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

If the underlying pathology of the syndrome of fat embolism is the presence of circulating emboli of neutral fat with adherent platelets and red blood cells, then one could expect certain changes in normal vascular cellular elements and fat metabolism, with resultant alterations in pulmonary function. In our series of 118 patients with fractures of the lower limbs we found that more than half of them exhibited hypoxemia as well as a decrease in the hematocrit and platelet counts with a concomitant increase in platelet adhesiveness. In addition, those patients with hypoxemia showed increased fibrinogen degenerative product levels indicating an increased fibrinolysis. We found only a slight temporary rise in the serum triglycerides, but the nonesterified fatty acid levels rose sharply over the first three days following trauma associated with an increase in serum lipase. Our study demonstrated that this increase in serum lipase occurred slightly before the peaking tendency observed in the nonesterified fatty acids. Following trauma, fat emboli with adherent platelets and other vascular cellular elements are formed; we would expect that these emboli would lodge in the capillaries and small vessels of the lung, thereby producing a physiological shunt. An increase in the A-aDo2 confirmed this hypothesis and was associated with a decrease in the arterial oxygen level in over half the patients studied. Although 58 of our patients showed evidence of hypoxemia associated with a fall in hematocrit and platelet count, not one of them showed clinical signs and symptoms of the fat embolus syndrome. This study suggests that a subclinical form of fat embolism does exist. What causes a small percentage of those patients with subclinical fat embolism to progress to a clinical fat embolism is still unknown. The majority of our patients spontaneously returned to normal within 5 days. Reviewing the results of those patients who developed hypoxemia and the two patients who developed clinical fat embolism, there seems to be no indication of what causes the progression. Hypotension and shock do not seem to be relevant to the progression of the subclinical condition. Not one of 110 reviewed had evidence of shock or persistent hypotension, yet 58 of these patients developed changes in arterial saturation, vascular elements, and evidence of disseminated intravascular coagulation.
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PMID:Alterations in pulmonary function, coagulation and fat metabolism in patients with fractures of the lower limbs. 125 90

In our opinion, this clinical study demonstrates the intravascular formation of globules, macroglobules and their aggregations both in the association with the type of general anaesthesia and with the operative osteosynthesis of long bones. Within the framework of this study changes in the level of lactic acid in blood serum and of total ketosubstances in blood were followed as well as the levels of total lipids, triglycerides, phospholipides, serum lipase, non-esterified and esterified fatty acids, changes in blood coagulation and 17-ketosteroides in blood. The observed changes supported the opinion that the development of fat globulemia was associated with humoral and physicochemical changes in blood. Repeated evaluations of fat globulemia in plasma are important for studies on pathogenesis and development of fat embolism. In practice, they help: to diagnose especially subclinical forms of fat embolism with non-marked clinical symptoms; to define a suitable term of both primary and delayed operation performed in the period of ending katabolic phase after severe trauma; to define an optimum time for the indication of osteosynthesis to the end of manifest fat embolism; to control positive effects of drugs used for the prophylaction and treatment of fat embolism. In this way it is possible to objective the effectiveness of a rational prophylaxis and treatment of fat embolism. Following factors contribute to macroglobulamia and to manifestation of F. E.: injuries to bones, tissues and organs; stress, posttraumatic shock; severe hemorrhagic hypotension; posttraumatic hypercoagulation with possible binding to the development of a consumption coagulopathy; heavy changes of acid-base balance; increase of catecholamines in plasma; hormonal and general metabolic disturbances; posttraumatic dyslipidemia with special regard to the decrease of beta-lipoproteins and of lipoproteinlipase activity together with the increase of lipoproteins having a very low density and with the occurrence of a significant lipoprotein coalescence. The prospective study on the globulemia changes is based on the following examinations: in 76 injured patients: a short time observation (24 hours) of the globulemia changer after osteosyntheses in general anesthesia. The operative interventions were usually performed 6 to 8 days after injury. in 60 injured patients with fractures (single or multiple fractures, fractures in polytrauma patients): a long-time observation (28 days) of the globulemia changes.
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PMID:Fat globulemia in early diagnostics of traumatic fat embolism. 308 41

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
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PMID:Acute pancreatitis: a multisystem disease. 804 85

We report a case of acute pancreatitis with diabetic ketoacidosis associated with increased serum myoglobin concentration, acute renal failure, and disseminated intravascular coagulation. A 49-year-old man suffering from diarrhea, vomiting, and somnolence was admitted to the hospital. He had had flu-like symptoms for 4 days prior to the onset of these symptoms. He was a habitual drinker and had been consuming 360 ml-900 ml of the drink "shochu" (distilled spirits containing 28% alcohol) daily for 30 years. Laboratory data on admission revealed elevated serum levels of pancreatic enzymes, including amylase, trypsin, lipase, pancreatic secretory trypsin inhibitor (PSTI), phospholipase A2 (PLA2), and elastase-1, as well as elevated levels of glucose (373 mg/dl), ketone bodies (3675 mumol/l), and myoglobin (229.8 ng/ml). Treatment with subcutaneous insulin and intravenous administration of electrolyte fluid and the systemic protease inhibitor, gabexate mesilate, was begun immediately. Early after the initiation of treatment, there was an increase in serum creatinine (4.9 mg/dl), and thromobocytopenia (15000/microliters) was observed. The patient completely recovered from renal failure and acute pancreatitis, but required insulin therapy. Alcohol ingestion and dehydration are thought to have played a major role in the triggering of the acute pancreatitis. We examined the relationship among acute pancreatitis, diabetic ketoacidosis, and hypermyoglobinemia in the literature.
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PMID:Acute pancreatitis with diabetic ketoacidosis associated with hypermyoglobinemia, acute renal failure, and DIC. 884 91

A twenty-year-old woman with anorexia nervosa (body mass index=11) suffered from severe liver dysfunction (aspartate aminotransferase 5,000 IU/l, alanine aminotransferase 3,980 IU/l, prothrombin time 32%), hypoglycemia (serum glucose 27 mg/dl), and pancreatic dysfunction (amylase 820 IU/l, lipase 558 IU/l). She fell into a depressive state with irritability, which was not improved by intravenous glucose. Despite treatment with plasmapheresis for the liver dysfunction, she subsequently developed pulmonary edema, acute renal failure, gastrointestinal bleeding, and disseminated intravascular coagulation. Hemodialysis, mechanical ventilation and drug therapy including prednisolone, prostaglandin E1, and branched-chain amino acid, improved her critical condition. In this case, malnutrition may have been the cause for the liver dysfunction and subsequent complications.
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PMID:Anorexia nervosa with severe liver dysfunction and subsequent critical complications. 1043 64

The case is described of a 32-year-old man suffering from alcoholism who came to the Emergency Unit with vomiting, fever and sharp epigastric pain irradiating to the chest and upper abdomen. A diagnosis of acute pancreatitis was made after high amylase and lipase levels were observed and the results of computed tomography scan revealed images typical of acute pancreatitis. Findings upon admission and after the initial 48 hours did not correlate with a severe or complicated course according to Ranson's criteria. On the third day after admission he suddenly developed decreased vision. A fluorescein angiogram showed arteriolar occlusion, retinal and choriocapillary ischaemia. Purtscher's retinopathy was suspected. After 4 weeks, the patient had recovered from acute pancreatitis, ophthalmoscopic examination showed normal results, and visual acuity had almost returned to normal. Activation of complement in acute pancreatitis could account for many haematologic acute disorders due to leucocyte emboli or other complement-mediated aggregates. Coagulation abnormalities may range from isolated intravascular thrombosis to severe disseminated intravascular coagulation. Purtscher's retinopathy, due to microembolizations in the choroidal and retinal arterioles, should be included among the various systemic effects of acute pancreatitis. This visual disorder is a rare systemic manifestation of acute pancreatitis which was not correlated to a severe or complicated clinical course. Treatment of these ocular complications remains to be established and outcome, therefore, depends upon resolution of the pancreatic disease.
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PMID:Acute pancreatitis with Purtscher's retinopathy: case report and review of the literature. 1114 85

An enzymatic, kinetic method for determining serum lipase activity was evaluated and compared to a standard manual method for use in dogs. The kinetic method was a commercial kit adapted for use on a tandem access clinical chemistry analyzer and utilized a series of coupled enzymatic reactions based on the hydrolysis of 1,2-diglyceride by lipase. The manual method was the Cherry-Crandall technique based on the titration of base against the acid formed by hydrolysis of an olive oil substrate by lipase. The correlation between the two methods was very good (r = 0.94). The reference range for 56 clinically healthy dogs assayed by the kinetic method was 90 to 527 U/L. Diseases associated with a greater than twofold elevation in serum lipase activity as determined by the kinetic method included pancreatitis, gastritis with liver disease, and oliguric renal failure with metabolic acidosis. In some cases, pancreatitis was seen with other clinical problems, such as gastroenteritis, diabetic ketoacidosis, duodenal mass, disseminated intravascular coagulation, and septic peritonitis. Diseases associated with serum lipase activity within the reference range or elevated less than twofold included gastritis, gastric ulcer, cholestasis, phenobarbital-induced hepatopathy, colitis, copper hepatopathy, abdominal hematoma, apocrine gland adenocarcinoma, and thrombocytopenia with pneumonia.
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PMID:Serum lipase determination in the dog: a comparison of a titrimetric method with an automated kinetic method. 1267 88

Thrombotic microangiopathy (TMA) is a rarely reported complication of acute pancreatitis. The prognosis is generally good, if diagnosis is made early and treatment is adequate. We present the case of a 74-year-old man who visited our emergency department due to acute abdominal pain. He had no history of alcohol abuse or pancreatitis. Blood tests indicated elevated lipase and amylase. An abdominal computerized tomography (CT) indicated mild pancreatitis. After admission, the patient suffered a seizure and developed anemia, thrombocytopenia, elevated lactic dehydrogenase (LDH) and elevated unconjugated bilirubin. A peripheral blood smear indicated fragmented red blood cells. We diagnosed the patient as having TMA. After plasma exchange and plasma infusion therapy, the LDH and platelet levels gradually improved. A differential diagnosis of disseminated intravascular coagulation (DIC) and TMA following pancreatitis is necessary because of the different treatment strategies. Our patient had a good prognosis following therapy for TMA. Such therapy may include plasma exchange, plasma infusion, corticosteroid therapy and splenectomy.
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PMID:Acute pancreatitis preceding an acute episode of thrombotic microangiopathy. 2017 26

Systemic complications related to acute pancreatitis include acute respiratory distress syndrome, multiple organ dysfunction syndrome, disseminated intravascular coagulation, hypocalcemia, hyperglycemia, and insulin dependent diabetes or diabetic ketoacidosis. In practice, the development of diabetic ketoacidosis induced by acute pancreatitis is rare and generally associated with hypertriglyceridemia. However, herein we report a case of a 34-year-old female without hypertriglyceridemia, who was diagnosed with acute pancreatitis complicated with diabetic ketoacidosis. The patient was admitted with complaints of febrile sensation, back pain, and abdominal pain around the epigastric area. Levels of serum amylase and lipase were elevated to 663 U/L and 3,232 U/L. Contrast-enhanced abdominal CT showed pancreatic swelling, peri-pancreatic fat infiltration and fluid collection. The patient was initially diagnosed with simple acute pancreatitis. Though the symptoms were rapidly relieved after initiation of treatment, severe hyperglycemia (575 mg/dL), severe metabolic acidosis (pH 6.9), and ketonuria developed at four days after hospitalization. However, serum triglyceride levels remained within the normal range (134 mg/dL). Finally, the patient was diagnosed with acute pancreatitis complicated with diabetic ketoacidosis unrelated to hypertriglyceridemia. She recovered through insulin and fluid therapy, and receives insulin therapy at the outpatient clinic.
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PMID:Acute Pancreatitis Complicated with Diabetic Ketoacidosis in a Young Adult without Hypertriglyceridemia: A Case Report. 2787 Nov 65