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TUBERCULOUS PLEURAL EFFUSION DISEASE
Created by:
Dessy Eva Dermawaty, S. Ked.
Gita Augesti, S. Ked.
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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
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ANAMNESIS Taken from : Autoanamnesis Date : June 8th, 2015 Time : 16.15
Chief Complain : Dyspnea Additional Complaint : Productive cough, chills,
fever, decrease appetite, colic pain.
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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.
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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.
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Family’s diseases History :Family’s Disease History is hypertention in his father.
Is there any family who suffer :Patient didn’t know
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Weight Average weight (kg) : - kg Height (cm) : 165cm Present Weight : 80 kg (if the patient doesn’t know certainly)
(-) steady(+) down(-) up
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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
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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
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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
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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 : (-)
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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
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Ear Deafnes : (-) Foramen : (-) Membrane tymphani : normal Obstruction : (-) Serumen : (-) Bleeding : (-) Liquid : (-)
Mouth Lip : (-) Tonsil : (-) Palatal : Normal Halibsts : No Teeth : (-)
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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
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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
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Cor Inspection : Ictus cordis invisible. Palpation : Ictus Cordis feel in ICS V left
midclavicula Percussion : difficult to essess Auscultation : Heart Sound 1 & 2 Regular
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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
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Stomach Inspection : distended , Symetrics Palpation : Stomach Wall: undulation (-), pain (-)
Heart : Hepatomegali (-)
Limfe : Splenomegali (-)
Kidney : Ballotement (-) Percussion : Shifting Dullness (-) Auscultation : Intestine Sounds (+)
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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 : (-)
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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
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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%
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Blood Chemistry Test. SGOT : 48 SGPT : 108 GDS : 113 Ureum : 26 mg/dl Creatinine : 1 mg/dl
BTA Test One Time : (-) Morning : (-) One Time : (-)
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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
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Anatomic Patology Test There is no malignancy detected, and the
morphology found was consistent with Tuberculous pathology anatomy
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CHEST X-RAY
PULMO: HIPERLUSENT, INTERCOSTAL SPACE INCREASE, FLATTER DIAFRAGHM
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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.
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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.
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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 (+)
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Differential Diagnose Destroyed Lung Pneumonia Ca Paru Bronchitis Cor abnormality
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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
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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
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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
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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
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Prognose
Quo ad Vitam : Dubia ad bonam Quo ad Functonam : Dubia ad bonam Quo ad Sanationam : Dubia ad bonam
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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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THANK YOUTHANK YOU:^):^)