Electrical alternans in a cardiac tamponade – the first sign of tuberculosis


Nicolae Dan Tesloianu , Andreea- Maria Ursaru, Anda Tesloianu


Pericarditis is a rare manifestation of tuberculous disease, occurring in approximately 1 to 2 percent of patients with extrapulmonary tuberculosis. Large pericardial effusions are uncommon, even fewer patients developing tamponade as the initial manifestation. Tuberculous pericardial effusion usually develops insidiously, presenting with nonspecific systemic symptoms, and is associated with immunosuppression, as in HIV infection, but extremely rare it can be the first manifestation of tuberculosis, as in the case of our patient.

pericarditis, tuberculosis, cardiac tamponade


Tuberculosis (TB) can involve any organ, lungs being the most common. Extrapulmonary tuberculosis (EPTB) is the term used to describe the occurrence of TB at body sites other than the lungs. It commonly involves lymph nodes, pleura, gastrointestinal tract, bone, central nerv-ous system, or genitourinary system. TB‐related peri-cardial disease is uncommon (<1% of EPTB), and the cases complicated by life‐threatening cardiac tamponade are extremely rare(1).

The total of TB cases in industrialized countries is constantly declining, pericardial tuberculosis being par-ticularly related to immunosuppression due to Human Immunodeficiency Virus (HIV)(2,3). We report a case of cardiac tamponade as first sign of tuberculosis (no TB history) in a mid-age patient without immunosuppres-sion factors.

Case report

A 43-year-old man without medical history was admit-ted for increased fatigue, fever and dry cough. As clinical features, the patient presented acute dyspnea with tachyp-nea, tachycardia, hypotension with reduced pulse pres-sure, jugular turgor, cardiac impulse difficult to palpate and muffled heart sounds. Laboratory studies showed currently inflammatory syndrome and mild iron defi-ciency anemia. Sinus tachycardia and QRS electrical alter-nans 2:1 were present on the electrocardiography (Figure 1). The chest radiograph revealed rounded appearance of the antero-posterior silhouette of the heart, mild bilateral pleural effusion, calcified lymph nodes and pleural fluid

within horizontal fissure (Figure 2a, Figure 2b). Transthoracic echocardiography showed: a large circum-ferential pericardial effusion, with early diastolic collapse of the right ventricle (Figure 3a); late diastolic collapse of the right atrium (Figure 3b) and “swinging heart” (Figure 3b, Figure 3c); distention of the inferior vena cava that didn’t diminish with inspiration (Figure 3d).

Emergency pericardiocentesis was needed, with drainage of 2.000 ml of hemorrhagic exudate, with intense monocytosis, adenosine deaminase (ADA) = 90 U/L, glucose 55 mg/dl, lactate dehydrogenase (LDH) = 120 mg/dl. The patient was redirected to the depart-ment of pneumology, where diagnostic thoracentesis evacuated 20 ml of haemoragic pleural effusion, exu-date, ADA=16 U/L, glucose 60 mg/dl, LDH 138 mg/dl. pH, lactate- and amylase-levels were in normal range in both pleural and pericardial liquid. The cytological exam for neoplasy was negative. Pleural biopsy was performed and the histopathological examination was highly sug-gestive for tuberculosis: pleural epithelioid cell granu-loma and Langhans giant cell (Figure 4).

It is worth mentioning that HIV test was negative and the patient remembers no TB contact in the last months.

Our patient had a favorable clinical outcome, without relapse under antituberculous therapy: the six-month course of therapy was completed uneventfully, with no evidence of the reconstitution of the inflammatory syn-drome. Corticotherapy was unnecessary. Ultrasound at the end of the 6 month-treatment demonstrated no residual pericardial or pleural effusion.





manTuberculosis presents with symptoms that vary with the anatomical site involved. The clinical manifestations of tuberculous pericarditis are various – chest pain, cough, dyspnea, fever, night sweats and fatigue may commonly arise. Patients may present subacutely with the development of constrictive pericarditis or, as described in our case, acutely, with signs of heart failure due to pericardial fluid accumulation leading to cardiac tamponade(4).

Tuberculosis can be a cause of acute pericarditis, but usually has more chronic symptoms. It can be accompa-nied by signs and symptoms of acute pericardial inflam-mation, but these patients are generally critically ill and other components of their illness typically dominate. However, in a tuberculous pericarditis, emergency man-agement and subsequent therapeutic interventions, mandatory in our case, are unusual(5).

Regarding the diagnosis of pericardial tuberculosis, the yield of Mycobacterium tuberculosis isolation from pericardial fluid is low. The probability of making a diagnosis is increased if both fluid and biopsy specimens are examined early in the effusive stage. Thus, there is a definite role for biopsy, the pericardial or pleural tissue revealing either granulomas or organisms in 80% to 90% of cases. Measurement of ADA, an enzyme produced by white blood cells, improves markedly the accuracy and speed of diagnosis, so that ADA higher than 40 units/ liter in the fluid has a sensitivity of approximately 88% and a specificity of approximately 83%(6). Increased interferon-gamma in pericardial fluid is an additional marker that, when combined with ADA, provides an even greater accuracy. Thus, measurement of ADA and interferon-gamma should be routine whenever tubercu-lous pericarditis is suspected or when there is no clue for diagnosis. PCR to detect Mycobacterium tuberculosis can be performed, but its usefulness is disappointing, with a sensitivity lower than 30%(7).

The short-term goal of therapy is to treat the symp-toms and tamponade, and the long-term goal is to pre-vent progression to constriction. Multidrug antimycobacterial treatment is mandatory: a 6-month therapy is the standard recommendation and has proved to greatly decreased mortality(8). However, effusions are likely to reaccumulate before the benefits of antimicro-bial therapy are obtained that is why the role of corti-costeroids is still debated(9). In our case the corticotherapy was unnecessary, considering the rapid response to the antituberculous therapy, with no reoccurrence of the pericardial fluid. Pericardiocentesis relieves tampon-ade, but open drainage and the establishment of a win-dow along with pericardial biopsy are recommended, especially when needed for diagnosis.

In our patient, due to the nonspecific nature of the presenting symptoms and physical findings, the initial high values of ADA in pericardial fluid and then the paradoxically low values in pleural fluid, the final diag-nosis was histological. However, the delays involved in making a diagnosis by culture were avoided and antitu-berculous drugs were early initiated. As a result, the patient had no recurrent pleural or pericardial effusion. Also, as a singularity of our patient, we would like to note the lack of the immunodeficiency status (tubercu-lous pericarditis being often a finding in HIV-infected individuals) and, of course, cardiac tamponade as being the clue that lead to the discovery of a TB disease.


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