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

Between 1 September and 24 October 1976, 318 cases of acute viral haemorrhagic fever occurred in northern Zaire. The outbreak was centred in the Bumba Zone of the Equateur Region and most of the cases were recorded within a radius of 70 km of Yambuku, although a few patients sought medical attention in Bumba, Abumombazi, and the capital city of Kinshasa, where individual secondary and tertiary cases occurred. There were 280 deaths, and only 38 serologically confirmed survivors.The index case in this outbreak had onset of symptoms on 1 September 1976, five days after receiving an injection of chloroquine for presumptive malaria at the outpatient clinic at Yambuku Mission Hospital (YMH). He had a clinical remission of his malaria symptoms. Within one week several other persons who had received injections at YMH also suffered from Ebola haemorrhagic fever, and almost all subsequent cases had either received injections at the hospital or had had close contact with another case. Most of these occurred during the first four weeks of the epidemic, after which time the hospital was closed, 11 of the 17 staff members having died of the disease. All ages and both sexes were affected, but women 15-29 years of age had the highest incidence of disease, a phenomenon strongly related to attendance at prenatal and outpatient clinics at the hospital where they received injections. The overall secondary attack rate was about 5%, although it ranged to 20% among close relatives such as spouses, parent or child, and brother or sister.Active surveillance disclosed that cases occurred in 55 of some 550 villages which were examined house-by-house. The disease was hitherto unknown to the people of the affected region. Intensive search for cases in the area of north-eastern Zaire between the Bumba Zone and the Sudan frontier near Nzara and Maridi failed to detect definite evidence of a link between an epidemic of the disease in that country and the outbreak near Bumba. Nevertheless it was established that people can and do make the trip between Nzara and Bumba in not more than four days: thus it was regarded as quite possible that an infected person had travelled from Sudan to Yambuku and transferred the virus to a needle of the hospital while receiving an injection at the outpatient clinic.Both the incubation period, and the duration of the clinical disease averaged about one week. After 3-4 days of non-specific symptoms and signs, patients typically experienced progressively severe sore throat, developed a maculopapular rash, had intractable abdominal pain, and began to bleed from multiple sites, principally the gastrointestinal tract. Although laboratory determinations were limited and not conclusive, it was concluded that pathogenesis of the disease included non-icteric hepatitis and possibly acute pancreatitis as well as disseminated intravascular coagulation.This syndrome was caused by a virus morphologically similar to Marburg virus, but immunologically distinct. It was named Ebola virus. The agent was isolated from the blood of 8 of 10 suspected cases using Vero cell cultures. Titrations of serial specimens obtained from one patient disclosed persistent viraemia of 10(6.5)-10(4.5) infectious units from the third day of illness until death on the eighth day. Ebola virus particles were found in formalin-
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PMID:Ebola haemorrhagic fever in Zaire, 1976. 30 56

Cerebral fat embolism was established as the cause of death in a 34-year-old man with acute pancreatitis. Encephalopathy complicating pancreatitis may be due to hypoxia secondary to pulmonary fat embolism, cerebral fat embolism, or the complicating syndromes of disseminated intravascular coagulation or hyperosmolality.
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PMID:Pancreatic encephalopathy. 32 Jun 76

Studies of coagulation were performed prospectively in 41 patients with mild to moderately severe acute pancreatitis. Six patients (15%) presented with coagulation data suggestive of defibrination; two of them had clinical signs of bleeding. No other cause than pancreatitis was found in these 6 patients to account for coagulation abnormalities. Comparing the patients who presented defibrination to those who did not, no difference was observed in clinical course and admission values of serum amylase, fibrinogen, urea, calcium, glucose, transaminase levels, white blood cell count and arterial partial pressure of oxygen. Platelets counts and serum creatinine levels were respectively lower and higher in the first group of patients.
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PMID:[Defibrination syndrome during acute pancreatitis: 6 cases. Prospective studies of coagulation in 41 patients (author's transl)]. 46 Nov 54

Fifty-eight patients with mild to moderately severe acute pancreatitis were randomly allocated to treatment with or without nasogastric suction (27 and 31 patients respectively). Intravenous fluids and pethidine hydrochloride were also given. The two groups were comparable clinically at the start of the study. There were no differences between the two groups in the mean duration of the following features: abdominal pain or tenderness; absence of bowel movements; raised serum amylase concentration; time to resumption of oral feeding; and days in hospital. Prolonged hyperamylasaemia (serum amylase greater than 0.33 mU/l) occurred in one patient in the suction group and in three patients in the non-suction group. A mild recurrence of abdominal pain after resumption of oral feeding occurred in three patients in the suction group and in two patients in the non-suction group. Two patients in the suction group developed overt consumption coagulopathy and two others pulmonary complications. No patient in the non-suction group had complications. The findings suggest that most patients with mild to moderately severe acute pancreatitis do not benefit from nasogastric suction. The procedure should be elective rather than mandatory in treating this condition.
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PMID:Is nasogastric suction necessary in acute pancreatitis? 69 50

Twenty-five patients with acute pancreatitis were studied prospectively in the first week of their admission using haematological and coagulation tests. Platelet counts initially fell and later returned to admission levels. Rising levels of plasma fibrinogen were recorded. The kaolin cephalin clotting time was shorter than its control in twenty-one patients. Eighteen patients had elevated fibrinogen degradation products and fourteen had a positive ethanol gelation test. It is suggested that by taking into account the results in series of individual patients a degree of intravascular coagulation may be a common feature of acute pancreatitis. In one patient (presented in detail) strong evidence for disseminated intravascular coagulation was found
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PMID:Haematological abnormalities in acute pancreatitis. A prospective study. 88 29

Splenic hematomas are infrequent complications of acute pancreatitis. In some cases, local factors that may play a role in the pathogenesis of the hematoma (thrombosis of the splenic artery or veins, intrasplenic pseudocysts, perisplenic adhesions, enzymatic digestion) are found. In the absence of local factors, the etiology of splenic hemorrhage remains unknown. We report two cases of splenic hematoma occurring during an acute necro-hemorrhagic pancreatitis associated with renal failure that required renal replacement therapy (hemodialysis and continuous arteriovenous hemodialysis). In both cases, more than half of splenic parenchyma was affected by multiple infarctions. No local factors responsible for the splenic abnormalities were detected in either case. Thrombosis of the splenic arterial microcirculation and a coagulation disorder consistent with disseminated intravascular coagulation was detected in one patient. In the second patient, coagulation disorders secondary to either liver disease, pancreatitis and its septic complications, or extracorporeal circuit heparinization for renal replacement therapy were present. Coagulation disorders should be considered whenever a splenic hematoma is found in a patient with acute pancreatitis. Disseminated intravascular coagulation may be the etiology of a splenic hematoma in acute pancreatitis.
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PMID:Splenic hematoma in acute pancreatitis. Role of coagulation disorders. 141 37

Pneumocystis carinii pneumonia (PCP) is a major opportunistic infection in acquired immunodeficiency syndrome (AIDS) and is treated with co-trimoxazole, pentamidine and others. The severe adverse reactions, including bone marrow suppression, by these therapeutic agents often preclude their continued use. A 14-year-old male HIV-positive hemophilia A patient, who was complicated by disseminated intravascular coagulation syndrome (DIC) following acute pancreatitis during treatment for PCP, was treated with proteinase inhibitors and anticoagulant agents. He was improved and discharged. As pentamidine may cause pancreatitis and develop DIC, it is important that pancreatic enzymes should be carefully followed when this agent administrated. In this case, granulocyte colony-stimulating factor and erythropoietin were effective for the bone marrow suppression, suggesting that importance of these agents for the prophylaxis of other secondary infections during the treatment.
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PMID:[HIV-1 seropositive hemophilia A complicated by disseminated intravascular coagulation syndrome and acute pancreatitis during treatment of Pneumocystis carinii pneumonia]. 143 51

In two patients receiving L-asparaginase therapy, severe acute pancreatitis complicated by disseminated intravascular coagulation (DIC) developed. In both cases it was successfully treated with continuous infusion of a synthetic protease inhibitor, nafamostat mesilate. In this report, we briefly discuss the clinical efficacy of the synthetic protease inhibitor in treating such cases.
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PMID:Use of a synthetic protease inhibitor for the treatment of L-asparaginase-induced acute pancreatitis complicated by disseminated intravascular coagulation. 162 61

ARDS occurs in patients with no underlying pulmonary diseases, induced by stresses, such as lung injury, acute pancreatitis or infections. It is an acute respiratory disorder which manifests as acute dyspnea, hypoxemia and lowered pulmonary compliance. Greene et al, used balloon pulmonary angiogram (BOPA) as diagnostic tool to morphologically observe the pulmonary disorder. To study the dynamic pulmonary circulation and morphology of the peripheral pulmonary artery of ARDS, we performed this method for acute cardiac failure and ARDS patients. Pulmonary hemodynamic changes in ARDS revealed mild pulmonary hypertension and increased PVR, while C.I. and PCWP remained within a normal range. The findings of BOPA in ARDS showed that the frequency of PAFD correlated with the the presence of an elevated PVR and DIC, and pulmonary vasoconstriction was detected by measurement of PA diameter (B/A2).
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PMID:[ARDS: circulatory factors and their evaluation]. 203 88

Acute pancreatitis complicated by acute renal failure (ARF) requiring dialysis is a rare condition with a mortality rate of 80%. During the period 1977-1988 419 patients were admitted to our hospital because of ARF requiring dialysis. Fourteen (3%) had ARF caused by acute pancreatitis. Ten patients developed respiratory failure, eight patients circulatory failure, four hepatic failure, and one disseminated intravascular coagulation. Three patients had complicating septicemia and two gastrointestinal bleeding. Ten patients (71%) died. All patients with four or more organ failures besides the pancreatic failure died. Median time from start of symptoms until death was 28 days. Mortality in this series does not differ from that reported over the last 40 years. The need of multicenter trials for the purpose of improving prognosis is emphasized.
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PMID:Prognosis in acute pancreatitis complicated by acute renal failure requiring dialysis. 227 48


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