Pancreatic encephalopathy (PE) is a syndrome of central nervous system damage complicated by acute pancreatitis, first proposed by Lowell in 1923, followed by Istvan in 1929 and Rotherich et al. in 1994 who reported 8 cases of abnormal mental status in patients with acute pancreatitis. PE is one of the more common complications of pancreatitis, and its occurrence is related to the clinical type of pancreatitis, and the incidence of PE in necrotizing pancreatitis is 7 times that of edematous pancreatitis. once PE is secondary to SAP, the prognosis is often poor and the death rate is high. 1, the pathogenesis of PE is not completely clear, but most authors believe that its pathogenesis is: ① the role of pancreatic enzymes: due to increased permeability of the blood-brain barrier in pancreatitis, escape to the blood of a large number of pancreatic enzymes (including trypsin, chymotrypsin, elastase, phospholipase A, vasoprotein, kinin, etc.) escape into the circulation, causing cerebral vascular lesions, venous stasis, followed by small hemorrhages Foci with cerebral softening soap and neuronal cell intoxication, edema, and metabolic disorders, resulting in various forms of psychoneurological symptoms. Most often seen in the acute reaction phase. Animal experiments have demonstrated that pancreatic enzymes can act on the central nervous system to cause demyelinating lesions; also similar foci were found in the brain tissue of patients who died of severe pancreatitis, so that pancreatic enzymes play a role in the development of PE. And one of them is phospholipase A (phospholipase A), especially phospholipase A2 is the most important: phospholipase A system is activated, which can cause multi-organ insufficiency and failure, and it can convert brain phospholipids and lecithin into hemolytic lecithin, and the latter has strong toxicity, which can destroy the phospholipid layer of cell membrane, affect cell permeability, and can break the blood-brain barrier into the brain circulation. It has strong neurophilic properties and acts directly on the phospholipid layer of brain cells, causing edema, hemorrhage, focal necrosis and demyelination of nerve cells in brain tissue, and also destroys tissue organelles, causing mitochondrial disintegration and structural changes in the nucleus and cell pulp, and destroys acetylcholine vesicles and inhibits the release of acetylcholine, thus affecting neuromuscular conduction, and hydrolyzes alveolar surface active It can affect neuromuscular transmission and hydrolyze alveolar surface active substances, which can damage the function of major organs. ②Severe infection poisoning: During the period of systemic infection and residual infection, the toxins of the pathogens act on the brain tissue due to secondary serious infections such as infectious shock, sepsis, and deep fungal infections, causing a series of neuropsychiatric symptoms similar to encephalitis. ③Alcoholism: acetaldehyde, a metabolite of ethanol, can act directly on the central nervous system or through the action of free catecholamines on sympathetic nerve endings or adrenal medulla, causing hypofunctioning of the central nervous system and a series of neuropsychiatric symptoms. ④Vitamin deficiency: prolonged fasting and insufficient exogenous supplementation lead to vitamin deficiency, which eventually affects brain cell metabolism and causes damage to brain tissue. It is customary to refer to encephalopathy due to VitB1 deficiency as Wernicke’s encephalopathy. ⑤ Other factors: severe water-electrolyte disturbances and hypoxemia can lead to impaired brain cell metabolism and edema, producing clinical manifestations of intracranial hypertension and brain herniation in severe cases. Studies on the autopsy of PE patients show that the histopathological examination of the brain reveals the presence of Lipolytic Demyelination, multiple small arteries and capillaries necrosis, hemorrhage, perivascular edema, reactive glial cell hyperplasia, and venous stasis. 2, clinical manifestations of PE typically manifest as mental abnormalities, audio-visual hallucinations, bizarre behavior, convulsive seizures, and even delirium or impaired consciousness. common symptoms of PE are unresponsiveness, disorientation, agitation, confusion, delirium, coma, depression, fear, delusions, hallucinations, transient confusion, language disorders, convulsions, ataxia, tremors, seizure-like epilepsy and focal neurological damage . Neurological examination reveals meningeal irritation, increased intracranial pressure, and encephalomyelopathy syndromes such as limb tonicity, muscle pain, and hyperreflexia or loss of reflexes. Patients presenting with coma suggest a poor prognosis and most of them die; most PE patients die from MSOF, and ARDS, respiratory failure, toxic encephalopathy, and renal failure are also common causes of death. Moreover, patients with severe pancreatitis often have ARDS, hepatic and renal insufficiency and failure, heart failure, etc., and the presence of PE on top of this increases the risk of death of patients. The EEG changes in PE patients are non-specific, mainly extensive slow waves, which return to normal after healing, and there may be changes in CT and MRI head examinations, especially the latter which mostly show periventricular and basal ganglia edema, small focal hemorrhage and demyelination, which are also non-specific changes. Cerebrospinal fluid examination may show a small number of lymphocytes, normal or mildly elevated protein, and normal sugar and chloride. 3, diagnosis and differentiation There is no uniform standard for the diagnosis of PE, according to clinical manifestations: those with a history of acute pancreatitis and typical psychoneurological disorders should be considered first. Symptoms in those with combined PE mostly appear 2 to 9 days after the onset of pancreatitis, and some occur 10 days after surgery. The symptoms last for 1-6 days, blood and urine amylase are higher than normal, and some patients have high blood glucose. CT and ultrasound can show the disease of the pancreas itself, which can help diagnose PE, while EEG, head CT and MRI can show abnormalities but are not specific, and cerebrospinal fluid tests play an auxiliary role in diagnosis. The treatment of PE focuses on The treatment of PE focuses on the active and effective treatment of pancreatitis. Some patients can improve with the remission of pancreatitis, especially to take appropriate therapeutic measures for the cause, such as the application of growth inhibitors such as enzyme-inhibiting preparations Sunnin and Stannin. In addition, the application of phospholipase A inhibitors such as gabex, etc. can play a role in eliminating the cause of PE, shortening the course of the disease and relieving mental symptoms. For patients with pancreatitis, timely treatment with anti-inflammatory drugs, nutritional support, gastrointestinal decompression, antacid, antitrypsin, correction of water-electrolyte disorders, anti-infection and surgical debridement and drainage, vitamin supplementation and other measures have a positive role in preventing the occurrence of PE and other complications. Secondly, measures are taken to treat neuropsychiatric symptoms: ① For severe psychiatric symptoms, Valium or suboxone can be given, and if necessary, chlorpromazine, procaine, colloidal glucose mixture intravenously and psychiatric drugs can be applied to eliminate symptoms and give the patient adequate rest. ②When there are signs of meningeal irritation or intracranial hypertension, dehydration therapy such as mannitol, hypertonic glucose, dexamethasone, albumin and other drugs can be taken to reduce intracranial pressure. (③Energetic synergists can help nerve cell function recovery, brain activator is effective in restoring consciousness and improving language function, and cytarabine can reduce the toxic reaction to the central nervous system. ④Conditioned units can use hyperbaric oxygen chamber treatment, which can rapidly improve the hypoxic state of brain cells. ⑤ Under the monitoring of serum insulin level, patients with lower than normal level can be treated with small doses of insulin, which can compensate for the decrease of insulin secretion caused by the massive destruction of pancreatic islet cells, and also promote the transfer of glucose to brain cells and enhance the utilization of glucose by brain cells to reduce the hypertonic state of blood caused by hyperglycemia. However, changes in blood glucose concentration should be dynamically observed during drug administration to avoid hyperglycemia and hypoglycemia from aggravating psychiatric symptoms. In addition, in the treatment of PE, appropriate application of magnesium preparations and some Chinese herbal formulas for draining the liver and Qi and clearing heat can also receive better results.