Pediatric Radiology

The Hemodynamic Significance of Massive Pneumopericardium in Preterm Infants with Respiratory Distress Syndrome Clinical andExperimental Observations 1 Charles B. Higgins, M.D.,2 Thomas W. Broderick, M.D., David K. Edwards, M.D., and Alan Shumaker, M.D.

Radiographic and clinical data were evaluated in 12 preterm infants with pneumopericardium complicating ventilator therapy of respiratory distress syndrome. Eight infants had massive or tension pneumopericardium, reflected by bradycardia, hypotension, and cyanosis of abrupt onset; cardiac size decreased dramatically but returned to approximately the former size after aspiration of the pneumopericardium. In puppies, pneumopericardium large enough to reduce heart size by 32 ± 3 % caused decreased mean arterial pressure (-22 ± 7 % ) and right ventricular peak systolic pressure (-11 ± 2 % ) and increased right ventricular diastolic and intrapericardial pressures. These findings suggest that pneumopericardium per se causes severe hemodynamic compromise. When it is large enough to reduce heart size, drastic circulatory impairment is produced and pericardiocentesis should be performed immediately. INDEX TERMS:

Heart, tamponade. Pneumopericardium, 5[5].823 • Respiratory distress syndrome, 6[0].781

Radiology 133:363-368, November 1979

ALTHOUGH positive-pressure ventilation therapy (PPVT) has increased the survival rate among preterm infants with respiratory distress syndrome (RDS), treatment is frequently complicated by extra-alveolar air leaks, producing interstitial emphysema, pneumothorax, or pneumomediastinum (1-5). It is well recognized that tension pneumothorax and interstitial emphysema may cause hemodynamic compromise, sometimes lethal. A relatively rare consequence of ventilator-induced air leaks is pneumopericardium, which has generally resulted in a very low survival rate (6-10). The hemodynamic importance of a large pneumopericardium is often obscured by associated abnormalities such as other types of air leaks, pulmonary parenchymal disease, and patent ductus arteriosus. However, we have noticed that symptoms of severe circulatory compromise are usually accompanied by a perceptible decrease in the size of the cardiac silhouette, suggesting that the pneumopericardium impedes cardiac filling. In order to determine the hemodynamic effect of a large pneumopericardium per se, we assessed the hemodynamic changes induced by graded pneumopericardium in newborn infants and puppies.

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MATERIALS AND METHODS

Patient Studies

Radiographic and clinical data were analyzed in 12 consecutive preterm infants (10 boys and 2 girls) who

exhibited pneumopericardium during mechanical ventilation (either continuous positive airway pressure or positive end-expiratory pressure). The average gestational age was 29.5 weeks, the average weight 1,521 g (TABLE I). Radiographs were available before, during, and in some cases following the resolution of pneumopericardium. The cardiothoracic ratio was measured as a semiquantitative estimate of heart size. In order to minimize the influence of variations in the height of the diaphragm on serial chest radiographs, the thoracic diameter was measured at the inner aspect of the eighth ribs in the mid-axilla. Expiratory radiographs were excluded. The severity of RDS was graded during the first day of life according to the criteria set by Tudor et a/., with Grade I indicating mild radiographic changes of RDS; Grade II, moderate changes; Grade III, moderate to severe; and Grade IV, severe (11). Each patient's chart was reviewed to define clinically evident declines in blood gases, blood pressure, and heart rate at the time of pneumopericardium. Anima/ Studies

Five puppies weighing 1-2 kg were anesthetized with morphine sulfate (1.5 mg/kg) and a-chloralose (50 mg/kg). Using a small paraxyphoid incision and without entering the pleural spaces, a flared-tip catheter was placed in the pericardial sac and stabilized with a purse-string suture. Catheters were placed through the femoral artery and vein into the thoracic aorta and right ventricle, respectively.

1 From the Department of Radiology, University of California Medical Center, San Diego, Calif. Presented in part at the Sixty-fourth Scientific Assembly and Annual Meeting of the Radiological Society of North America, Chicago, 111., Nov. 26-Dec. 1, 1978. Revised version received June 26, 1979 and accepted July 10. 2 Recipient of USPHS Research Career Development Award Grant 1 K04 HL00201 from the National Heart and Lung Institute. sjh

363

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CHARLES B. HIGGINS AND OTHERS

TABLE I:

CASE

Underlying Disease

GestaBirth Weight tlonal (g) Age (wk.)

November 1979

CLINICAL DATA

Respirator Therapy

Associated Air Leaks

Outcome

Cause of Death

Massive Pneumopericardium I.

Respiratory distress syndrome (11)*

32

1,780

CPApt PEEP

II.

Respiratory distress syndrome (IV)

31

1,280

CPAP PEEP

2 22

None

Died on Day 7

Intracranial hemorrhage, necrotizing enterocolitis

III.

Respiratory distress syndrome (IV)

24

980

CPAP PEEP

2 22

Interstitial emphysema, tension pneumomediastinum

Died on Day 2

Hyaline membrane disease (IV)

IV.

Respiratory distress syndrome (I)

28

1,100

CPAP PEEP

2 24

Interstitial emphysema

Died on Day 3

Massive pneumopericardium

V.

Respiratory distress syndrome (II)

29

1,220

CPAP PEEP

2 28

Interstitial emphysema

Died on Day 2

Massive pneumopericardium

VI.

Respiratory distress syndrome (II)

28

1,200

CPAP PEEP

4 22

Interstitial emphysema, pneumothorax, pneumomediastium

Survived (pericardiocentesis)

VII.

Respiratory distress syndrome, patent ductus arteriosus (I)

33

1,800

CPAP PEEP

4 22

Interstitial emphysema, pneumothorax

Survived (pericardiocentesis)

VIII.

Respiratory distress syndrome (III)

36

3,850

CPAP PEEP

2 24

Pneumothorax

Pericardiocentesis on Day 2; died on Day 5

Intracranial hemorrhage, disseminated intravascular coagulation

IX.

Hyaline membrane disease (III)

28

1,050

CPAP PEEP

3 34

Interstitial emphysema, pneumothorax

Died on Day 7

Hyaline membrane disease (IV)

X.

Hyaline membrane disease (III)

28

1,300

CPAP PEEP

4 26

Interstitial emphysema, tension pneumomediastinum

Died on Day 2

Hyaline membrane disease (IV); tension interstitial emphysema

XI.

Hyaline membrane disease, patent ductus arteriosus (II)

28

1,077

CPAP PEEP

4 22

Interstitial emphysema

Died

Intracranial hemorrhage

XII.

Hyaline membrane disease, patent ductus arteriosus (III)

32

1,616

CPAP PEEP

4 24

Tension pneumothorax

Survived

4 26

Interstitial emphysema, pneumothorax, pneumomediastinum

Survived (pericardiocentesis)

mc~enmlPneumopericardwm

* See text for explanation of grading system. t CPAP = continuous airway pressure; PEEP = positive end-expiratory pressure. Units are mm Hg. Arterial, right ventricular, and intrapericardial pressures and heart rate were recorded continuously in the control period and after graded injections of air into the pericardial catheter (1O-ml increments, total 60 ml). At each stage of pneumopericardium, chest radiographs were obtained on Polaroid film. The cardiac area was determined by planimetry of the heart shadow on each radiograph. Changes in hemodynamic variables and heart size compared to

control values were tested for statistical significance using Student's paired

t-test. RESULTS

Clinical Observations Eight infants experienced cyanosis, hypotension, and

MASSIVE PNEUMOPERICARDIUM IN RESPIRATORY DISTRESS SYNDROME

Vol. 133

365

Pediatric Radiology

1a,b

Fig. 1.

a and b.

Chest radiographs taken before (a) and after (b) the development of pneumopericardium in an infant. Massive (tension) pneumopericardium is indicated by the drastic reduction in heart size.

2a ,b

Fig. 2.

a and b.

Chest radiographs taken before (a) and after (b) the development of pneumothorax and pneumopericardium . Pneumopericardium was frequently associated with other air leaks. A drastic reduction in heart size is again evident.

bradycardia of abrupt onset. During episodes of acute clinical deterioration , chest radiographs demonstrated a large amount of air distending the pericardium (massive pneumopericardium) and a small heart (Figs. 1 and 2). In each of these 8 infants, the cardiothoracic (CIT) ratio duringpneumopericardiummeasured less than 0.50. When expiratory films were excluded, the mean CIT ratio declined from 0.54 ± 0.01 (standard error of the mean) prior to pneumopericardium to 0.43 ± 0.02 during pneumopericardium; and in 5 infants the CIT ratio after peri cardiocentesis approximated the pre-pneumopericardium value (Fig. 3). Additional air leaks were radiographicall y evident in 7 of these 8 infants (TABLE I); interstitial emphysema was present in 6. Nevertheless, heart size varied with the onset and aspiration of the pneumopericardium. Four infants treated by pericardiocentesis survived the

acute episodes . In 3 of them , recurrent pneumopericardium prompted the percutaneous insertion of a catheter into the pericardial sac. One of these 4 infants eventually died of disseminated intravascular coagulation and intracranial hemorrhage (TABLE I). A small (incidental ) pneumopericardium developed in 4 other infants. Only one exper ienced an abrupt episode of cyanosis, hypotension, and bradycardia, and he died as a result of tension pneumothorax . Two others eventually died of causes other than massive air leaks , though air leaks were present. Chest radiographs showed a small amount of air in the pericardial sac and no reduction of the cardiac silhouette. Experimental Findings

Injection of 2':20 ml of air into the pericardial sac of

366

CHARLES

8. HIGGINS AND OTHERS

the mean arterial pressure by 22 ± 7 %, decreased the right ventricular peak systolic pressure (RVPSP)by 11 ± 2 %, and increased the right ventricular end-diastolic ·pressure (RVEDP) from 8 ± 1 to 13 ± 2 mm Hg. Additional increases in the pneumopericardium did not decrease the cardiac area further but did induce drastic increases in intrapericardial pressure, hypotension, and bradycardia (Figs. 4 and 5). An example of the reduction in heart size associated with severe hypotension is shown in Figure 6. After aspiration of air from the pericardial sac, all hemodynamic changes were immediately reversed. In two dogs, the bradycardia observed with a large pneumopericardium was reversed after cholinergic blockade.

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DISCUSSION

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Pneumopericardium in preterm infants with RDS has been associated with a mortality rate of >70% (7-10). This is understandable, since it generally develops in infants with severe lung disease, requiring rigorous positive-pressure ventilatory support. In most instances, additional pulmonary air leaks are present. Even in this complicated clinical setting, the onset of massive pneumopericardium in the current study and in previous reports (6-10, 12-16) has been associated with an abrupt and drastic decline in hemodynamic status, characterized by cyanosis, hypotension, and bradycardia. In the current study, pericardiocentesis produced dramatic clinical improvement in several instances, suggesting that the pneumopericardium per se was the major cause of the severe circulatory compromise. With massive pneumopericardium, there was invariably a marked reduction in heart size. After pericardiocentesis, it returned to approximately its former size. A similar phenomenon is illustrated in previous reports (6-10,

.30 __ _ _--J PRE PNEUMO· PNEUMO· POST PNEUMO· PERICARDIUM PERICARDIUM PERICARDIUM ,"--_~

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Fig. 3. Individual cardiothoracic ratios in the 8 infants with massive pneumopericardium. In each instance the ratio is larger on the pre-pneumopericardium chest radiograph compared to the later study. * = survivors; t = fatalities. One infant survived the pneumopericardium but died later of another cause (*t).

puppies resulted in a reduced cardiac area on chest radiographs (Fig. 4). Significant hemodynamic impairment occurred after the injection of 40 ml of air, which reduced the cardiac area by 32 ± 3 % (Figs. 4 and 5), decreased

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