Exocrine and endocrine function of the pancreas was assessed in the early postoperative period (< or = 2 months) and subsequently (mean, 25 months; range, 3 to 120) in 103 patients (69 men, 34 women; mean age, 42.4 +/- 11.6 years) undergoing operation for chronic pancreatitis. Alcohol was the main causative agent (69%) and pain the most frequent indication (87%) for operation. Drainage procedures (n = 23) did not alter pancreatic function either initially or on long-term follow-up. In the early postoperative period, distal pancreatectomy (n = 42) often impaired endocrine function without affecting exocrine function; seven patients (17%) became diabetic, and results of oral glucose tolerance test showed deterioration in 23 of 28 patients (82%, p < 0.05). On subsequent follow-up, 11 patients developed exocrine failure (p < 0.01) and 10 patients endocrine (p < 0.01) failure. Proximal pancreatectomy (n = 38) precipitated clinical exocrine failure in 14 patients (37%, p < 0.01), yet pancreolauryl tests in 18 patients showed little objective change in exocrine status (0.50 > p > 0.10). Endocrine function was initially spared after proximal pancreatectomy, but six additional patients (16%, p < 0.05) required treatment for diabetes at a mean of 19 months (range, 3 to 34). Deterioration in pancreatic function is thus not an invariable immediate consequence of pancreatic drainage procedures or partial pancreatectomy for chronic pancreatitis. Progression of disease must account, in part, for failure of both exocrine and endocrine function on long-term follow-up. Drainage operations appear to delay this progressive decline in pancreatic function.

To assess the contribution of parenchymal hypertension to pain, pancreatic tissue pressures were measured intraoperatively in 17 patients with chronic pancreatitis and in four other patients undergoing pancreatic surgery (reference group). The technique involved direct fine needle cannulation of the pancreas using a flow infusion system, which measured parenchymal resistance to this infusion. Three to six recordings were obtained at each site. In chronic pancreatitis the pressure (mean +/- s.e.m.) was substantially elevated in all regions of the pancreas compared with reference subjects: head (257 +/- 59 versus 19 +/- 5 mmHg, P less than 0.05); body (201 +/- 51 versus 13 +/- 6 mmHg, P less than 0.05) and tail (161 +/- 45 versus 11 +/- 3 mmHg, P less than 0.05). Elevation was greater in areas of calcific disease (281-383 mmHg) than in non-calcific disease (81-120 mmHg, P less than 0.05). Mean pancreatic ductal pressure in 10 patients (seven with calcific disease) was 20 +/- 4 mmHg. Differential pressure measurements within the pancreas helped determine the extent of resection in six patients with diffuse disease. The greatly increased tissue pressures in chronic pancreatitis, especially in the presence of calcification, suggest a possible 'compartment syndrome'.

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A 32-year-old woman with a choledochal cyst (Todani type I) developed recurrent acute pancreatitis leading to calcific chronic pancreatitis. She had previously been treated with two cyst drainage procedures and subtotal cyst excision. This association between choledochal cyst and chronic pancreatitis has not been previously reported. Severe continuing symptoms led to pylorus-preserving proximal pancreatoduodenectomy, which was undertaken to prevent future carcinoma in the cyst remnant and progression of the chronic pancreatitis

Portal vein thrombosis is an unusual potential complication of liver resection. In our case it was due to ligation of the right branch of the portal vein during right hepatectomy in a patient without portal vein bifurcation. Hepatic angiography can delineate this abnormality and influence the choice of surgical management.