Pancreatic encephalopathy

Abstract

SUMMARY A 58 year old woman presenting with abdominal distress and a neuropsychiatric disturbance with evidence of focal neurological deficit is described. A diagnosis of pancreatic encephalopathy was made, and the patient was treated accordingly with pancreatic anti-enzymes. A survey of the literature is presented.The syndrome of pancreatic encephalopathy was first described by Rothermich and von Haam in 1941and Vogel (1950, 1951a investigated the pathogenesis of this condition. A few cases have been published, but the pathophysiology of the disease has not been completely elucidated. Because of the high mortality and the therapeutic value of the anti-enzymes, early diagnosis and treatment are essential. CASE REPORTA 58 year old woman was admitted as an emergency case to the surgical department, complaining of severe abdominal pain, nausea, and constipation. The onset of pain was sudden, 12 hours before admission. It was localized to the upper abdomen, and accompanied by vomiting. From her previous history it emerged that she was suffering from latent diabetes. Thirteen years before admission she had undergone gynaecological surgery for a prolapse of the vaginal vault, and three years before admission she had undergone an appendicectomy.On physical examination there was tenderness to palpation in the periumbilical area but the abdomen was soft, and active peristaltic sounds were audible. No other physical signs were elicited. The day after admission the patient became confused and afterwards stopped talking entirely. Straight radiographs of the abdomen, as well as an electrocardiogram, were within normal limits.The haemoglobin level was 13-4 g/100 ml., a leucocyte count was 24,000/c.mm, plasma glucose was 95 mg/100 ml. and urea 43 mg/100 ml. Plasma sodium level was 134 m-equiv/l.; chlorides were 98 m-equiv/l. The CO2 combining power was 20 volumes; plasma potassium 4-8 m-equiv/l.; cholesterol 285 mg/100 ml. The thymol turbidity was 1 u.; transaminase 21 u.; alkaline phosphatase 1-7 Bodansky units. Plasma calcium was not estimated. The (Fig. 1).The patient's condition deteriorated into a state of akinetic mutism with incontinence of faeces and urine. Re-examination showed no progression of the slight right hemiparesis described above. However, tenderness of the skull on the left side, and a palmomental reflex on the right side had appeared. The aphasia remained unchanged.A left carotid angiogram revealed a considerable deviation of the anterior cerebral artery from left to 'Trasylol, Bayer.

Acute Pancreatitis in a Patient with Subarachnoid Hemorrhage: A Causal Link or a Mere Coincidence?

“…Absence of known etiological factors, suggest that AP might have occurred secondary to SAH, and deterioration in sensorium could have been additionally contributed by pancreatic encephalopathy which manifests in the early stage of AP. [7][8][9] Likely mechanisms of pancreatic injury in SAH include oxidative stress and SIRS. 10 After SAH, cardiopulmonary and renal complications get early attention, and gastrointestinal complications remain unnoticed.…”

Haemorrhagic shock and encephalopathy

“…This led to the hypothesis of trypsin activity in the vascular system and different organs as the pathogenetic mechanism. Pancreatitis, in which trypsin is also released from the pancreas, may indeed lead to a syndrome which resembles HSE in some aspects including the encephalopathy [7,8,11]. We have only very limited data on pancreatic enzymes in our patients: in Case 1 lipase and amylase were increased (440 and 91 U/1 respectively; normal values 40-240 U/1 and 20-77 U/l) and in Case 2 trypsin (1150ng/ml; normal value 140-400 ng/ml) and amylase (538 U/l) were markedly increased and al antitrypsin decreased (105 mg/dl; normal values 200-400 mg/dl).…”

Rare and Unusual … Or Are They? Less Commonly Diagnosed Encephalopathies Associated with Systemic Disease

“…[13][14][15][16][17][18] Less frequent manifestations include depressed mood, seizures, tremor, aphasia, hemiparesis, clonus, signs of meningeal irritation, frontal release signs, ataxia, nystagmus, akinetic mutism, and coma. [16][17][18][19][20][21][22][23] Pancreatic encephalopathy usually begins within 2 weeks of the presentation of acute pancreatitis, often between the second and fifth days. 14,15,21,22 Several patients will have the onset of their symptoms within the first 24 hours, with neurological manifestations evident from time of admission.…”