tuberculous pericarditis



Overview.

Tuberculous pericarditis is characterized by fibrinous and hemorrhagic pericarditis in the early stages, followed by pericardial effusion and subsequent pericardial hypertrophy, which may be converted to a subacute or chronic phase, and partially progresses to pericardial constriction. Early treatment of tuberculous pericarditis is of great importance to the prognosis, and once the diagnosis is clear, anti-tuberculosis treatment or surgical treatment is adopted. Tuberculous pericarditis occupies an important position in pericardial diseases in China, accounting for 21.3% to 35.8% of pericardial diseases. Active control of the prevalence of tuberculosis can significantly reduce the incidence of tuberculous pericarditis.

Etiology

Tuberculous pericarditis is usually caused by direct spread of tracheal, peribronchial and mediastinal lymphatic tuberculosis, or hematogenous dissemination of primary pulmonary tuberculosis or pleural tuberculosis infection, and rarely pericardial involvement is caused by hematogenous dissemination of distal urinary tuberculosis and bone tuberculosis. Tuberculous pericarditis is characterized by fibrinous and hemorrhagic pericarditis in the early stages, followed by pericardial effusion, followed by pericardial hypertrophy, which may be converted to a subacute or chronic phase, and partially develops into pericardial constriction.

Symptoms

Patients are mostly young, more common in males, with slow onset, mainly non-specific systemic symptoms, often fever, chest pain, palpitations, cough, dyspnea, loss of appetite, lethargy and night sweats. They often appear in the stage of pericardial effusion or advanced constrictive pericarditis. Chest pain is less severe than that of acute viral or nonspecific myocarditis, and cough and hemoptysis may be present if combined with tuberculosis.  

The main signs of tuberculous pericarditis are: tachycardia, heart enlargement, distant heart sounds, occasional pericardial friction, 40%-50% and pleural effusion, a large number of people may lead to cardiac tamponade, jugular venous aneurysm, peculiar veins, enlarged liver, sedentary respiration, and lower limb edema. When tuberculous pericarditis develops into chronic constrictive pericarditis, there are no symptoms such as fever, night sweats, etc., but the prominent manifestations are jugular vein raging, low blood pressure and pulse pressure, abdominal distension, abdominal effusion and edema.

Examination

1. Tuberculin test

Positive tuberculin test and the presence of tuberculosis foci in other parts of the body are helpful for diagnosis. 25% of patients have negative tuberculin test.  

2. Pericardial puncture fluid examination

Similar to the exudate of tuberculous pleurisy, there may be bloody pericardial effusion. Confirmation of the diagnosis depends on finding tubercle bacilli in the pericardial fluid, but the positive rate is low, with 20%-50% of cases having a positive culture for Mycobacterium tuberculosis. Adenosine deaminase ADA in pericardial fluid is significantly increased to help the diagnosis.  

3. Pericardial biopsy

Caseous granulation tissue can be seen. 

4. Other auxiliary examinations

(1) X-ray examination is very important for the determination of pericardial effusion. When the effusion is >300~500 ml, the shadow of the heart is enlarged into a pear shape or flask shape under fluoroscopy, the original arc shape disappears, and the heart beat is weakened or disappears. The shadow at the base of the heart widens and becomes spherical when supine. The aorta becomes smaller and the superior vena cava widens.

(2) Electrocardiography ①S-T segment elevation Early (hours to days), except for the S-T segment of aVR and V1, the S-T segment of other leads is elevated, which is obvious in V5 and V6, with the bowing back down, and then gradually decreases to return to the equipotential line. ② T-wave changes Early T-wave is upright, and when the S-T segment returns to the baseline, the T-wave is gradually flattened or inverted. After the inflammation subsides (within weeks to months), the T wave gradually returns to normal. If it becomes chronic, T-wave inversion may persist for a long time. (iii) The QRS wave is seen to be under-voltage. Sinus tachycardia. ⑤ A large amount of pericardial effusion may cause electrical alternation of P, QRS and T waves. And right bundle branch conduction block can be seen.  

(3) Echocardiography 15 milliliters of fluid can be detected.  

5. Isotope scan

Cardiac scanning with intravenous 131I-labeled clear protein or intravenous 99mTc, compared with cardiac shadows on radiographs, can determine the presence of effusion.

Diagnosis

Tuberculous pericarditis should be thought of first in any patient with unexplained fever and a large amount of pericardial effusion, especially bloody effusion. Tuberculous pericarditis may also occur during treatment for tuberculosis. The diagnosis can be established if antacid bacilli can be found in pericardial effusion or pericardial biopsy specimens in the early stages of the disease. It should be emphasized that a negative pericardial biopsy does not exclude tuberculous pericarditis; moreover, if antacid bacilli are not seen in granulomatous or caseous material, a firm diagnosis of tuberculous pericarditis cannot be made, since these substances may also be seen in chronic rheumatic or sarcoidal pericardial lesions. Surgical pericardial biopsy may be performed when necessary. In patients with acute pericarditis of unknown cause, laboratory tests should include a tuberculin skin test; a negative tuberculin skin test alone does not negate tuberculous pericarditis. Elevated adenosine deaminase activity in pericardial fluid (normal <45 U/L) is helpful in the diagnosis of tuberculous pericarditis.

Complications

Common complications of this disease include cardiac tamponade and cardiogenic cirrhosis.  

1. Cardiac tamponade

Tuberculous pericarditis has a large amount of pericardial exudate, but the rate of production is slow and usually does not cause acute hemodynamic complications. However, there may be signs and symptoms of chronic pericardial tamponade. 

2. Cardiogenic cirrhosis

Due to chronic pericardial constriction, the hypertrophied and rigid pericardium restricts ventricular filling, which increases the right ventricular diastolic pressure and right atrial pressure, obstructs hepatic venous return, dilates the intrahepatic blood sinusoids and stagnant blood, compresses the neighboring hepatocytes, and promotes hepatocyte atrophy and accelerates the proliferation of fibrous tissue. In addition, the permeability of hepatic sinusoids increases, the fluid with high protein infiltrates into the Disse cavity, and the edema of the paracentral hepatic sinusoids hinders the diffusion of nutrients from the plasma to the hepatocytes, which exacerbates the hepatic damage. Eventually, cardiogenic cirrhosis is formed.

Treatment

1. Anti-tuberculosis treatment

Triple antituberculosis chemotherapy: isoniazid, rifampicin and streptomycin or ethambutol, treatment for 9 months can achieve satisfactory results. If there is still pericardial exudation or recurrence of pericarditis in the course of anti-tuberculosis treatment, adrenocorticotropic hormone, such as prednisone (prednisone), can be added. It can reduce the number of pericardiocentesis and the mortality rate, but cannot reduce the occurrence of constrictive pericarditis.  

2. Surgical treatment

Pericardial constriction, cardiac tamponade, or exudative constrictive pericarditis are all indications for surgical removal of the pericardium, and should be pursued at an early stage.

Questions you may be concerned about

What to do for Tuberculous Pericarditis

Tuberculous pericarditis can be treated with medication and surgery.

1. Drug treatment: Tuberculous pericarditis is mostly caused by tuberculosis mycobacterium infection, and is usually treated with quadruple therapy, i.e. isoniazid, rifampicin, pyrazinamide and streptomycin, or ethambutol, etc., and most of the patients get better results after about 9 months to one year of treatment.

2. Surgical treatment: If the condition is more serious and presses the heart, it can be treated by pericardiocentesis and pericardiectomy. If left untreated, it may cause myocardial atrophy and can affect heart function.

Tuberculous pericarditis requires the use of medications under medical supervision. In addition to timely medical treatment, during the recovery period, it is necessary to go to the hospital for regular checkups, and eat a reasonable diet, which can include some vegetables and fruits that can replenish the nutrients needed by the body.

Prognosis

The prognosis of exudative pericarditis is better, especially if it is treated early. The prognosis of constrictive pericarditis is worse. Prompt surgical treatment can improve the prognosis and many patients can be cured. If surgery is performed too late, the myocardium is susceptible to severe damage and the outcome is poor.

Prevention

Aggressive control of the prevalence of tuberculosis can significantly reduce the incidence of tuberculous pericarditis.