothesis for the pathogenesis of primary tuberculous pleural effusion is that a subpleural caseous focus in the lung ruptures into the pleural space 6–12 weeks after a primary infection. Mycobacterial antigens enter the pleural space and interact with T-cells previously sensitized to mycobacteria resulting in a delayed hypersensitivity reaction and the accumulation of fluid. It seems that this reaction of the pleura augments the entry of fluid into the pleural space by increasing the permeability of pleural capillaries to serum proteins, and thereby increasing the oncotic pressure in the pleural fluid.

Involvement of the lymphatic system probably also contributes to the accumulation of pleural fluid. An impaired clearance of proteins from the pleural space has been reported in human tuberculous effusions.

CLINICAL MANIFESTASION

TB was the third leading cause of large or massive pleural effusion (12%) after malignancy (55%) and pneumonia (22%).

The most frequent symptoms are cough (70%), which is usually non-productive and chest pain (70%), which is usually pleuritic in nature. If both cough and pleuritic pain are present, the pain usually precedes the cough.

Most patients are febrile but approximately 15% will be afebrile.

Patients with tuberculous pleural effusions may be dyspneic if the effusion is large.

On occasions the onset of tuberculous pleuritis is less acute with mild chest pain, at most a low grade fever, a non-productive cough, weight loss and easy fatigability.

The pleural effusions secondary to tuberculous pleuritis are usually unilateral and can be of any size.

PLEURAL FLUID CHARACTERISTICS

The pleural fluid with tuberculous pleuritis is invariably an exudate. Indeed, the pleural fluid protein level frequently exceeds 5 g/dL and this finding suggests tuberculous pleuritis.

The pleural fluid glucose level with tuberculous pleural effusions may be reduced but it usually is similar to the serum level.

The pleural fluid pH is usually above 7.30, but it also may be reduced.

DIAGNOSIS

Mycobacterial stain and culture

One test that is frequently overlooked in the diagnostic work-up of patients with an undiagnosed pleural effusion is examination of the sputum for mycobacteria. Conde and associated prospectively evaluated the diagnostic yield of mycobacterial smears and cultures in 84 patients with tuberculous pleuritis. They induced sputum in those unable to spontaneously expectorate. They reported that the sputum studies were positive in 44 of the 84 patients (52%). In 10 of the 44 patients, sputum smears were positive, whereas cultures were positive in all. The sputum was positive in 35 of 64 patients (55%) who had a normal chest radiograph except for the effusion and in whom the sputum was induced. Probably sputum examination is underutilized in the diagnosis of tuberculous pleuritis.

Adenosine deaminase

Testing for pleural fluid ADA levels is an easy and inexpensive method for establishing the diagnosis of TB pleuritis.

Sensitivity and specificity of ADA in the diagnosis of pleural TB were 92% and 90%, respectively.

The most widely accepted cut-off value for pleural fluid ADA is 40 U/L. The higher the level, the greater the chance of the patient having TB while the lower the level the lesser the chance of the patient having TB.

Pleural Biopsy

The most common way to make the diagnosis of tuberculous pleuritis over the past 50 years has been with a blind needle biopsy of the pleura.

TREATMENT

The treatment of tuberculous pleuritis has three goals:

to prevent the subsequent development of active TB,

to relieve the symptoms of the patient, and to prevent the development of a fibrothorax.

CHEMOTHERAPY

The recommendation for the treatment all of pulmonary and ekstrapulmonary TB are as follow.

The initial phase of a 6-month regimen should consist of a 2-month period of isoniazid (INH), rifampicin and pyrazinamide. Ethambutol should be included in the initial regimen until the results of drug susceptibility studies are available, unless there is little possibility of drug resistance.

The second phase of the treatment should be INH and rifampin given for 4 months. Directly observed therapy (DOT) is recommended. Nine-month regimens using INH and rifampicin are also effective when the organisms are fully susceptible to the drug.

With treatment, the patient’s symptoms and radiological abnormalities gradually abate. The typical patient becomes afebrile within 2 weeks, but temperature elevations may persist as long as 2 months.

The mean time for the complete resorption of pleural fluid is approximately 6 weeks, but it can be as long as 12 weeks.

CORTICOSTEROIDS

The role of corticosteroids in the treatment of tuber- culous pleurisy is controversial. In two controlled studies in which therapeutical thoracentesis was performed there were no benefits. In a third study in which no therapeutical thoracentesis was performed, the duration of fever and the time required for fluid resorption were decreased. The administration of corticosteroids did not decrease the degree of residual pleural thickening and 6 or 12 months after therapy was initiated in any of the three studies.

The recommended approach to the patient with tuberculous pleuritis is as follows. If the patient is more than mildly symptomatic, a therapeutical thoracentesis is recommended. If the patient continues to have severe systemic symptoms (fever, malaise, pleuritic chest pain) after the therapeutical thoracentesis, the administration of 80 mg of prednisone every other day until the acute symptoms have subsided is recommended. Thereafter the corticosteroids are rapidly tapered.

REFERENCE

Buku Ajar Ilmu Penyakit Dalam Jilid III Edisi V (2009)

Buku Interna Harrison Konsensus PDPI (Tuberculosis Pedoman

Diagnosis dan Penatalaksanaan di Indonesia 2003)

Yew, Wing.W, Migliori, Giovanni.B, Lange,C. 2010. Update on Tuberculous Effusion Pleura. Respirology J. 15 : 451–458.

H. Hamm and R.W. Light. 1997. Pleural tuberculosis. Eur Respir J, 10: 942–947.

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