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CASE REPORT
Year : 2022 | Volume
: 11
| Issue : 2 | Page : 54-56
Pyopericardium manifesting as cardiac tamponade: A rare presentation of a common disease
Parvathareddy Krishna Mala Konda Reddy, Praveen Nagula, Naga Venkata Raghava Balla, Syed Zia Hussain
Department of Cardiology, Osmania General Hospital, Hyderabad, Telangana, India
Correspondence Address:
Dr. Praveen Nagula
Department of Cardiology, Osmania General Hospital, Hyderabad - 500 012, Telangana
India
Source of Support: None, Conflict of Interest: None
DOI: 10.4103/rcm.rcm_6_22
Pyopericardium is a rare fatal pericardial disease. It manifesting as cardiac tamponade is rare and because of tuberculosis is extremely rare. We present the case of a 20-year-old female who presented with worsening dyspnea, low-grade fever, and weight loss. Echocardiography showed pericardial effusion with tamponade. After pericardiocentesis, the purulent aspirate on analysis confirmed the etiology as tuberculosis. The patient improved after the initiation of antituberculosis therapy and steroids.
Keywords: Antitubercular therapy, cardiac tamponade, pericardiocentesis, pyopericardium, tuberculosis
Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid in the pericardial space, resulting in reduced ventricular filling and subsequent hemodynamic compromise. It is a cardiac emergency requiring immediate intervention to relieve the compression of cardiac chambers.
Pyopericardium is a rare pericardial disease with a high mortality rate. Pyopericardium is usually secondary to pneumonia, empyema, thoracic surgery, and hematogenous spread of sepsis. The most common organisms attributed are Staphylococcus aureus, Klebsiella pneumoniae, Escherichia More Details coli, and Mycobacterium tuberculosis.
Case ReportA 20-year-old female presented with worsening dyspnea of 1-month duration. Before the onset of dyspnea, there was a history of low-grade intermittent fever with night sweats for 6 months. She had a weight loss of 10 kg over 6 months. There was a history of localized pain in the left lower limb and hip of 2-month duration.
On physical examination, she had a pulse rate of 122 beats/min. Her blood pressure was 90/60 mmHg over the right upper arm in the supine position. The oxygen saturation on room air was 86%. She was tachypneic (40/min). On cardiac examination, the jugular venous pulse was raised, and the heart sounds were muffled. The lungs were clear. Bedside echocardiography revealed large pericardial effusion in tamponade [Figure 1]a. An emergency pericardiocentesis stabilized the patient. Approximately 300 ml of thick pus was aspirated [Figure 1]b. The aspirated pus sample was sent for routine biochemical, pathological, and microbiological parameters along with adenosine deaminase (ADA) levels and cartridge-based nucleic acid amplification test (CBNAAT) for M. tuberculosis.
Figure 1: (a) Echocardiographic parasternal short axis view showing large pericardial effusion (red arrow) and both ventricles, D-shaped left ventricle is also seen. (b) The pus aspirated from the pericardial space, RV -right ventricle, LV - left ventricleThe laboratory evaluation of the pus sample showed low glucose (34 mg/dl), elevated proteins (7.8 g/dl). The ADA level was elevated (124U/L) and lactate dehydrogenase level was 3135U/L. The erythrocyte sedimentation rate was 100 mm/h. The CBNAAT for M. tuberculosis was positive. Imaging evidence of pulmonary tuberculosis was confirmed on computed tomography (CT) of the chest. The magnetic resonance imaging (MRI) of the spine showed lytic lesions in the vertebrae and paravertebral space, suggestive of Pott's spine. She was initiated on antitubercular therapy. She responded well to the treatment and is under regular follow-up.
DiscussionPurulent pericarditis (also known as pyopericardium) is diagnosed when pus is drained from the pericardium or bacteria are grown from the pericardial specimen. It accounts for <1% of total cases of pericarditis.[1] It usually presents with fever and chest pain. Hypotension and raised jugular venous pressure are usually present. The presence of pulsus paradoxus gives clues regarding the presence of tamponade.[2]
Although approximately one-third of cases of pericardial effusion secondary to tuberculosis is massive, only <3% of them present as pyopericardium.[3],[4] The usual mechanism of pericardial involvement is by retrograde lymphatic spread from the peritracheal, peribronchial, and mediastinal lymph nodes. Contiguous spread from pulmonary tuberculosis or by hematogenous spread from a distant primary tuberculosis infection is relatively uncommon.[5] In our case, the patient had disseminated tuberculosis involving the lungs, pericardium, and spine. Four pathological phases of tuberculous pericarditis (TBP) are shown in [Table 1].[6]
Due to the purulent nature of fluid and negative stain for the acid-fast bacilli (AFB), bacterial etiology was suspected, and the patient was started on high-end antibiotics after emergency pericardiocentesis. In Reuter et al., study of 233 cases with pericardial effusion, the presence of fever, night sweats, weight loss, and peripheral blood leukocyte count (<10 × 109/l) were independent predictors of TBP. A value of >40 u/l (ADA) in pericardial fluid has 87% sensitivity and 89% specificity.[7] In our case, the patient has all the above features as shown in the [Table 1], hence, pyopericardium secondary to disseminated tuberculosis was considered as a probable diagnosis.
Echocardiographic-guided pericardiocentesis is safe and effective. During the evaluation of pericardial disease, CT and MRI are better because of simultaneous visualization of mediastinal structures, better soft-tissue contrast when compared to echocardiography.[8] As the CBNAAT was positive for AFB, the patient was initiated on antitubercular therapy. Other supporting evidence in favor of AFB came from the CT chest which showed a tree in bud opacities in the upper lobes of the lung, and an MRI of the spine which showed lytic lesions in the spine confirming the diagnosis as Pott's spine.
The diagnostic yield of AFB from the smear and culture of pericardial fluid is variable. It varies from 53% with conventional culture method using Lowenstein‒Jensen medium, and up to 75% detection with double-strength liquid medium of Kirchner.[9] In our study, AFB staining was negative. A strongly positive tuberculin skin test as seen in our patient may increase the suspicion of TBP, but a negative test does not exclude this diagnosis.[7] The sensitivity and specificity of polymerase chain reaction, ADA (value of >38 IU/l) are 74% and 88%, 81%, and 90%, respectively, in diagnosing tuberculous effusions.[10] In our case, the patient had high ADA levels (124U/L) and positive CBNAAT for AFB.
Time-tested therapies for the prevention of constrictive pericarditis include the early use of corticosteroids, colchicine, and fibrinolytic therapy in a patient with effusion. Tapering the dose of the prednisolone over 6 weeks in patients with TBP without HIV infection is recommended (their use is avoided in HIV-infected individuals because of the increased risk of malignancy). We used corticosteroids for 2 weeks during the hospital stay and achieved an excellent therapeutic response with prompt pericardial drainage and anti-TB therapy.
ConclusionTimely judgment and diagnosis along with accurate microbiological analysis will determine the prognosis in pyopericardium. The case is reported for its rarity and fatal clinical outcome if the diagnosis is delayed.
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