Pleural effusions are often associated with acute pancreatitis. In one study, 3 to 17% of patients with acute pancreatitis acquire pleural effusions. Most effusions were left sided, although some were bilateral. Pleural fluid amylase concentration was increased up to 30 times over the simultaneous serum value and remained elevated even after the serum concentrations had returned to a normal level. Large pleural effusions were associated with subdiaphragmatic collections of fluid. The immobility of the diaphragm induced by local inflammation seems to be responsible in part for these pleural complications. Interestingly, in 25 patients with amylase-rich pleural effusions, 4 patients had evidence of either acute or chronic pancreatitis. In those patients, the pancreatic isoenzyme was dominant in the pleural fluid, while the salivary type predominated in the remaining 21 patients free of pancreatic disease.
A reduced Pa02 on hospital admission has been long regarded as a prognostic factor for the severity of acute pancreatitis. In 1973, Ranson et al reported that 58% of the patients hospitalized for acute pancreatitis had arterial hypoxemia within 48 h after admission. During this period, clinical signs were obvious in 5% and radiologic signs were seen in 8% of the patients. Arterial hypoxemia was not correlated with the severity of acute pancreatitis, serum amylase concentration, or fluid administration. In a subsequent study, 43% of the patients with acute pancreatitis were moderately hypoxemic on room air (Pa02 < 68 mm Hg).
In 1978, de Troyer et al reported that in 22 patients with uncomplicated acute pancreatitis (without clinical or radiologic evidence of pulmonary injury), the Pa02 was < 75 mm Hg in only 4 patients. However, most patients had a marked decreased in the vital capacity and FEV1. The functional residual capacity was normal and the total lung capacity was moderately decreased. By contrast, the pulmonary diffusing capacity for carbon monoxide was significantly reduced (78% of predicted values). Interestingly, an increase in lung vascular permeability to plasma proteins within 48 h after hospital admission (measured by the labeled transferrin technique) was present in the patients who later died (p < 0.01). The index remained within normal limits in the patients who survived. Although all patients with an abnormal index were hypoxemic, the Pa02 values did not reflect the extent of increased lung vascular permeability.