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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The autopsy of a 10-month-old infant girl who died suddenly after a 2-day illness revealed acute pancreatitis and DIC. While the definitive etiology remains unknown, retention of pancreatic juice accompanying proliferation of papillary epithelium within the pancreatic duct adjacent to the ampulla Vater was suggested. Acute interstitial pancreatitis was assumed to have resulted from suppurative inflammation of the pancreatic duct. DIC was probably caused by the release of pancreatic enzymes.
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PMID:Sudden death due to infantile pancreatitis. 713 2

Acute necrotizing (hemorrhagic) pancreatitis was induced in 12 dogs by infusing oleic acid into their pancreatic ducts. There were decreases in blood pH, complement, antithrombin III, blood platelets, 24- and 48-hour plasminogen, and 24-hour haptoglobin and modest decreases in serum albumin. There were increases in fibrinogen, 48- to 120-hour haptoglobin, and 96-hour and 120-hour plasminogen and prolongations of prothrombin and activated partial thromboplastin times. The latter 2 changes together with decreases in antithrombin III, platelet numbers, and complement were indicative of consumption coagulopathy. A clinically innocuous but statistically significant decrease in serum total and ionized calcium despite significant acidosis was noted. This indicates that serum total and ionized calcium is helpful in making the diagnosis of acute necrotizing pancreatitis. Methemalbuminemia of 6 mg/dl at 24 hours and 7 mg/dl at 48 hours indicates that methemalbuminemia is a valuable diagnostic and prognostic finding in association with acute necrotizing pancreatitis.
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PMID:Biochemical and coagulation changes in a canine model of acute necrotizing pancreatitis. 725 99

An analysis was made of 41 cases of disseminated intravascular coagulation in dogs, with the objective of evaluating routine and nonroutine laboratory tests used in making the diagnosis. The dogs were grouped on the basis of underlying disease, which included neoplasia (39%), pancreatitis (30%), chronic active hepatitis (15%), heat stroke (12%), and sepsis (4%). Of the diagnostic tests evaluated, those for determination of activated partial thromboplastin time, antithrombin III activity, prothrombin time, and the platelet count were the most valuable. Of the clotting factors, factor V activity was decreased more frequently than the activity of factor VIII:C (factor VIII: procoagulant). The factor VIII:C activity was in conflict with prevailing dogma that reflects depression of this factor in disseminated intravascular coagulation. Factor VIII:C activity was decreased in only 29% of dogs studied. Activation of the fibrinolytic system was manifested by decreased plasminogen activity in 49% of the dogs studied. Sixty-one percent of the dogs had increased amounts of fibrin (ogen) degradation products.
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PMID:Disseminated intravascular coagulation: antithrombin, plasminogen, and coagulation abnormalities in 41 dogs. 726 67

The coagulation changes observed in acute experimental pancreatitis were compared with those after the intravenous infusion of pancreatic juice and ascitic fluid exudate obtained from bile-induced pancreatitis in dogs. The coagulation changes after acute pancreatitis was induced by the intraductal injection of autologous bile, trypsin or elastase showed decreased platelet counts, decreased plasma fibrinogen levels, prolonged partial thromboplastin and prothrombin times, shortened euglobulin clot lysis time and increased fibrin degradation products. Multiple microemboli were observed in the lung and, occasionally, in the kidney, an indication of consumption coagulopathy. The effects upon blood coagulation after the intravenous injection of pancreatic juice included decreased platelet counts, decreased plasma fibrinogen levels and prolonged partial thromboplastin and prothrombin times. The intravenous injection of pancreatic exudate produced greater changes than did those of an equal amount of pancreatic juice. There was a shortening of euglobulin clot lysis time and a marked increase in fibrin degradation products. Pancreatic exudate which accumulates during acute pancreatitis may contain a toxic substance or substances which contribute to the consumption of coagulation factors during acute pancreatitis.
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PMID:The effects upon blood coagulation in dogs of experimentally induced pancreatitis and the infusion of pancreatic juice. 726 8

It has been noticed that hyperamylasemia occurs after hepatic resection. Between July 1973 and April 1991, hyperamylasemia was observed in 57 (42%) of 136 patients with hepatocellular carcinoma and 13 (32%) of 41 patients with metastatic liver cancer. The incidence was not correlated with extent of resection, blood loss, hypoxemia, disseminated intravascular coagulation, liver cirrhosis, or hepatitis B virus infection. There were three patterns: salivary-type dominant hyperamylasemia (type I), pancreatic-type dominant hyperamylasemia (type II), and a mixture of types I and II (type III). The point at issue is whether types II and III indicate postoperative pancreatitis. Although the pathogenesis remains unclear, surgeons should be alert to this complication and take reasonable measures with regard to the types of hyperamylasemia.
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PMID:Hyperamylasemia after hepatic resection. 768 77

We reported a case of acute pancreatitis occurring during administration of valproic acid for epilepsy. About four years prior to the first onset of acute pancreatitis, treatment with valproic acid for his seizures was started. The first pancreatitis improved by conservative therapy within a week. He continued valproic acid after the first episode. Two months later, the second acute pancreatitis occurred. The second episode was complicated with disseminated intravascular coagulation, but responded to conservative therapy. After the second episode, the valproic acid was discontinued and pancreatitis has not recurred. Pancreatitis associated with valproic acid may be severe, and therefore valproic acid should be used with caution.
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PMID:[A case of acute pancreatitis during administration of valproic acid]. 839 36

We reported a case of motor neuropathy with pyramidal sign following prolonged administration of a high dose of muscle relaxant, pancuronium bromide (Myoblock). A 40-year-old male was admitted to our hospital with acute episode of pancreatitis. He was treated with artificial ventilation and Myoblock to manage delirious state, disseminated intravascular coagulation and multiple organ failure. Total dose of 823 mg (24 mg/day) of Myoblock was given intravenously over 36 days. After Myoblock was discontinued, he regained his consciousness and marked muscle weakness with atrophy was noted in both limbs, more severe in distal lower limbs, without any noticeable sensory and sphincter disturbances. Motor nerve conduction studies showed normal nerve conduction velocities with markedly decreased amplitude of compound muscle action potentials. Repetitive nerve stimulation studies revealed decrement response after tetanic stimulation, which disappeared later. Needle EMG showed active denervation potentials and marked polyphasic motor unit potentials. Muscle biopsy revealed neurogenic muscle atrophy with fragmented acetylcholine esterase-positive postsynaptic sites. Sural nerve biopsy showed slight to moderate degree of axonal degeneration of myelinated fibers. Clinical, electrophysiological, and pathological studies above indicated that the main affected sites were neuromuscular junctions including the terminal twigs of motor neurones and postsynaptic membrane, and pyramidal tracts, predominant in lower limbs. About one month after the recognition of the muscle weakness, his muscle strength improved gradually, however, spasticity with hyperreflexia and pathologic reflexes of both legs were found, and became more prominent thereafter. Intensive physiotherapy and rehabilitation led improvement to the point that he became able to ambulate with walking-aids about 7 months later, but marked spasticity persisted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of motor neuropathy with pyramidal sign due to prolonged administration of high dose of pancuronium bromide (Myoblock)]. 840 81

Extraneural manifestations of toxoplasmosis often are not recognized antemortem in patients with AIDS. We describe a patient who was seropositive for human immunodeficiency virus and presented with lethargy, abdominal tenderness, rapidly progressive ventilatory failure, rhabdomyolysis, myoglobinuria, and disseminated intravascular coagulation. Although the diagnosis of pancreatitis was not considered while the patient was alive, an autopsy demonstrated pancreatic necrosis associated with toxoplasmal cysts. No other infection was evident. This case suggests that Toxoplasma gondii can cause severe pancreatitis in patients with AIDS.
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PMID:Necrotizing pancreatitis and multisystem organ failure associated with toxoplasmosis in a patient with AIDS. 845 54

Five cases of gastric infarction were observed in adolescent or adult cynomolgus monkeys (Macaca fascicularis) over a 20-month period. Gastric infarcts were encountered as striking and unexpected findings at necropsy. Gross and microscopic findings included gastric necrosis, hemorrhage, and edema that involved large areas of the fundus and pylorus. A consistent finding was the presence of thrombi in the gastric microvasculature, particularly in the venous system. All animals had acute clinical episodes with substantial tissue damage resulting from a variety of causes, including trauma, pancreatitis, necrotizing cystitis, and intestinal intussusception. In addition, three animals had microvascular thrombosis in nongastric tissues. Our findings suggest that cynomolgus monkeys may be predisposed to developing gastric infarction under conditions of severe systemic insult that predispose to disseminated intravascular coagulation.
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PMID:Gastric infarction in cynomolgus monkeys (Macaca fascicularis). 880 10

The etiology of acute pancreatitis is based on several causes, among which idiopathic nature (< 30%) is second to biliary stone disease (60-70%). It is still under debate whether alcohol as the main cause of chronic pancreatitic disease can cause acute pancreatitis. Based on Opie's "obstruction theory" of 1901 and experimental data, it is now widely accepted that the gallstone passage into or through the terminal biliopancreatic ductal system triggers acute (necrotizing) pancreatitis by causing pancreatic ductal obstruction. However, the sequential intracellular mechanisms in the pathogenesis of acute pancreatitis remain unclear. A co-localization hypothesis has been proposed to explain the premature intracellular activation of trypsinogen to trypsin: due to a yet unknown defect in the intracellular protein transport and sorting system within the acinar cell, lysosomal hydrolases (i.e. cathepsin B) and secretory proteins (i.e. trypsinogen) co-localize in a fragile postgolgi vacuole where activation can occur. In addition, alterations of exo- and endocytosis at the apical pole exist (i.e. secretion block). The pathophysiological events are characterized by local and systemic hypovolemia and (micro)circulatory failure aggravating necrosis, followed by ARDS, renal failure and several other severe complications (i.e. sepsis and DIC). The systemic overflow of proteolytic enzymes (i.e. PLA-2) and kinins plays a major role as mediating factor in severe cases, resulting in multiorgan failure.
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PMID:[Etiology, pathogenesis and pathophysiology of acute pancreatitis]. 928 10


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