A note of caution for the doctor on duty: take the acute attack in chronic pancreatitis seriously!

Abstract

Dear Sir, Three different typical pain profiles have been described during the evolution of chronic pancreatitis: Repeated episodes of acute pancreatitis in the early stages. Spontaneous lasting pain relief in association with severe pancreatic insufficiency in the late stage of uncomplicated chronic pancreatitis. Persistent severe pain (or frequent recurrent episodes of pain), usually in association with local complications such as pseudocysts and ductal hypertension or extrapancreatic complications such as partial obstruction of the common bile duct, peptic ulcer and opiate addiction [1]. Pain has been attributed to increased intrapancreatic pressure, pancreatic ischaemia, pancreatic fibrosis leading to increased intraductal pressure in the chronically inflamed organ and to the presence of pancreatic pseudocysts causing compression of adjacent structures. Immunohistological reports have shown that the amount of neurotransmitters is increased in afferent pancreatic nerves, and a correlation between pain and immune cell infiltration of the nerves has been found (‘neurogenic inflammation’) [1]. Faced with the large number of publications concerning this fascinating theory, we felt that acute inflammation occurring at different stages of the disease has been rather neglected as a cause of pain. Therefore, we reviewed retrospectively the data of 21 patients (17 male, four female; age 48.2 ± 11.2 years, mean ± SD), who were admitted to our department from 2003 to 2006 with an acute attack of chronic pancreatitis. The diagnosis of chronic pancreatitis was made on the basis of abnormal morphology, i.e. pancreatic calcifications in all cases [2]. The aetiology of the disease was alcohol-related in 17 patients (16 male, one female) and unknown in four patients (one male, three female). All patients had their amylase and lipase levels measured on admission, with two exceptions, and all underwent contrast-enhanced computed tomography (CT), which is the gold standard for the differentiation between interstitial and necrotizing pancreatitis. The CT was performed within 96 h after admission and the findings were scored according to Balthazar et al. [3, 4]. None of our patients had acute respiratory and/or renal failure on admission (arterial pO2 < 60 mmHg; serum creatinine >2 mg dL−1 after rehydration). Only one (patient 14) required a stay on the intensive care unit. Mean hospital stay was 13.6 days (range 3–90 days). It is generally believed that the increase in pancreatic enzymes during an acute attack of chronic pancreatitis is low or even nonexistent, as the pancreas in this state is unable to release enough pancreatic enzymes into the bloodstream. Amylase and lipase were normal in 36% and 24%, respectively, of the attacks; however, they were increased to three times the upper limit of normal, which is generally considered to be diagnostic for acute pancreatitis, in 20% and 60% of the attacks. In all cases CT showed substantial changes: interstitial pancreatitis in 20 examinations (74%), necrotizing pancreatitis in seven (26%). However, interstitial pancreatitis was severe in 11 patients (Balthazar score E4), and usually one-third of such patients will already have organ failure (Table 1) [5]. Enzyme elevation and the CT findings were not significantly correlated (Mantel–Haenszel chi-square, 0.51 and 0.94). To our knowledge, this is the first conservative assessment of the severity of acute attacks of chronic pancreatitis. However, there are three surgical studies (two very old, one recent) which state that pancreatic necroses were found in 7–11% of patients who had undergone surgery for chronic pancreatitis [6–8]. These reports and our results support the necrosis–fibrosis sequence in the development of chronic pancreatitis [9]. Apart from the small contribution that this study makes to our understanding of acute attacks in chronic pancreatitis and their possible importance for the development of the disease, it also has some implications for the doctor on duty. First, similar to acute pancreatitis, the degree of enzyme elevation is not an indication of the severity of the disease [10]. Secondly, acute (necrotizing) pancreatitis is frequent in chronic pancreatitis patients hospitalized with acute pain on admission. Thus, the acute attack in chronic pancreatitis is not harmless. It should be taken seriously, ensuring that the guidelines laid down for acute pancreatitis are followed [11]. No conflict of interest was declared.