Pathogenesis of pancreatic encephalopathy in severe acute pancreatitis

BACKGROUND: Pancreatic encephalopathy (PE) is a serious complication of severe acute pancreatitis (SAP). In recent years, more and more PE cases have been reported worldwide, and the onset PE in the early stage was regarded as a poor prognosis sign of SAP, but the pathogenesis of PE in SAP still has not been clarified in the past decade. The purpose of this review is to elucidate the possible pathogenesis of PE in SAP. DATA SOURCES: The English-language literature concerning PE in this review came from the Database of MEDLINE (period of 1991-2005), and the keywords of severe acute pancreatitis and pancreatic encephalopathy were used in the searching. RESULTS: Many factors were involved in the pathogenesis of PE in SAP. Pancreatin activation, excessive release of cytokines and oxygen free radicals, microcirculation abnormalities of hemodynamic disturbance, ET-1/NO ratio, hypoxemia, bacterial infection, water and electrolyte imbalance, and vitamin B1 deficiency participated in the development of PE in SAP. CONCLUSIONS: The pathogenesis of PE in SAP has not yet been fully understood. The development of PE in SAP may be a multi-factor process. To find out the possible inducing factor is essential to the clinical management of PE in SAP.

Pancreatic encephalopathy and Wernicke encephalopathy in association with acute pancreatitis: A clinical study

AIM： To investigate clinical characteristics and therapy of pancreatic encephalopathy （PE） and Wernicke encephalopathy （WE）. METHODS： In a retrospective study of 596 patients with acute pancreatitis （AP）, patients with PE were compared to those with WE in regards to history, clinical manifestation, diagnosis, treatment and outcome. RESULTS： There were 93 patients with severe acute pancreatitis （SAP）. Encephalopathies were discovered in 10 patients （1.7%）. Six patients with PE all developed in SAP （6.5%）, and three of them died （3% of SAP, 50% of PE）. Four patients with WE developed in AP （0.7%）, and two of them died （0.3% of AP, 50% of WE）. Two patients with WE were treated with parenteral thiamine and survived. Global confusions were seen in all patients with encephalopathy. Ocular abnormalities were found. Conjugate gaze palsies were seen in 1 of 6 （16.7%） patients with PE. Of 4 patients with WE, one （25%） had conjugate gaze palsies, two （50%） had horizontal nystagmus, three （75%） had diplopia, and one （25%） had myosis. Ataxia was not seen in all patients. None of patients with WE presented with the classic clinical triad. CSF examinations for 2 patients with WE showed lightlyincreased proteins and glucose. CT and MRI of the brain had no evidence of characteristic abnormalities. CONCLUSION： PE occurs in early or reiteration stage of SAP, and WE in restoration stage of SAP/AP. Ocular abnormalities are the hallmarks of WE, and horizontal nystagmus is common. It is difficult to diagnose earlier an encephalopathy as PE or WE, as well as differentiate one from the other. Long fasting, hyperemesis and total enteral nutrition （TPN） without thiamine are main causes of thiamine deficiency in the course of pancreatitis.