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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Critically ill patients with severe pancreatobiliary disease exhibit multiple nutritional alterations compounded by the stress response. Acute pancreatitis may present as a life-threatening illness; patients are likely to be hypermetabolic and may have hyperglycemia and hypocalcemia. Nutritional support from parenteral or enteral feeding will probably be required in patients presenting with three or more positive risk factors as determined by Ranson criteria. Nutritional therapies for liver disease vary according to the specific disorder manifested. Patients with fulminant hepatic failure need to be monitored for profound hypoglycemia. Encephalopathy may develop in patients with acute-on-chronic liver disease, necessitating a protein restriction. Patients undergoing liver transplant are a perioperative challenge due to the combination of preoperative malnutrition, an extensive surgical procedure, and postoperative stress. Such patients require individualized assessment and management.
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PMID:Nutritional support for the patient with pancreatobiliary disease. 844 1

Pancreatic encephalopathy is a severe complication of acute pancreatitis. Proinflammatory cytokines may play a role in the development of multi-organ failure during pancreatitis. In the present study, we measured the changes in the blood-brain barrier (BBB) permeability concomitantly with the determination of serum tumor necrosis factor (TNF) and interleukin-6 (IL-6) levels in rats before, as well as 6, 24 and 48 h after the beginning of intraductal taurocholic acid-induced acute pancreatitis. Cytokine concentrations were measured in bioassays with specific cell lines (WEHI-164 for TNF and B-9 for IL-6), while the BBB permeability was determined for a small (sodium fluorescein, molecular weight (MW) 376 Da), and a large (Evans' blue-albumin, MW 67000 Da) tracer by spectrophotometry in the parietal cortex, hippocampus, striatum, cerebellum and medulla of rats. The serum TNF level was significantly (P < 0.05) increased 6 and 24 h after the induction of pancreatitis, while the IL-6 level increased after 24 and 48 h. A significant (P < 0.05) increase in BBB permeability for both tracers developed at 6 and 24 h in different brain regions of animals with acute pancreatitis. We conclude that cytokines, such as TNF and IL-6, may contribute to the vasogenic brain edema formation during acute pancreatitis.
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PMID:Experimental acute pancreatitis results in increased blood-brain barrier permeability in the rat: a potential role for tumor necrosis factor and interleukin 6. 953 Sep 27

Rare neurological complication in course of severe acute pancreatitis was described. A 38-year old woman developed Multiple Organ Dysfunction Syndrome ((MODS) and neurological complications such as transient encephalopathy and polineuropathy in a form of tetraplegy.
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PMID:[Unusual complication in the course of acute pancreatitis]. 1057 25

Acute renal failure (ARF) associated with liver disease is a commonly encountered clinical problem of varied etiology and high mortality. We have prospectively analyzed patients with liver disease and ARF to determine the etiology, clinical spectrum, prognosis and factors affecting the outcome. Other than hepatorenal syndrome patients, out of 221 cases, 66 developed ARF secondary to various liver disease like cirrhosis (n = 29, mortality 8, risk factors-older age p < 0.01, grade III/IV encephalopathy p < 0.05), fulminant hepatic failure (n = 25, mortality 15, risk factor-prolonged prothrombin time p < 0.01), and obstructive jaundice (n = 12, mortality 7, risk factor-sepsis p < 0.01). In these three groups the factors leading to ARF were volume depletion (24), gastrointestinal bleed (28), sepsis (34), drugs (27) [aminoglycosides (9) and NSAID (18)] along with hyperbilirubinemia. Various types of ARF with contemporaneous liver injury were malaria (n = 37, mortality 15, risk factors-higher bilirubin p < 0.001, higher creatinine p < 0.05, anuria p < 0.05 and dialysis dependency p < 0.05), sepsis (n = 36, mortality 22, risk factors-age p < 0.001, higher bilirubin p < 0.01, oliguria p < 0.05), hypovolemia with ischemic hepatic injury (n = 14, mortality 5, risk factors-higher creatinine p < 0.05 and SGPT p < 0.01), acute pancreatitis (n = 12, mortality 4, risk factors-higher bilirubin p < 0.001, higher SGPT p < 0.01, dialysis dependency p < 0.05), rifampicin toxicity (n = 10, no mortality), paroxysmal nocturnal hemoglobinuria (n = 3, no mortality), CuSO4 poisoning (n = 3 mortality 2), post abortal (n = 11, mortality 6, risk factors higher creatinine p < 0.05 and SGPT p < 0.01), ARF following delivery including HELLP syndrome (n = 12, mortality 4, risk factors-higher bilirubin p < 0.01 and SGPT p < 0.01), and of uncertain etiology (n= 14 mortality 4). 133 patients (60.2%), required hemodialysis hemodialfiltration or peritoneal dialysis. ARF associated with liver disease is having high mortality (42.5%). Avoidance of dehydration, hypotension, nephrotoxic drugs and sepsis, with promote dialytic support are necessary to reduce mortality and morbidity.
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PMID:Acute renal failure associated with liver disease in India: etiology and outcome. 1104 Dec 94

Pancreatic encephalopathy is a rare complication of acute pancreatitis. Clinical features include focal neurological signs and acute onset of dementia. This picture can fluctuate over time: cyclic progression with remission and relapses has been described. We present the case of a 43-year-old man who, after an acute episode of pancreatitis, experienced five relapses, with alternating focal signs. The patient has improved, but cognitive impairment persists after a 7-year follow-up.
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PMID:Pancreatic encephalopathy: a 7-year follow-up case report and review of the literature. 1253 91

Severe hepatotoxicity is a rare but potentially life-threatening side effect of antiretroviral therapy. In this case report we describe an HIV-positive patient who was admitted to our clinic with evidence of severe acute pancreatitis 18 months after the introduction of antiretroviral treatment, which included stavudine and didanosine. Shortly afterwards, she developed lactate acidosis and acute hepatic failure associated with renal failure. Renal support (hemofiltration) was required for three days. The patient subsequently developed grade III encephalopathy, as well as a large pleural effusion and ascites. Although the reported outcome of patients with liver failure due to antiretroviral treatment is poor, with a high mortality rate, our patient fully recovered after intensive supportive care and cessation of the antiretroviral agents. Liver biopsy revealed microvesicular steatosis and giant mitochondria, which are the typical hallmarks of mitochondrial damage, the presumed mechanism of antiretroviral drug toxicity. More than three years later the patient has an excellent clinical status with a stable HIV infection and no need for antiretroviral treatment. This case report indicates the need for increased awareness of the potential hepatotoxicity of an antiretroviral therapy, as severe side effects may occur more frequently with increasing use of such treatment.
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PMID:Acute hepatic failure and lactate acidosis associated with antiretroviral treatment for HIV. 1267 93

Acute pancreatitis, developing in a patient with chronic renal failure, was complicated by a fatal neurological illness during which MRI showed pontine and extrapontine changes consistent with pontine and extrapontine myelinolysis. At post mortem, acute pancreatitis was confirmed but the neuropathological findings were more in keeping with an unusual presentation of acute haemorrhagic leucoencephalitis, perhaps even representing a form of 'pancreatic encephalopathy'. Although the development of CT and MRI scanning has greatly increased the resolution of neuroimaging and facilitated diagnosis during life, the value of autopsy examination is confirmed in cases such as this. Sometimes the findings may raise more questions than may have been answered - this too is an important function!
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PMID:Fatal brain stem event complicating acute pancreatitis. 1276 45

A case of a 22-year-old woman with rare neurologic complications including encephalopathy and acute axonal sensorimotor polyneuropathy in the course of acute pancreatitis is reported. The encephalopathy emerged 3 weeks after the onset of the illness with complete remission being noted 1 week later. The polyneuropathy presented as quadriplegia and respiratory failure that required intubation and partially remitted gradually. There was no pancreatic lesion, no major pancreatic surgery, no sepsis, and no multiple organ failure, all of which had been proposed as the predisposing factors. Severe inflammatory response syndrome (SIRS) that developed during the clinical course of this patient might have induced these neurologic complications.
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PMID:Encephalopathy and acute axonal sensorimotor polyneuropathy following acute pancreatitis: a case report and review of the literature. 1578 9

The paper presents the experience gained in performing 100 operations associated with removal of intravascular malignant tumors [tumorous thrombi (TT)] from the inferior cava vein (ICV), which were made without using artificial and assisted circulation. This approach is substantiated. The variants of TT extent and its associated surgical technical features are shown. The procedure developed by the authors for anesthesia and infusion therapy in performing these highly specific interventions is described. The postoperative period ran with complications in 27 patients: pulmonary thromboembolism (PTE) (n=6); pneumonia (n=5); acute renal failure (n=4); encephalopathy (4); acute pancreatitis (n=4); cardiac arrhythmia (n=4); hepatic failure (n=2); adult respiratory distress syndrome (n=2); sepsis with evolving multiple organ deficiency (n=1), gastrointestinal hemorrhage (n=2); intestinal paresis (n=1); ICV thrombosis (n=1); recurrent myocardial infarction (n=1). Intraoperatively, 3 patients died from massive PTE (n=1) and hemorrhage (n=2). In the early postoperative period, 2 patients died from hemorrhage and hypovolemic shock (n=1) and recurrent myocardial infarction (n=1). Two patients died from pyoseptic complications on days 11 and 35. Thus, the vast majority of patients successfully tolerate a surgical intervention when certain conditions (the stepwise design of an anesthesia scheme keeping in mind the specific features of the course of an operation, hemodynamic and laboratory monitoring, adequate venous access, efficient infusion-transfusion therapy, timely use of cardiovascular stimulants, use of intraoperative hardware reinfusion of autoerythrocytes) are met.
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PMID:[The specific features of anesthesiological provision of operations removing malignant neoplasms with a tumorous thrombus in the inferior cava vein]. 1631 42

Immunosuppressive therapy, and particularly corticosteroids with or without azathioprine, can achieve a remission in more than 80% of patients with autoimmune hepatitis (AIH). By contrast, the usefulness of corticosteroid therapy in severe forms of AIH remains a subject of debate. Between 1986 and 2005, 16 patients (14 females, 2 males; mean age: 36.6 +/- 13.1 yr) presenting with acute, severe, or fulminant disease due to type 1 AIH (n = 13) or type 2 AIH (n = 3) were admitted to our liver intensive care unit. At admission, 10 of 16 (62.5%) patients presented with encephalopathy. Median international normalized ratio (INR), bilirubin, alanine aminotransferase (ALT), and creatinine values were 5.36 (range, 1.7-12.2), 425 micromol/L (range, 278-850), 678 IU/L (range, 60-2867), and 72 muicrool/L (range, 52-133), respectively. A total of 12 patients received corticosteroid therapy: 8 had started in the referring center a median of 2.5 days (range, 1-89) previously, and this therapy was initiated in 4 patients at their admission to our unit (median: 2 days; range: 0-5). Four patients were not treated because of a rapid deterioration in their AIH. Before treatment, 4 of 12 patients had been suffering from encephalopathy. The median duration of corticosteroid therapy was 7 days (range: 2-135). Of 16 patients, 13 underwent liver transplantation (LT) (81%), at which time all were encephalopathic. Median values for INR, total bilirubin, and ALT were 7.2 (range: 3.3-15.9), 400 micromol/L (range: 301-550), and 706 IU/L (range: 69-1,932), respectively, at the time of transplantation. All patients treated with corticosteroids had experienced a clinical (encephalopathy) and biochemical (Model for End-Stage Liver Disease [MELD] score) deterioration at the time of transplantation. Histological findings did not reveal any features of underlying chronic liver disease. Of the 13 patients undergoing transplantation, 10 had received prior corticosteroid therapy. Of the 2 nontransplanted patients treated with corticosteroids, a clinical improvement was observed in only 1 patient. Severe septic complications occurred in 3 patients under corticosteroid therapy (gram-negative septicemia n = 2; disseminated aspergillus n = 1). Nine of the treated patients are still alive; 1 died after liver transplantation (LT) (recurrence of AIH, acute pancreatitis, sepsis), 1 survived without LT, and 1 died without LT. Among the untreated patients, 3 survived after LT and 1 died without LT. In conclusion, corticosteroid therapy is of little benefit in severe and fulminant forms of AIH; it may favor septic complications and should not delay LT.
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PMID:Usefulness of corticosteroids for the treatment of severe and fulminant forms of autoimmune hepatitis. 1737 Mar 35


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