Recognition of complications

Remote organ dysfunction typically supervenes early in the attack and justifies close ICU monitoring. Regular assessment of pulmonary gas exchange, acid-base status, fluid balance, central venous pressure determination, and, in selected cases, pulmonary artery catheterization, indirect calorimetry, and gastric tonometry, are valuable diagnostic and management tools which contribute to understanding of the pathophysiological mechanisms. Relevant biochemical work-up includes regular determinations of blood glucose, electrolytes, calcium, urea and creatinine, coagulation tests, hematocrit, and full blood count.

Local complications typically prevail after day 15, although severe arterial hemorrhage, intestinal or colonic perforation, or infection of pancreatic necrosis may occur earlier. Close monitoring of the regional inflammatory process and necrosis is mandatory throughout, particularly in those patients who are deteriorating or not responding to conservative management and in whom surgery or percutaneous drainage might be contemplated. Repeated abdominal CT scanning is preferable, particularly for diagnosis, accurate localization and follow-up (diameter, walls) of any acute pseudocyst, pseudoaneurysm formation, pancreatic hemorrhage, pancreatic necrosis, peripancreatic fluid collections, and, occasionally, fistulous tracts and portal, mesenteric, or splenic vein thrombosis.

Bacterial or fungal infection of devitalized areas inside and outside the pancreas is responsible for 80 per cent of deaths from severe acute pancreatitis. Early identification is crucial, since drainage and often surgical debridement are mandatory. The associated mortality is directly related to any delay in diagnosis and proper treatment. Persistent remote organ failure or unexpected clinical deterioration (epigastric pain, vomiting, abdominal distension with guarding or rebound) should raise the suspicion of regional infection and prompt appropriate investigation. Clinical and biochemical indicators of pancreatic infection include the combination of fever exceeding 38.5°C, base excess above 4 mmol/l, and hematocrit below 35 per cent. However, precise differentiation between inflammatory sterile and infected collections cannot be made reliably on clinical and laboratory grounds. Fever and leukocytosis are absent in 15 to 20 per cent with infected pancreatic necrosis or pancreatic abscess who may present with a disarmingly indolent course. Conversely, sterile necrosis may mimic abdominal sepsis. Serial CT evaluation is the best method for early definite diagnosis of infection, either by demonstrating extraintestinal gas in or outside the gland (15-20 per cent) or, more reliably, by enabling percutaneous fine-needle aspiration sampling of inflammatory collections with subsequent Gram staining and aerobic/anaerobic cultures. This technique is safe and accurate (> 90 per cent correct) for early recognition of regional infection. It enables a more timely and rational basis for percutaneous or operative interventions and for optimal antibiotic treatment, avoiding the excessive mortality rate associated with delayed recognition. Importantly, since bacterial contamination is heightened by necrosis, needle aspiration should be preferentially directed to all non-perfused areas as identified by intravenous contrast. Similarly, all potentially septic foci such as pseudocysts should be sampled. With a protracted course and initial sterile sampling, serial percutaneous aspiration should be performed. Preoperative CT is helpful in localizing infected collections and areas of necrosis to be removed by the surgeon.

Ultrasonography is useful for delineating the number, size, and location of acute pseudocysts, pancreatic ascites, and portal or splenic thrombosis. As with CT, it may guide fine-needle aspiration of suspected areas of infection.

Angiography should be the preoperative diagnostic step for ruptured pseudoaneurysm and subsequent severe hemorrhage. Other indications for angiography include identification of splenic vein thrombosis with subsequent variceal hemorrhage.

Elevated fluid amylase and protein levels are diagnostic clues of pancreatic fistula. ERCP or percutaneous pancreatic ductography under CT or ultrasound guidance further aid diagnosis and management.

The varying diagnostic modalities for the acute episode, the causal factor, and each stage of the attack are outlined in Tab!e.3.

Table 3 Diagnostic work-up for acute pancreatitis

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