Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

22 patients with severe preeclampsia-eclampsia were treated in our Intensive Care Unit from 1972 to 1978. Control of convulsions was achieved by diazepam, diphenylhydantoin and phenobarbital. In 11 comatose patients brain monitoring was carried out by frequent neurological examination and use of computerized x-ray tomography; aspiration of gastric contents was prevented by nasotracheal intubation. Brain oedema therapy included controlled hyperventilation, steroids and mannitol (7 patients). 10 patients with respiratory failure (due to pulmonary oedema, "shock lung" or aspiration pneumonitis) were treated by mechanical ventilation. Diastolic blood pressure above 100 mm Hg was reduced by hydralazine. Diuresis was induced by normalization of hypovolaemia with albumin and plasma expanders. Six patients died (27%); main causes of death included intracerebral haemorrhage, brain oedema, heart failure, acute pulmonary thromboembolism and bleeding from DIC.
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PMID:[Intensive care of severe preeclampsia-eclampsia. A report on 22 cases (author's transl)]. 742 60

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

A retrospective study of 42 newborns who were admitted to the Hospital Universiti Sains Malaysia for spontaneous bleeding and prolonged prothrombin and partial thromboplastin times during 1987-1988 was conducted to determine the epidemiology, clinical features, laboratory findings, treatment, and outcome of hemorrhagic disease of the newborn (HDN). The infants came from households in the rural state of Kelantan. In Kelantan, the estimated overall annual incidence of severe HDN was 1/1900 live births. None of the infants had bleeding due to inherited coagulopathy or disseminated intravascular coagulation. The categories of HDN were classical HDN (48%), early onset HND (29%), and late onset HND (24%). The most frequent clinical manifestations of HDN were pallor, jaundice, umbilical cord bleeding, tense fontanelle, convulsions, and hepatomegaly. 81% of the infants were delivered at home. Only 7 infants received vitamin K at birth. Anemia was common, especially in cases with massive intracranial bleeds. Most intracranial hemorrhages were subdural hemorrhages. The mothers of all infants, except one, breast fed. All infants received intravenous vitamin K at an initial dose of 1-5 mg/daily, which returned the prolonged prothrombin time and partial prothrombin time to normal. 33 infants recovered completely. One infant with classical HDN was mentally retarded and had hydrocephalus. Another infant also with classical HDN was mentally retarded. The overall case fatality rate was 14%. The case fatality rate for late HDN was 30%. These findings stress the importance of vitamin K prophylaxis in the newborn.
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PMID:Haemorrhagic disease in newborn and older infants: a study in hospitalized children in Kelantan, Malaysia. 782 97

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 study of 10 fatal cases of amniotic fluid embolism, confirmed by autopsy and post-mortem histological examination, that occurred in Singapore between 1983-1992, showed that the majority (9 cases) were multiparous, with between 2-4 previous normal pregnancies each. Seven had uneventful antenatal histories. In all cases, the clinical onset was sudden and unexpected, having occurred during the first stage of labour in 8 subjects and being associated with convulsions in 5. There were seven cases of coagulopathy, with 6 of disseminated intravascular coagulation. Overall, foetal survival was poor. Three cases were associated with induction of labour, while another 3 occurred after augmentation. Emergency caesarean sections were performed in 5 cases. Autopsy demonstrated moderate to severe pulmonary oedema in 9 cases, accompanied by pulmonary haemorrhage in 6. Mild coronary atheroma was present in 6 cases, with 3 showing subendocardial haemorrhage. Significant utero-cervical ruptures or lacerations were found in 3 cases. Microscopy demonstrated the presence of squamous epithelial emboli within the pulmonary vasculature in all cases. Other histological features included fibrin microthrombi (3 cases), alveolar and pulmonary interstitial inflammation, focal myocardial and hepatocellular necrosis, and myocardial interstitial inflammation. Although the precise pathogenesis of amniotic fluid embolism has remained somewhat enigmatic, recent evidence points towards a combination of a severe haemodynamic disturbance followed by secondary coagulopathy in about 40% of patients who survive the initial event. Leucotrienes, prostaglandins and other vasoactive substances contained in amniotic fluid are postulated to play a fundamental role in its pathogenesis. Amniotic fluid is also thought to possess thromboplastin-like properties.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amniotic fluid embolism: a review of 10 fatal cases. 793 17

Fifty-seven cases of meningococcemia were evaluated retrospectively. The age of the patients ranged between 2 and 17 years. Of the 57 patients investigated for the efficacy of antibiotic treatment, 31 (54.4%) were treated with benzylpenicillin plus chloramphenicol and 26 (45.6%) with ampicillin plus sulbactam. Patients with criteria for a poor prognosis (presence of disseminated intravascular coagulation, low arterial blood pressure, and altered consciousness) were divided equally into two treatment groups. There were no statistically significant differences between the two treatment groups except for the higher incidence of convulsion in the group given penicillin plus chloramphenicol. The mortality rate was 19.3 percent for patients treated with benzylpenicillin plus chloramphenicol and 7.6 percent for patients treated with ampicillin plus sulbactam (p = 0.19; overall mortality rate 14%).
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PMID:Comparative therapeutic results of penicillin plus chloramphenicol versus ampicillin plus sulbactam in childhood meningococcemia. 824 99

A case of sinus thrombosis occurring during combination chemotherapy with CDDP and VP-16 (PE) for a suprasellar germ-cell tumor is presented. A 5-year-old girl developed polyuria, polydipsia and headache in April, 1991 and became unconscious on May 10, 1991, when MRI and CT demonstrated a suprasellar tumor and marked hydrocephalus. After a ventriculo-peritoneal shunt operation, radiotherapy and two courses of PE therapy were carried out. During the second course of PE therapy, diabetes insipidus became quite difficult to control and severe hypovolemic hypernatremia developed. While it was being treated, the patient developed a clonic convulsion of her left extremities and visual disturbance. CT scan demonstrated a right parietal hemorrhagic infarction and IV-DSA suggested thrombosis of the superior sagittal sinus. Laboratory data disclosed DIC. The main cause of sinus thrombosis in this patient was considered severe dehydration. It is also possible that cisplatin and steroid played a role. In addition to these, dysfunction of hypothalamus, which is one of the regulatory centers of the plasma concentration of factor VIII, may have contributed to the acceleration of blood coagulation. This case re-emphasized the importance of preventing dehydration and monitoring the blood coagulation fibrinolytic system during PE therapy in patients with a suprasellar germ-cell tumor accompanied with diabetes insipidus.
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PMID:[Sinus thrombosis during CDDP and VP-16 (PE) therapy for suprasellar germ-cell tumor: case report]. 825 77

Antidepressant drugs are among the most commonly encountered causes of self-poisoning. These drugs include tricyclics, tetracyclics, bicyclics and monocyclics, as well as monoamine oxidase (MAO) inhibitors and selective serotonin reuptake inhibitors (SSRIs). Of these, the tricyclic antidepressants (TCAs) are generally more toxic in overdose, with major toxicity usually manifesting within the first 6 hours after overdose. Various studies indicate that patients at risk of toxicity from TCA overdose may be identified by neurological, cardiovascular and electrocardiography status, together with a quantitative estimate of the plasma drug concentration. While there are various methods available for such chemical estimations, the most satisfactory appears to be fluorescence polarisation immunoassay which gives rapid quantitative results for a variety of TCAs. The selective MAO-A inhibitor antidepressants and the SSRIs are relatively nontoxic when taken alone. However, overdoses of combinations of MAO inhibitors and either SSRIs or TCAs with serotonin reuptake blocking activity may result in a serotonin syndrome with a severe or fatal outcome. Features of this syndrome include hyperpyrexia, disseminated intravascular coagulation, convulsions, coma and muscle rigidity, which may not develop until 6 to 12 hours after overdose. While quantitative chemical identification of these drugs following overdose is helpful in confirming the diagnosis, it is not mandatory. The increasing use of MAO-A inhibitors and SSRIs in the treatment of depression suggests that careful clinical observation is required when combination overdoses are suspected.
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PMID:Antidepressant toxicity and the need for identification and concentration monitoring in overdose. 852 78

Reported is a case of hemorrhagic shock and encephalopathy syndrome (HSE) with extensive white matter involvement. A three year old, previously healthy boy was presented with an acute onset of fever, loss of consciousness and convulsions. He had disseminated intravascular coagulation, metabolic acidosis, non-ketotic hypoglycemia and hepatorenal dysfunction. The computed tomography (CT) scan of his head on the second day of illness demonstrated symmetric, extensive low-density areas in the cerebral and cerebellar white matter. The child died on the 13th hospital day. A post-mortem histopathological examination of the liver revealed centrilobular necrosis and infiltration of fatty acid droplets. The concentrations of serum 2',5'-oligoadenylate synthetase and urinary neopterin were markedly elevated, indicating excessively activated cell-mediated immunity. This overproduction of inflammatory cytokines might play an important role in the pathogenesis of the brain lesion as well as in other clinical and laboratory manifestations. The patient had a decreased serum level of alpha l-antitrypsin, which may have been associated with the development of uncontrolled inflammation and coagulation disorder.
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PMID:Extensive white matter involvement in hemorrhagic shock and encephalopathy syndrome. 874 21

During a 3-year period, 6 of 50 children with systemic malignacies developed neurologic complications such as hemiparesis, convulsions and loss of consciousness. The children consisted of 1 boy and 5 girls, from 3 to 12 years old, 3 with acute lymphoblastic leukemia and 3 with malignant lymphoma. Four patients received induction treatment that included intravenous administration of L-asparaginase and/or intrathecal administration of methotrexate. One patient received induction treatment and consolidation treatment that included intravenous administration of L-asparaginase. One patient received induction and consolidation treatment, and the protocol for peripheral blood stem cell transplantation. Laboratory examinations revealed coagulation dysfunction in 3 patients treated with L-asparaginase and 1 patient with disseminated intravascular coagulation (DIC). Magnetic resonance imaging (MRI) was performed on a 1.5-T unit, using spin-echo or fast spin-echo sequences. T1-weighted, T2-weighted, and proton density-weighted images were obtained in the axial and/or coronal plane (section thickness, 4 mm; inter-section gap, 2 mm). MRI was initially performed within 36 hours after the onset in all patients, and follow-up MRIs were performed for 6 months. MRI showed lesions involving the cortex and subcortex in 4 patients with coagulation dysfunction. In 2 of these 4 patients, Gd-enhanced T1-weighted images showed contrast enhancement in the surface of the gyrus, suggesting focal vascular stasis. Serial MRI revealed nearly complete resolution of the lesions. Symptoms were relieved in every case. The lesions on MRI were presumed to be due to venous thrombosis related to the coagulation dysfunction caused by L-asparaginase or DIC. On the other hand, in 2 patients with onset after intrathecal administration of high-dose methotrexate and cytarabine, MRI revealed multiple lesions involving the centrum semiovale and periventricular white matter. No Gd-enhancement of the lesion was detected. This MRI finding was consistent with leukoencephalopathy. As time passed, the symptoms improved completely, and the lesions became better demarcated. MRI is useful for differentiating lesions related to coagulation dysfunction from leukoencephalopathy.
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PMID:[MRI abnormalities of the brain in neurologic complications following treatment of cancer in children]. 875 96


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