Spontaneous pneumopericardium an unusual complication in a patient of HIV and pulmonary tuberculosis

Abstract

Pneumopericardium is defined as a collection of air or gas in the pericardial cavity. It is a rare entity and spontaneous pneumopericardium is even rarer. It is a rare complication of tuberculosis and human immunodeficiency virus and just three cases have been reported so far.

INTRODUCTION

Pneumopericardium is defined as a collection of air or gas in the pericardial cavity. Pneumopericardium most commonly results from trauma (in approximately 60% of the reports).[1] Other reported causes can be noniatrogenic or iatrogenic. It is a rare entity and spontaneous pneumopericardium is even rarer.[1] Development of spontaneous pneumopericardium is a very rare complication of tuberculosis with coexisting human immunodeficiency virus (HIV) infection.[1] To the best of our knowledge only three cases of pneumopericardium with pulmonary tuberculosis concomitant with HIV infection[1–3] have been reported so far.

CASE REPORT

A 30-year-old HIV-positive male smoker on antiretroviral therapy (ART) presented with complaints of cough with expectoration and fever for two and a half months. Cough was moderate in intensity and was present throughout the day with worsening at night. Expectoration was thick, whitish in color, and nonfoul smell. Patient had intermittent fever with an evening rise. There were associated complaints of decreased appetite and loss of weight. There was no history of dyspnea, chest pain, or vomiting. There was no history of trauma or preexisting respiratory or cardiac disease. There was no history of any procedure in the past.

Clinical examination of the patient showed stable vitals. Pulse rate was 102/min and was regular, synchronous, and good volume. BP was 110/70 mm of Hg and temperature was 99.2°F with a respiratory rate of 20/min. Oral sores were present. Chest examination revealed bilateral coarse crepitations in bilateral infra-clavicular and mammary areas. Cardiac examination was normal. There was no murmur and there were no signs of cardiac tamponade.

Routine laboratory investigations were within normal limits. Erythrocyte sedimentation rate (ESR) was 98 mm in first hour. Sputum examination was positive for acid fast bacilli (AFB). Electrocardiogram (ECG) showed normal sinus rhythm.

X-ray chest revealed patchy infiltration in bilateral upper zones. A thin hyper-lucent line was present lining the lateral cardiac borders suggesting possibility of pneumopericardium [Figure 1]. The air or gas in X-ray chest did not rise above the upper level of pericardium in standing erect position differentiating it from pneumothorax and pneumomediastinum. There was no evidence of cardiomegaly. Computed tomography (CT) scan of the chest confirmed the presence of pneumopericardium [Figure 2]. There was no peumomediastinum or pericardial effusion. It also showed a well-defined thick walled cavity with necrotic areas in apicoposterior segment of left upper lobe and bilateral infiltration with minimal bronchiectatic changes [Figure 3].

Figure 1.

X-ray chest PA view showing patchy infiltration in both the upper zones with pneumopericardium

Figure 2.

CT scan showing bilateral infiltration with pneumopericardium

Figure 3.

CT scan showing cavitary lesion on the left side with pneumopericardium

Barium swallow fluoroscopy ruled out any esophagopericardial fistula. The patient did not have any symptoms related to pneumopericardium and its detection was purely incidental. Patient was started on anti-tubercular treatment (ATT) as per the guidelines of revised national tuberculosis control program. Patient showed clinical improvement after 4 weeks of treatment. Repeat X-ray chest also showed resolution of pneumopericardium.

DISCUSSION

Pneumopericardium was first described by Bricheteau in 1844 who named bruit de Moulin (water wheel sound) associated with pneumopericardium.[4] Pneumopericardium occurs typically because of the breech of the pericardium by traumatic or nontraumatic causes. In adults, 60% of pneumopericardium results from trauma either sharp or blunt. Other causes attributed to pneumopericardium can be noniatrogenic or iatrogenic. Iatrogenic factors include thoracocentesis, thoracic surgery, endotracheal intubation, sternal bone marrow puncture, or positive pressure mechanical ventilation. Noniatrogenic causes can be underlying disease processes like infected fluid or gas producing organisms in the pericardial sac, fistulous communication between pericardium and other air containing structures such as bronchus,[3] esophagus, or stomach and amebic liver abscess. Other causes also include foreign body aspiration,[5] physical exertion,[6] parturition, severe cough, acute asthma,[7] cocaine inhalation, chlorine gas exposure, and forceful emesis.[4]

The possible mechanism of pneumopericardium in this case could either be a severe bout of cough or a fistulous communication of pericardium with an infected contiguous organ.[8] The rise in intra-alveolar pressure above atmospheric pressure due to increased bout of coughing may lead to rupture of alveoli and the released air moves to hilar area, mediastinum, and through pericardial reflections on the pulmonary vessels in the pericardial cavity.[4] The parietal pericardium is reflected on the visceral pericardium near ostia of the pulmonary veins, the weakest histological area.[5] Nectrotizing pulmonary process like tuberculosis in the setting of HIV could have resulted in the fistulous communication between the lung and pericardium leading to pneumopericardium in this patient.

Pneumopericardium may be symptomatic or asymptomatic depending upon the quantity of air in the pericardium. The patient with a small pneumopericardium may be asymptomatic and the cardiac examination may be normal. It may only be diagnosed incidentally on a chest radiograph and the gas usually does not rise above the upper limit of the pericardium in the erect position, which differentiates the pneumopericardium from pneumomediastinum[4] as in this patient. In large pneumopericardium the patient may be symptomatic and the note may be tympanic and heart sounds may be metallic. The commonest symptoms are dyspnea and precordial chest pain. Other symptoms if present are associated with the underlying etiology. Tension pneumopericardium leading to cardiac tamponade occasionally complicates pneumopericardium. This complication is thought to be caused by a ball valve mechanism preventing air from leaving the pericardial space.

Pneumopericardium unlike pneumothorax often does not require any specific treatment and is usually self-limiting as in the present case. The treatment of small or asymptomatic pneumopericardium is usually directed toward the underlying disease. Treatment is required in cases of large and symptomatic pneumopericardium or in patients of tension pneumopericardium, which can be a needle aspiration or tube decompression. Oxygen therapy in high concentrations as in management of pneumothorax can also be helpful in absorption of air.