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Tuberculosis Induced Pericarditis 1.General Information A. Chief Complaint (CC) SOB, PND, DOE > ½ mile, 2 Pillow Orthopnea 2.History of Present Illness.

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Presentation on theme: "Tuberculosis Induced Pericarditis 1.General Information A. Chief Complaint (CC) SOB, PND, DOE > ½ mile, 2 Pillow Orthopnea 2.History of Present Illness."— Presentation transcript:

1 Tuberculosis Induced Pericarditis 1.General Information A. Chief Complaint (CC) SOB, PND, DOE > ½ mile, 2 Pillow Orthopnea 2.History of Present Illness (HPI) Mr. J C is a 49 yr old male that originally came from Rancho Los Amigos Hospital complaining of exacerbations of PND, DOE and SOB. He state that he was able before to walk over ½ mile without DOE. He also has identifiable lower extremity (LE) bilateral 1+ pitting edema. Mr. J C requires 2 pillows instead of one when lying down to sleep. He denies chest pain (CP) and nausea or other complaints.

2 3. Patients Family History Father (65 died)and Mother (died 58) both had a history of DM-2 and heart disease. The father, mother and sister had HTN. The sister stated by the patient had a heart problems. 4. Patients Family History + smoking 1-2 PPD, ETOH heavy drinker 6 pack of beer each day for 15 years, but quit 4 years ago. Lives currently with wife Hilda. Occupation was a construction worker, and is currently on disability 5. Drug History Lasix unknown dosage Clonidine“ Benazapril“ Felodipine“ Denies elite drug use and has now known drug allergies

3 6. Past Medical History (PMI) +PND 4 years, CHF, HTN, DM-2 X 10years, HCV, +PPD, Neuropathy, Nephropathy, BPH 7. Physical Exam (PE) 7/10/01 VS: T 98.7, P66, BP 189-158/121-88 GEN: Middle aged man overweight HEENT: EOMI, PERRL, NECK: supple no bruits, JVD RESP: CTA. COR: RRR, +2/6 systolic murmur no rubs no gallops ABD: +BS, NTND PULSES: 2+R/L Carotid Radial and Brachial EXT: 2+ pitting edema LL +1 edema LR legSKIN: NA NEURO: A&OX3

4 9. Abnormal or Pertinent Results of Initial Laboratory Tests

5 9. Abnormal or Pertinent Results of Initial Laboratory Tests Cont. Mr. J C has a known Chronic Pericardial Effusions who on Echo Cardiogram (ECG) on 7/13/01 showing positive pericardial effusions and right atrial and ventricular collapse in diastole. Repeat Echo on 7/13/01 showed circum-pericardial effusions with preserved left ventricular function. ECG on 7/10/01 showed normal sinus rhythm, with inferior infarct He was diagnosed with PPD + for tuberculosis with the date unknown at this time.

6 10.Patients Problem List and Work-up A.Pericardial Effusion a)Consult Cardiology for Pericardial Centisis B.Diabetes Mellitus 2 A.Monitor C.Hypertension (HTN) a)Decrease fluids and monitor in and out fluids (I/O) D.BPH a)Continue on Hytrin therapy and monitor PSA level E.Nephropathy a)Secondary to DM2 monitor 24 hour urine F.HCV a)Monitor Liver Function Tests (LFTs)

7 11. Patient’s Hospital Course A.Pericardial Effusion The patient on 7/25 was given an intervention biopsy in the form of a sub pericardial drain implant. The drain was to decrease the increase fluid on the pericardial sack and drain into the abdominal cavity. Thereupon the patient was put on TB medications (prophylactic dose of INH 300mg PO QD, Vit B6 25 mg PO QD) for 9 months. Also Lasix 40mg PO BID decreased to 20mg 7/16 Diabetes Mellitus 2 On admission PT has a blood glucose of 220-197 thereupon the level decrease the level to 95 mg/dl the PT was given insulin 70/30 5 U SQ QPM Hypertension (HTN) On admission the patient (PT) has a BP of 189-158/88-121 and the PT was put on 7/10 Lasix 40mg PO BID then 7/16 HCTZ 12.5 mg PO QD and on 7/30 BP 116/60 was appropriately reduced and signs and symptoms (DOE< SOB, and PND) and given at DC Baycol.3mg PO QHS, Benazapril 20mg PO Bid BPH Patient was given Hytrin 5 mg PO QD and at DC

8 Nephropathy Considered secondary to DM I/O were monitored and the original level of Scr 1.6 and increased to 1.9 on 7/13 but continued with the 20 range. BUN on 7/20 of 19 stayed within the 20 throughout the hospital stay HCV On admission the AST (61) continued to stay within the range. Alt at 33 stayed with the 30 range both high normal 12.Discharge Data Patient was discharged 7/30 from LACUSC on home with a follow-up of a TEE (Transesophogeal echocardiogram)

9 Epidemiology World TB Day, 24 March 2002 Centers for Disease Control (CDC) 2001 Worldwide approximately 3.8 million new cases of tuberculosis (90 % of them from developing countries). As of 1999 the US census rate of 5.8% and 2000 6.4% was reported to the CDC World Health Organization (WHO) 2000 Tuberculosis kills 2 million people each year. Between 2000 and 2020, nearly one billion people will be newly infected 200 million people will get sick, and 35 million will die from TB In terms of numbers of cases, the biggest burden of TB is in south-east Asia. Over 1.5 million TB cases per year occur in sub-Saharan Africa. This number is rising rapidly as a result of the HIV/AIDS epidemic. Nearly 3 million TB cases per year occur in south-east Asia. Over a quarter of a million TB cases per year occur in Eastern Europe..

10 Etiology  Tuberculosis is one of the oldest diseases known diseases and is been identified in Egyptian mummies.  The Greeks called the disease phthisis ("consumption"), emphasizing the dramatic aspect of general wasting with untreated cases.  Europe industrial revolution 17 th -18 th centuries,TB 20 percent of all deaths..  In the early 19 th century of the United States, 4 per 1000 population. Robert Koch's discovery of the tubercle in 1882. Mycobacteria, family Mycobacteriaceae, order Actinomycetales M bovis tuberculosis transmitted by unpasteurized milk M africanum M leprae M. tuberculosis rod-shaped, non-spore-forming, aerobic bacterium Acid fast organism due to the mycolic acids, long-chain cross-linked fatty acids.  Very low permeability of the cell wall most antibiotics  Purified protein derivative (PPD) tuberculin, a mixture of non-species- specific molecules in an extract from a culture filtrate.

11 Pathophysiology (TB induced Pericarditis) Mycobacterium tuberculosis Primarily is spread as a aerosolized airborne particle from an infected individual to a susceptible host’s lung. Initial manifestations is a dormant tuberculosis in a non-immunocompromised individual M tuberculosis grows slowly as a obligate aerobe/facultative intracellular mononuclear phagocytes parasite. Invades lymph nodes via hematogenous routes. Sanctuaries Typical infected sites are apices of the lungs, kidneys, bones, meninges, eye. Mycobacteria host immune reactions on sites of infection cause collateral damage Bacterial antigenicity due to cell wall parts glycoproteins, phospholipids

12 Etiology I.Tuberculosis is usually classified as either pulmonary or extra pulmonary 1.Prior to the onset of HIV into the human population 80% of all TB case were primarily lung in origin. 2.Today 2/3rds of of HIV infected AIDS patients may have both forms of TB Pulmonary and Extra pulmonary II.Pulmonary Tuberculosis 1.Primary or post primary(secondary) 1.Contracted of tubercle bacilli from high prevalence areas mostly seen in children. 2.Organism locates in middle to lower lung field forming tracheal lymphadenopathy which can heal spontaneously or form into a (Ghon lesion) a calcified nodule 3.Effusions in a majority of the cases resolve but tuberculosis emphysema may ensue in multibacillary necrosis and acute cavitations forming a primary TB and necrosis of the underling tissue 4.Enlarged lymph notes compress Bronchi and lung collapse 5.Bacilli that enter the blood stream form the pulmonary or lymph nodes dissimate into body organs and form glaucomatous lesions.

13 Secondary tuberculosis (adult type, reactivation, secondary TB) 1.Reactivation of latent infection and is usually localized to the apical and posterior segments of the upper lobes, III.Extra pulmonary Tuberculosis Pericardial Tuberculosis (Tuberculosis Pericarditis) Pleural Tuberculosis; Tuberculosis Of The Upper Airways, Lymph-Node Tuberculosis (Tuberculosis Lymphadenitis) Genitourinary Tuberculosis Skeletal Tuberculosis Gastrointestinal Tuberculosis Miliary Or Disseminated Tuberculosis Tuberculosis Meningitis And Tuberculoma HIV-Associated Tuberculosis

14 Diagnosis (TB) 1.Early in the course Nonspecific consisting mainly of weakness or fatigue, weight loss, no appetite, chills fever, sweating at night 2.Majority of cases, cough, initially nonproductive to purulent sputum. Blood streaking of the sputum Massive hemoptysis Pleuritic chest pain sometimes develops Dyspnea Physical findings are of limited use in pulmonary tuberculosis. Rales in inspiration, especially after coughing Rhonchi due to partial bronchial Systemic fever (often low-grade and intermittent),wasting In some cases, pallor and finger clubbing develop. mild anemia and leukocytosis

15 Diagnosis Pericardial Tuberculosis Due to direct progression of a primary focus within the pericardium Due to reactivation of a latent focus Rupture of an adjacent lymph node, pericardial tuberculosis has often been a disease of the elderly in countries with low tuberculosis prevalence but develops frequently in HIV-infected patients and into cardiac tamponade The effusion, detectable on chest radiography, is exudative in nature, with a high count of leukocytes(predominantly mononuclear cells). Hemorrhagic effusion is frequent. Culture of the fluid reveals M. tuberculosis in about 30 percent of cases, while biopsy has a higher yield. Without treatment, pericardial tuberculosis is usually fatal. Even with treatment, complications may develop, including chronic constrictive pericarditis with thickening of the pericardium, fibrosis, and sometimes calcification, which may be visible on a chest radiograph. A short course of glucocorticoids may prevent constriction.

16 Tuberculous Pericarditis (TBP) 1) TBP is responsible for 4% of acute pericarditis and 7% of tamponade in US Hospitals Calcific (chronic) pericardial constriction, occurring in 30% to 50% of cases. Pathology TBP originates from direct spread from pulmonary lesions or lymphoid spread, from hematogenous, mediastinal or peribronchial nodes There are four stages: Initially the inflamed dry or fibrinous, lacking bacilli with little fluid accumulation. 2) Post flammatory response of mononuclear infiltrate and necrotic tissue 3) Pericardial fluid increases (600 to 1500 ml) and a subsequent hemodynamic compromise. 4) Effusion resolves fibrous adhesions develop in between the pericardium and surrounding tissues adhesions become calcified constrict clinical constriction and radiographic calcification.

17 Treatment Drug Therapy (Both Pulmonary and Extra Pulmonary) Proper isolation in a negative-pressure room.. Health department notified of all cases of TB, contacts identified, compliance with therapy can be ensured by directly observed therapy (DOT) A.Chemotherapy. At least two drugs to which the organism is susceptible must be used because of the high frequency with which primary drug resistance to a single drug develops. INH (5 mg/kg; maximum, 300 mg PO qd), RIF (10 mg/kg; maximum, 600 mg PO qd), pyrazinamide (PZA, 15–30 mg/kg PO qd), and either ethambutol EMB, 15 mg/kg PO qd) or streptomycin (15 mg/kg; maximum, 1.5 g IM qd) If the isolate proves to be fully susceptible to INH and RIF, EMB (or streptomycin) can be dropped and INH, RIF, and PZA continued to finish 8 weeks, followed by 16 weeks of INH and RIF. After at least 2 weeks of daily therapy, the medications can be administered twice a week at adjusted doses.

18 When INH resistance is documented, the INH should be discontinued, and the remaining three drugs should be continued for the duration of therapy. Therapy should include at least three drugs to which the organism is susceptible. Careful documentation of bacteriologic sputum culture conversion is important, and therapy should be continued for at least 12 months and possibly as long as 24 months after cultures convert to negative. 3.Extrapulmonary disease in adults can be treated in the same manner as pulmonary disease, with 6- to 9-month short-course regimens. B.Monitoring. Patients with pulmonary TB whose sputum smears are positive before treatment should submit sputum for acid-fast bacilli smear and culture every 1–2 weeks until smears become negative. C. Adverse reaction monitoring. Baseline laboratory evaluation at the start of therapy that includes ASL,ALT, bili, CBC, SCr level. D.Glucocorticoid administration. In TB, the administration of glucocorticoids is controversial. Prednisone, 1 mg/kg PO qd initially, has been used in combination with antituberculous drugs for life-threatening complications such as meningitis and pericarditis.

19 III. Chemoprophylaxis. Untreated, approximately 5% of persons with latent TB infection (LTBI)develop active TB disease within 2 years of infection. An additional 5% will develop TB disease during their lifetime. A.Criteria for a positive TST are (1) 5-mm induration in patients with HIV infection or another defect in cell-mediated immunity, close contacts of a known case of TB, patients with chest radiographs typical for TB, and patients with organ transplantation or other immunosuppression (>15 mg/day prednisone for >1 month); (2) 10-mm induration in immigrants from high-prevalence areas (Asia, Africa, Latin America, Eastern Europe), prisoners, the homeless, parenteral drug abusers, nursing home residents, the medically underserved, low-income populations, patients with chronic medical illnesses, and those people having frequent contact with these groups (e.g., health care workers, prison guards); and (3) 15-mm induration in individuals who are not in a high-prevalence group). B.Prophylactic therapy (treatment for LTBI) should be administered only after active disease has been ruled out by a proper evaluation (chest radiography, sputum collection, or both). INH, 300 mg PO qd for 9 months,

20 Double blind randomised placebo controlled trial of adjunctive prednisolone in the treatment of effusive tuberculous pericarditis in HIV seropositive patients (HEART 1 August 2000) OBJECTIVE: Eeffect of adjunctive prednisolone on morbidity, mortality in HIV seropositive patients with effusive tuberculous pericarditis. DESIGN: Placebo controlled double blind randomised. SETTING: Harare, Zimbabwe medical schools PATIENTS: 58 HIV seropositive and tuberculous pericarditis positive patients aged 18–55 INTERVENTIONS: All patients received standard short course antituberculous chemotherapy and received prednisolone or placebo for six weeks. rifampicin, isoniazid, pyrazinamide, and ethambutol for two months, followed by rifampicin and isoniazid for a further four months in standard doses Prednisolone and placebo were made as identical “5 mg” tablets. The intervention consisted of prednisolone/placebo tablets starting at a dose of 60 mg (12 tablets) and tapering by 10 mg per week until completion at the end of the sixth week. MAIN OUTCOME MEASURES: Improved clinically, ECG, radiologic pericardial fluid resolution, and death. RESULTS: 29 patients were assigned to prednisolone and 29 to placebo. After 18 months of follow up there were five deaths in the prednisolone treated group and 10 deaths in the placebo group. Mortality was significantly lower in the prednisolone group, hepatomegaly, ascites.. However, there was no difference in the rate of radiologic and echocardiographic resolution of pericardial effusion. CONCLUSIONS: Adjunctive prednisolone for effusive tuberculous pericarditis produced a pronounced reduction in mortality. It is suggested prednisolone should be added to standard short course chemotherapy to treat HIV related effusive tuberculous pericarditis.

21 Controlled Clinical Trial of Complete Open Surgical Drainage and of Prednisolone in Treatment of Tuberculois Pericardial Effusion in Transkei (Lancet Oct 1988) OBJECTIVE:To compare of open surgical drainage of pericardial fluid compared with early and open percutaneous pericardiocentisis when required and the role of prednisolone compared to placebo. DESIGN: Double blind placebo controlled SETTING:South Africa Medical Centers PATIENTS: INTERVENTIONS. 240 patients with active TB pericardial effusions received a 4 drug antiTB regiment for 6 months followed for 24 months and given random surgical drainage of pericardial fluid, percutaneous pericardiocentisis and randomly given prednisolone or placebo for 11 weeks. MAIN OUTCOME MEASURES: End point was death of subjects RESULTS:During the 24 months, 3 % prednisolone and 14% of the placebo group died CONCLUSIONS: Cortical steroids increase the rate of clinical improvement in conjunction with TB medication and probably reduce the rate of death and the decision of a pericardectomy

22 Relevance of Adenosine Deaminase and Lysozyme Measurements in the Diagnosis of TB Pericarditis (General Cartiology 2000) OBJECTIVE: To assess the value of pericardial fluid Adenosine Deaminase (ADA) and Lysozyme (Lys)as a measure of TB Pericarditis DESIGN: Paired wise comparisons prospective study of three separate groups different pericarditis SETTING Single hospital Athens Greece PATIENTS: 41 Patients ranging from age 17-77 into three groups TBP, with neoplastic TBP, and Idiopathic TBP INTERVENTIONS: diagnostic MAIN OUTCOME MEASURES: ADA and Lys pericardial levels RESULTS:Ada levels >_ 72U/I and Lys >_ 6.5ug/dl were indicators of sensitivity of diagnostic TB pericarditis CONCLUSIONS: prognosis of outcome decreased with ADA level

23 Bibliography Catanzaro, AntoninoThe Role of Clinical Suspicion in Evaluating a New Diagnostic Test for Active Tuberculosis:Results of a Multicenter Prospective Trial JAMA Volume 283(5) 2 February 2000 pp 639-645 Constadina Aggeli Revenace of ADA and Lys Measurements in the Diagnosis of Tuberculosis Pericarditis Cardiology 2000; 94:81-85 Hakim, J G Double blind randomised placebo controlled trial of adjunctive prednisolone in the treatment of effusive tuberculous pericarditis in HIV seropositive patientsHEART Volume 84(2)1 August 2000 pp 183-188

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