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

We have recently experienced a case of Vibrio vulnificus septicemia which occurred in a patient with hepatic cirrhosis, and as we were able to give early antibiotic treatment, the patient survived. We would like to report this case here together with another case experienced 2 years ago. Case 1 was a 58-year-old male who was attending our hospital as an outpatient for hepatic cirrhosis. At 5:30 pm on August 8, 1987, he consumed abalone and giant clam and at 9 pm complained of high fever with shaking chills. He was admitted to our department as an emergency case. Cefoperazone was administered resulting in a decline of fever on the following day. During the course of treatment he fell transiently into pre-DIC, but due mainly to the administration of antibiotics his condition was subsided. Case 2 was a 53-year-old male who was under medical care in our hospital for grave hepatic cirrhosis. On October 11, 1985, he consumed sushi and two days later suffered chills and pyrexia. A blood culture revealed Vibrio vulnificus. His condition improved transiently with administration of Cefazolin, but oliguria, hypotension and ascites occurred subsequently, and finally the patient died on the 22nd day.
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PMID:[Two case reports of septic shock due to Vibrio vulnificus with liver cirrhosis]. 250 32

In Burma, clinicopathological studies were carried out in three young farmers who died 15, 52 and 36 h after being bitten by Russell's vipers. Clinical features included local swelling, spontaneous systemic bleeding, defibrination, shock, cardiac arrhythmia, hypoglycaemia, coma and oliguria. On admission to hospital, 15, 48 and 21 h after the bites, serum venom antigen concentrations ranged from 50 to 130 ng/ml. Autopsies revealed widespread congestion and bleeding in the lungs, gastrointestinal and renal tracts, adrenals, heart, brain and anterior pituitary. There was histopathological evidence of focal haemorrhage and fibrin deposition at the site of the bite and in the pituitary, lungs and kidneys and acute tubular necrosis. Deposition of fibrin microthrombi results from the action of venom procoagulants. Shock was attributed to increased capillary permeability, revealed clinically by conjunctival oedema. Acute pituitary/adrenal failure in one case was explained by fibrin deposition and haemorrhage in the anterior pituitary--resembling Sheehan's syndrome. Acute tubular necrosis resulted from ischaemia caused by fibrin deposition and to prerenal factors. An intractable cardiac tachyarrhythmia may have been caused by subendocardial and myocardial haemorrhages.
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PMID:Contribution of focal haemorrhage and microvascular fibrin deposition to fatal envenoming by Russell's viper (Vipera russelli siamensis) in Burma. 256 58

Fifty patients of acute renal failure following Viperine snake bite were studied. Oliguria (100%), local swelling (48%) and bleeding tendencies (42%) were the predominant clinical features encountered. Of the 25 patients in whom detailed coagulation studies were done, 24 patients had disseminated intravascular coagulation (DIC) and 1 had primary fibrinolysis. DIC was commoner with Russell's viper bite (62%) in comparison to Echis carinatus bites (40%). Renal histology obtained in 29 cases revealed tubular necrosis (35%), cortical necrosis (24%) tubular degeneration (17%) and glomerular changes (17%). Ballooning of glomerular capillaries (59%), splitting of glomerular basement membrane (40.7%), swelling of endothelial cells (29.6%), and focal proliferation of mesangial cells (17%) were the significant glomerular changes encountered. 20 (40%) patients succumbed, DIC (50%), irreversible shock (30%) and septicaemia (20%) being the immediate causes of death. Development of oliguria within 24 hours of snake bite and cortical necrosis were associated with higher mortality.
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PMID:Clinicopathological study of acute renal failure following viperine snake bite. 261 61

Burn injury causes dynamic alterations in the coagulation and fibrinolysis, and so-called DIC often occurs in burned patients. In this study the clinical significance of heparin therapy combined with antithrombin III concentrate in animal experiments and clinical experiences were discussed. The changes in blood coagulation, fibrinolysis and kidney function and the effect of anticoagulation therapy using heparin were investigated in rabbits with third degree burn covering 35% of the total body surface area. The animals were subjected to determinations for various kidney function tests, blood coagulation and fibrinolysis tests, blood viscosity and hematocrit value before induction of the burn and after 8 and 24 hours respectively. Thirty rabbits were divided into a non-therapy group, an intravenous infusion group, a heparin group, an antithrombin III group, and an antithrombin III plus heparin group and the results were compared among them. Oliguria and a disturbance of kidney function were noted even at hour 8 after burn in the non-therapy group. In the intravenous infusion group urine volume was maintained well although the early stage of non-oliguric renal insufficiency was noted. The changes noted in the intravenous infusion group were prevented almost completely in the heparin group at hour 8, but FENa and CH2O were elevated at hour 24 probably because antithrombin III activity was depressed markedly. In the antithrombin III group and the antithrombin III plus heparin group, however, creatinine clearance was moderately elevated while FENa and CH2O remained unchanged as compared with the values before the burn. The antithrombin III plus heparin group showed slightly better results than the antithrombin III group in Ucr/Pcr ratio, creatinine clearance and CH2O. The results of the present study indicate that it is extremely effective to initiate appropriate fluid infusion therapy immediately after a burn and administer antithrombin III concentrate in combination with or without heparin for the prevention of acute renal insufficiency in patient with a severe burn. The effects of antithrombin III concentrate when used clinically were also discussed.
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PMID:[Alteration in coagulation and fibrinolysis after burn injury and significance of anticoagulation therapy using heparin and antithrombin III concentrate]. 381 36

The process of adaptation for extrauterine life can be easily disturbed by respiratory insufficiency. The surfactant deficiency as well as anatomical and physiological immaturity of a newborn can be considered as etiological factors in some diseases, such as respiratory distress syndrome (RDS), transient tachypnoea (TT) syndrome, segmental atelectasis or pneumonia complicated by atelectasis. The widespread used method of treatment is based on mechanical increase of difference between alveolar and atmospheric pressure. So-called constant distending pressure (CDP) increases functional residual capacity (FRC), keeps alveoli open and finally increases oxygenation of arterial blood. During 3 years period continuous positive airway pressure by nasal route (n-CPAP) was used as only one method in 26 newborns. The newborns were treated because of RDS (15 cases) and pneumonia with atelectasis (11 cases). n-CPAP was starting with pressure 8 cm H2O (0.8 kPa) and FIO2 0.5, if atelectasis with severe dyspnea, hypoxia and forced hyperventilation were found. This method was very well tolerated. 22 newborns treated for 2-7 days--survived, 4 small-for-date babies--died. The most common cause of death was septicaemia complicated by disseminated intravascular coagulation. The moderate hyperbilirubinemia, oliguria with tissue oedema was observed in many cases. The light nostril decubitus were only complications. No pneumothorax was detected. We found n-CPAP as a simple, safe method in treatment of atelectasis in newborns.
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PMID:[Continuous positive pressure respiration by nasal route (n-CPAP) as a preferred treatment method in various types of acute respiratory insufficiency in newborn infants]. 637 92

The renal venous thrombosis is mostly produced by severe dehydration. The following, however, are also predisposing factors: infections, birth traumata, paranephritic processes, lack of oxygen, diabetes of the mother and cyanotic heart defects. The diagnosis is correctly made by means of the palpable flank tumor, the macrohematuria, together with the urogram and sonography. The most urgent therapeutic measure is the balancing of the water and electrolyte deficit to eliminate the dehydration, i.e. the existing oliguria or anuria. The therapy is primarily always conservative. In the event of a consumption coagulopathy, a therapeutical attempt can be undertaken with heparin but if this is unsuccessful, an immediate nephrectomy must be performed. A further nephrectomy will be necessary if hypertony persistent infection and renal atrophy occur. Two infants with renal venous thrombosis were used for this study on the causes and diagnosis of, and the therapy for the illness.
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PMID:[Renal venous thrombosis in the newborn (author's transl)]. 746 39

The maternal mortality rate associated with eclampsia ranges from 100 to 6000 per 100,000, and the perinatal mortality rate ranges from 150 to 400 per 1000. Both eclampsia and its preceding condition, pregnancy-induced hypertension, occur in varying degrees in different parts of India. The warning signs of imminent eclampsia are 1) systolic blood pressure of 160 mmHg or more on two occasions six hours apart when the patient is on bed rest; 2) proteinuria of 5 g or more in 24 hours or 3 + or more by semiquantitative assay; 3) oliguria or anuria; 4) cerebral or visual disturbances; 5) pulmonary edema or cyanosis; and 6) epigastric/right hypochondriac pain, impaired liver function, and thrombocytopenia and coagulation disorders. Eclampsia is classified as the acute fulminating type, which can occur without warning, and the insidious type. Most cases (61%) show onset of eclampsia during the prenatal period. Treatment of eclampsia involves 1) control of convulsions (through an injection of magnesium sulphate or diazepam or the intravenous administration of phenytoin); 2) correction of hypoxia and acidosis; 3) a gradual lowering of blood pressure with hydralazine hydrochloride, nifedipine, atenolol, labetalol, oxprenolol, or metoprolol); and 4) steps to effect delivery. Diagnosis of HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) requires a complete blood count, blood film for platelet count and red blood cell fragmentation, and a coagulation screen for diagnosis of disseminated intravascular coagulation. Efforts to induce delivery in cases of prenatal eclampsia can take place 12-24 hours after convulsions have stopped. There is no reason to prolong pregnancy in the interests of the fetus, and in some cases Cesarean section may be required. Adequate prenatal care should allow the identification of almost every potential case of eclampsia and allow the prompt treatment of pre-eclampsia or termination of pregnancy when necessary. Medical staff must receive proper training to diagnose pre-eclampsia and treat the condition.
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PMID:Eclampsia. 765 39

In a retrospective study we analyzed the clinical and blood chemical data of 12 patients with severe tropical malaria in the intensive care units of the University Hospital Zurich and the Stadtspital Triemli, Zurich, between 1991 and 1994. None of the 12 patients had been exposed to malaria before or had taken drugs for chemoprophylaxis. 7 patients survived, 5 died from complications of malaria. According to the criteria of severe tropical malaria defined by the WHO, the following pathological clinical and blood chemical parameters were noted on admission: cerebral coma (2/12); blood hemoglobin < 5 g/dl (0/12), < 8 g/dl (2/12); serum creatinine > 265 mumol/l (3/12); blood glucose < 2.2 mmol/l (0.12); circulatory collapse/shock (0/12); bleeding/signs of disseminated intravascular coagulation in laboratory tests (4/12); acidosis with pH < 7.25 (1/12). Further signs of severe tropical malaria were: hyperparasitemia > 5% (9/12); qualitative and quantitative disturbances of consciousness (6/12); thrombocytopenia < 30 x 10(9)/l (9/12); hyponatremia 125-135 mmol/l (9/12), < 125 mmol/l (2/12); rhabdomyolysis with creatine kinase > 1000 U/l (4/12). The basic treatment consisted of parenteral quinine hydrochloride in all patients; doxycycline was added in 8 cases, clindamycin in 3. Adjuvant therapy with desferrioxamin was given in 3 cases. 6 patients had exchange transfusions. Parasitemia cleared in all patients within 5 to 6 days. Later in the course, 5 patients developed acute respiratory distress syndrome, 6 required hemofiltration due to oliguria, and one became comatose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intensive care aspects in severe tropical malaria: clinical aspects, therapy and prognostic factors]. 777 Jul 59

Hemolytic uremic syndrome (HUS) is defined as microangiopathic hemolytic anemia, thrombocytopenia and uremia. It is an important cause of acute renal failure (ARF) in children all over the world. The present study was carried out to assess the incidence, clinical presentation, hematological and biochemical profile of children presenting with HUS from 1987 to 1990. Out of the 100 cases who presented with ARF 22 had HUS. A majority of these children were males below 1 year of age, and had a prodromal phase of mainly gastrointestinal manifestations lasting for about a week. Anemia was a constant feature followed by bleeding diathesis, mainly melena and purpura. Neurological manifestations included altered sensorium, irritability, coma, hypertensive encephalopathy and convulsions. Renal problems mainly included oliguria, hypertension, hematuria and edema. Investigations revealed thrombocytopenia and microangiopathic hemolytic anemia in all cases. Evidence of disseminated intravascular coagulation (DIC) was observed in 3 cases as decreased fibrinogen levels, increased fibrinogen degradation products and deranged clotting studies. Blood biochemistry revealed azotemia in all cases, hyponatremia in 5 cases, hypernatremia in 3 cases and hyperkalemia in 12 cases. Stool culture showed the presence of Shigella in 8, E. coli in 6 and Klebsiella in 4 cases. Out of 22 cases of HUS, 15 were treated conservatively; of these 2 died. Both of these deaths were due to DIC 7 children were put on peritoneal dialysis; only 1 child died in this group. Factors affecting the outcome were duration of oliguria, levels of blood urea and presence of encephalopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A clinico-hematological profile of hemolytic-uremic syndrome. 788 99

A 44-year-old Spanish woman travelled in Kenya without doing correct malarial prophylaxis. Upon her return to Spain, she suffered from Plasmodium falciparum malaria. She was initially treated with chloroquine for three days, but her state worsened and she was admitted to our intensive care unit. On admission, parasitaemia was 22%. She had hyperpyrexia, obtundation, hypotension, tachycardia, tachypnoea, jaundice, digestive haemorrhage, petechiae in her soles, oliguria with elevation of serum uraemia and creatinine, anaemia, thrombocytopaenia, hypoproteinaemia, hyponatraemia, hypocalcaemia, metabolic acidosis and parameters of disseminated intravascular coagulation. She was given quinine, sulfadoxine-pyrimethamine and clindamycin. An exchange transfusion was performed, during which an acute pulmonary oedema appeared, initially with high pulmonary artery wedge pressure. She required mechanical ventilation for 16 days and haemodialysis for 11 days. She remained in coma and had seizures which required diazepam, phenitoin and thiopentone. She received a total amount of 22 units of packed erythrocytes, 55 of platelets and 15 of plasma. After the first week, she had nosocomial infection due to Escherichia coli, Staphylococcus and Pseudomonas aeruginosa and was treated with the corresponding antibiotics. She cured completely. This case report gives us the possibility of discussing on frequent problems in the prevention and treatment of malaria, and on the treatment of severe, life-threatening malaria in the setting of the intensive care unit.
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PMID:[Multiple organ failure in Plasmodium falciparum malaria]. 853 25


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