Pneumopericardium in a Patient with AIDS

Abstract

In 1997, a 53-year-old male smoker was admitted for progressive shortness of breath associated with a productive cough and yellowish sputum, pleuritic chest pain, and low-grade fever. There was no history of trauma. A posterior–anterior chest radiograph showed a diffuse infiltrate through the right lung field and an air space parallel to the lateral border of the heart. A computed tomographic scan of the chest confirmed pneumopericardium, with no associated pericardial effusion. It also showed a cavitary infiltrate in the anterior basal segment of the right lower lobe, but no definite neoplasm. Cultures of the sputum grew Staphylococcus aureus. The patient had positive antibodies to human immunodeficiency virus (HIV), hepatitis A, and hepatitis B. A bronchial biopsy from the right lower lobe showed well differentiated infiltrating squamous cell carcinoma with an acute inflammatory exudate. No bronchopericardial fistula was noted. After antibiotic treatment, a repeat chest radiograph showed resolution of pneumopericardium and improvement of the chest infiltrate. Repeat computed tomography of the chest showed that the pneumopericardium had resolved, but now revealed a large pericardial effusion. No bronchopericardial fistula could be demonstrated. Unfortunately, our patient refused further investigation.

Pneumopericardium is a rare disorder. In adults, pneumopericardium most commonly results from trauma. Although many other reports link pneumopericardium to an underlying disease process, our patient with HIV antibodies developed pneumopericardium despite having no history of trauma and no documentation of a communicating fistula. To our knowledge, there has been no previous report of pneumopericardium in association with acquired immunodeficiency syndrome. (Tex Heart Inst J 2002;29:51–3)

In 1997, a 53-year-old male smoker was admitted for progressive shortness of breath associated with a productive cough and yellowish sputum, pleuritic chest pain, and low-grade fever. There was no history of trauma. The patient was afebrile, in mild respiratory distress, with a respiratory rate of 24 breaths/min, a pulse of 98 beats/min, and a blood pressure of 120/80 mmHg. Chest examination showed bronchial breath sounds over the lower half of the right chest with scattered crackles bilaterally. There were E-to-A changes over the basal portion of the right lung. Cardiac examination revealed normal S₁ and S₂, and a systolic ejection murmur at the left sternal border.

The white-blood-cell count was 15.6 × 10⁹/L, with a lymphocyte profile of 0.949 × 10⁹/L total lymphocytes and 0.094 × 10⁹/L T-helper cells. The hematocrit level was 21%, blood urea nitrogen was 12 mg/dL, and creatinine was 1.3 mg/dL. The patient's erythrocyte sedimentation rate was 139 mm/hr and his lactic dehydrogenase level was 271 IU/L. Electrocardiography showed normal sinus rhythm with J-point elevation in the inferior leads.

A posterior–anterior chest radiograph (Fig. 1) showed a diffuse infiltrate through the right lung field, with areas of consolidation. There was an air space parallel to the lateral border of the heart, separating it from a curvilinear line that could have represented the reflected parietal pericardium. There was no evidence of hilar adenopathy. A lateral chest radiograph showed evidence of air surrounding the proximal aorta, a finding that could have indicated pneumomediastinum or possibly pneumopericardium (although air was not noted around the inferior surface of the heart). A computed tomographic (CT) scan of the chest (Fig. 2) did clarify this issue by confirming pneumopericardium, with no associated pericardial effusion. It also showed a cavitary infiltrate in the anterior basal segment of the right lower lobe, although no definite neoplasm was noted. The CT image, which shows shifting of the air, is not compatible with pneumomediastinum.

Fig. 1 Posterior–anterior chest radiograph shows curvilinear opacity (arrow) parallel to the left border of the heart. Note that the air within the pericardial sac does not completely outline the heart.

Fig. 2 Computed tomographic scan of the chest confirms pneumopericardium (arrow). Note the change in position of the pericardial gas, in comparison with its location on the chest radiograph. It migrates superiorly (away from the dependent position).

A Gram stain of the sputum revealed many white cells and a few gram-positive cocci in pairs; cultures grew Staphylococcus aureus. Serologic tests for Mycoplasma spp. and Legionella spp. were negative. The patient had positive antibodies to human immunodeficiency virus (HIV), hepatitis A, and hepatitis B, but not to hepatitis C. Acid-fast bacillus smears and cultures from sputum and bronchial brushings were negative. A bronchial biopsy from the right lower lobe showed well differentiated infiltrating squamous cell carcinoma with an acute inflammatory exudate. No bronchopericardial fistula was noted. Computed tomographic scans of the pelvis and abdomen were normal.

On day 4, the repeat chest radiograph in our patient showed resolution of pneumopericardium and improvement of the chest infiltrate after antibiotic treatment. Repeat CT of the chest (Fig. 3) showed that the pneumopericardium had resolved, but now revealed a large pericardial effusion. No bronchopericardial fistula could be demonstrated. Unfortunately, our patient did not consent to any further investigations and signed out against medical advice.

Fig. 3 Three days later, the pneumopericardium resolved, but was replaced by a much larger pericardial effusion (arrow), seen upon repeat computed tomography. No bronchopericardial fistula can be seen.

Discussion

Pneumopericardium, the presence of air in the pericardial space, is a rare disorder. In adults, pneumopericardium most commonly results from trauma (in approximately 60% of reports) or from an underlying disease process. In premature infants, it can be a complication of respiratory distress syndrome when that condition requires prolonged positive pressure ventilation. ¹ If the cause is chest trauma, the magnitude of the trauma must be great enough to cause pleuropericardial and bronchial tears. If the cause is an infectious disease, pneumopericardium can occur secondarily via fistulous communication with an infected contiguous organ, ² or primarily by infection with a gas-forming organism within the pericardium. ³ There have been isolated case reports of pneumopericardium in association with nonmalignant gastropericardial fistula as a late complication of surgical repair of hiatal hernia, ⁴ cytomegaloviral infection in a lung-transplant recipient, ⁵ invasive aspergilloma in patients on aggressive chemotherapeutic regimens, ⁶ bronchogenic ⁷ or esophageal ⁸ carcinoma that has perforated the pericardium, and the probable passage of air, in lung-transplant recipients, during dissection of the pulmonary veins. ⁹ Pneumopericardium may also be encountered in adults who have undergone various abdominothoracic procedures, such as colonoscopy. ¹⁰ In small children, pneumopericardium has occurred during attempted manual ventilation in the presence of a closed glottis; ¹¹ in very low birth-weight infants, it is associated with rising oxygenation indices and subsequent acute deterioration. ¹² Spontaneous pneumopericardium is even rarer.

Although many case reports link pneumopericardium to an underlying disease process, our patient with HIV antibodies developed an apparently spontaneous pneumopericardium, with no history of trauma and no documentation of a communicating fistula.

To our knowledge, there has been no previous report of pneumopericardium in association with HIV infection.