Alterations in coagulation factors have been reported during acute pancreatitis. Therefore the relationship of coagulation measurements to complications of pancreatitis was evaluated prospectively in 35 patients in whom 130 serial coagulation profiles were performed, consisting of fibrinogen, platelet count (PC), fibrinogen-fibrin-related-antigen (FR-antigen), prothrombin time (PT), partial thromboplastin time, thrombin time, euglobulin clot lysis, and Factors II, V and VII-X levels. During attacks of acute pancreatitis, over-all mean initial fibrinogen and PC of 268 mg. per 100 ml. and 214,000 per cubic millimiter rose significantly (p less than 0.005) to peaks of 362 mg. per 100 ml. and 477,800 per cubic millimeter by day 6 to 10. Mean initial FR-antigen of 4.8 microgram per milliliter rose to peak 7.4 microgram per milliliter on day 5. In 21 patients with mild pancreatitis, mean highest fibrinogen, PC, FR-antigen, and PT were 329 mg. per 100 ml., 361,500 per cubic millimeter, 5.3 microng per milliliter and 14.1 seconds. These values were significantly higher (p less than 0.05 to 0.01) in patients with severe pancreatitis, being 422 mg. per 100 ml. 528,000 per cubic millimeter, 13.7 microng per milliliter, and 15.5 seconds, respectively. Evaluation of the relationship of coagulation measurements to early clinical features showd that mean initial fibrinogen levels were significantly higher (p less than 0.05 to 0.01) in patients with initial amylase greater than 1,000 Somogyi units percent, serum glutamic oxaloacetic transaminase (SGOT) greater than 250 S.F.U. percent, and initial 72 hour PAO2 less than 75 mm. Hg. Early hypoxemia also correlated (p less than 0.05) with elevated initial FR-antigen levels. Impaired early renal function correlated (p less than 0.01) with elevated initial PC only. Early hypocalcemia did not correlate with coagulation measurements. These findings demonstrate that marked changes in coagulation parameters occur during acute pancreatitis and are related to over-all morbidity. Correlation of early coagulation measurements with amylase levels and with respiratory, renal, and hepatic dysfunction suggests that enzyme-related intravascular coagulation may be implicated in the pathogenesis of these complications of pancreatitis.

Acute Disease↗

PubMed1976

Relationship of sodium, intravascular coagulation, and respiratory distress.

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Animals↗

PubMed1976

Pulmonary capillary permeability - a transfusion lesion.

Massive transfusion of bank blood has been implicated as a major etiologic factor in the evolution of pulmonary insufficiency after injury. In spite of the demonstration of significant debris, including aggregates, in stored blood, a precise and reproducible pulmonary effect of transfusion has not previously been demonstrated. Since clinical pulmonary insufficiency is frequently accompanied by increased lung water, these experiments were designed to measure pulmonary capillary permeability and its response to transfusion of blood and blood components in rats. These experiments demonstrate that: 1) the rat lung is a target organ with regard to blood transfusion; 2) the lung lesion with transfusion is attributable, at least in part, to a selective and acute increase in pulmonary capillary permeability; 3) pulmonary capillary permeability is highly responsive to viable platelets; 4) prolonged storage of blood in polyvinyl chloride containers may enhance its ability to induce pulmonary capillary permeability; 5) increased capillary permeability with transfusion is largely eliminated when platelets and buffy coat are eliminated.

Animals↗

PubMed1975