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

In 18 cases of perinatal intraventricular haemorrhage, continuous ventricular drainage was applied. As a result, ICP hypertension was inhibited and thus brain damage prevented. The early intervention prevented the formation of hydrocephalus (evoidence of shunt dependence) and aspiration of the bleeding prevented DIC and maintained coagulation factors.
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PMID:Successful treatment of perinatal intraventricular haemorrhage. 54 18

A comparative investigation of the pathogenetic factor in symptomatic cerebral vasospasm was made by quantitative histological and clinical studies in four patients who died immediately of symptomatic cerebral vasospasm (Cases 1-4) and in two who died without fatal cerebral vasospasm (Cases 5 and 6). Histological examination of the brain from Cases 1 and 2 found many white and fibrin microthrombi together with ischemic and infarctic changes in the territories of spastic arteries, which corresponded to the low-density areas (LDAs) observed on computed tomographic (CT) scans and the typical neurological symptoms. In Case 3, who had suffered severe vasospasms in bilateral anterior cerebral and middle cerebral arteries, bilateral LDAs were observed on CT scans and multiple fibrin thrombi were seen diffusely throughout the brain. In Case 4, extensive bilateral LDAs (lt greater than rt) were observed on CT scans, and multiple microthrombi were seen diffusely but predominantly in the left cerebral hemisphere. Only in Case 3 the possible complication of disseminated intravascular coagulation could not be ruled out. Only negligible thrombi were observed in Cases 5 and 6, whose immediate cause of death was considered to be acute hydrocephalus and aneurysmal rerupture, respectively. Distributions of microthrombi were significantly greater in the regions clinically identified to have been ischemic or infarctic.
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PMID:Cerebral microthrombosis in symptomatic cerebral vasospasm--a quantitative histological study in autopsy cases. 169 46

Vitamin K deficient hemorrhagic diathesis is well known as a cause of infantile intracranial hemorrhage. Its occurrence, however, as a post-surgical complication is rare and has never been reported previously. Two cases are presented here which illustrate the existence of such a hazard. Case 1. A 73-year-old woman admitted with subarachnoid hemorrhage (WFNS IV) underwent microsurgical exploration of a left internal carotid aneurysm, and neck clipping of the aneurysm was performed. She had an uneventful postoperative course, but her neurological condition deteriorated suddenly on the fifth postoperative day. CT scan revealed a large epidural hematoma. Case 2. A 6-year-old boy was admitted due to the dysfunction of a ventriculo-peritoneal shunt system that had previously been placed for hydrocephalus. This dysfunction was thought to be caused by meningitis. Twelve days after ventricular drainage and antibiotic therapy, sudden intraventricular hemorrhage occurred. In both cases, PT and APTT were markedly prolonged, FDP slightly increased and fibrinogen slightly decreased. SFMC was positive in case 2. After the administration of vitamin K, PT and APTT were immediately normalized. Recent reports emphasize the adverse effect of antibiotics that leads to vitamin K deficient hemorrhagic diathesis, especially, in patients in a cachectic state. In these two cases, such a cachectic condition was not observed. We presume that the cause of vitamin K deficiency would be, along with the administration of antibiotics, a preliminary condition of disseminated intravascular coagulation which is encountered in some neurological disorders including subarachnoid hemorrhage. We conclude that attention should be paid for these pitfalls in perioperative neurosurgical care.
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PMID:[Postoperative intracranial hemorrhage due to vitamin K deficiency: report of two cases]. 173 30

At the Kiel University Department of Gynaecology, 21 patients between the 21th and 39th week of gestation were treated in 1987 and 1988 following diagnosis of HELLP syndrome. At the time of diagnosis all patients presented an advanced gestosis/eclampsia. 9 patients developed the classical signs and symptoms, while hospitalised. The typical signs of gestosis, hypertension, proteinurea, oedema and hypoproteinaemia preceded the changes in laboratory values caused by the HELLP syndrome. Upper abdominal pain and increase in transaminase values occurred on the average 3.4 or 2.7 days prior to the decrease of, thrombocyte count. In 19 of the 21 cases, pregnancy was terminated by caesarean section. Severe peripartal complications occurred in 7 cases e.g. foetal death in utero (n = 3), eclampsia (n = 5), renal failure (n = 2), cerebral oedema (n = 1), intracerebral haemorrhage (n = 1), disseminated intravascular coagulation (n = 1), abdominal wall haematoma (n = 1). 6 of these patients were admitted after complications had occurred prior to admittance. All 18 infants born alive survived the neonatal period. The average birth weight was 1,571 g. 11 infants were discharged clinically normal. The remaining infants included 5 cases pointing to retinopathy and 3 cases of cerebral palsy. One infant developed post-haemorrhagic hydrocephalus.
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PMID:[Development of symptoms and perinatal complications in HELLP syndrome]. 177 22

Localized suppuration involving the spinal cord is uncommon. A case of spinal subdural empyema is reported. The patient is 54-year-old male who had been suffering a diabetes mellitus but did not receive any treatment. His initial symptom was lumbago. Then he noticed a palpitation and general malaise which made him visit a hospital. Because he did not show any improvement by a fluid therapy, he was transferred to our institute for the further evaluation. On admission, physical examination showed no abnormality. Blood pressure was 170/90 mmHg, heart rate 128/min. and body temperature 37.1 degrees C suggesting a septic shock state. Neurological examination revealed slight consciousness disturbance, mild tetraparesis and bilateral hypesthesia lower than the level of L3. Laboratory examination showed the elevated leukocyte count and fasting blood sugar and urine ketone body levels of 20,500/mm3, 257 mg/dl and 226 mg/dl respectively. Blood culture proved a septicemia of Streptococcus agalactiae afterwards. On the second day of admission, lumbar puncture revealed a purulent cerebrospinal fluid, though X-ray CT of lumbar spine did not confirm a diagnosis. Spinal magnetic resonance imaging (MRI) revealed a widespread abnormal intensity of the spinal canal from the level of Th11 to L4. On the T1-weighted image (TR 300 msec., TE 40 msec.), cerebrospinal fluid space was abnormally isointense. On the T2-weighted image (TR 2,000 msec., TE 80 msec.), subdural and cerebrospinal space was filled with an abnormal high-intense lesion especially on the ventral side. He developed semicoma due to hydrocephalus following a intraventricular empyema. He was also complicated disseminated intravascular coagulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Spinal subdural empyema diagnosed by MRI and recovered by conservative treatment]. 257 46

Diffuse neonatal hemangiomatosis is an often fatal disorder characterized by widespread capillary hemangiomas of the skin and visceral organs. Ultrasound and computed tomographic scans may be useful in determining the extent of visceral disease. The organs most commonly affected are the gastrointestinal tract, brain, liver, and lung. Complications include high-output cardiac failure, gastrointestinal bleeding, hydrocephalus, and consumption coagulopathy. Despite therapy with corticosteroids, the mortality rate is high.
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PMID:Diffuse neonatal hemangiomatosis. 395 31

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

Cerebellar infarcts have been neglected for a long time and are now shown well by CT and especially MRI. Some infarcts involve the full territory supplied by a cerebellar artery. They are frequently complicated by edema with brain stem compression and supratentorial hydrocephalus, requiring at times emergency surgery, and are often accompanied by other medullary, medial pontine, mesencephalic, thalamic and occipital infarcts. On the other hand, partial territory infarcts are usually confined to the cerebellum and have a benign outcome with total recovery or minimal disability. They are more common than full territory infarcts. However, clinical presentations are similar to those full territory infarcts, differing mainly by the lack of drowsiness or unconsciousness. The main symptoms are vertigo, headache, vomiting, unsteadiness of gait and dysarthria. Signs include ipsilateral limb dysmetria, ipsilateral axial lateropulsion, ataxia and dysarthria. Vertigo is more severe and rotary in posterior inferior cerebellar artery territory infarcts, whereas dysarthria and ataxia are prominent in superior cerebellar artery territory infarcts. A few brain stem signs are sometimes added. In these territorial cerebellar infarcts, cardioembolism is the most common cause. Atherosclerotic occlusion comes next, involving the intracranial part of the vertebral artery and, less frequently, the lower basilar artery, both locations inaccessible to surgery. Other causes are artery to artery embolism from a vertebral artery origin stenosis, or the aortic arch, in situ intracranial branch atherosclerotic occlusion, and vertebral artery dissection. Border zone cerebellar infarcts occur in one third of the cases. They are small cortical or deep infarcts. They have the same symptoms and signs as territorial infarcts except for more frequent postural symptoms occurring over days, weeks or months after the ischemic event. The infarcts mainly have a thromboembolic mechanism, and sometimes have a hemodynamic mechanism: 1) focal cerebellar hypoperfusion due to large artery occlusive disease in more than half the cases, 2) small or end (pial) artery disease due to hypercoagulable state (thrombocythemia, polycythemia, hypereosinophilia, disseminated intravascular coagulation), arteritis or intracranial atheroma, and 3) rarely systemic hypotension due to cardiac arrest.
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PMID:[Cerebellar infarctions and their mechanisms]. 809 Oct 85

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

Kasabach-Merritt syndrome is characterized by thrombocytopenia and bleeding tendency leading to disseminated intravascular coagulation with giant hemangiomas. We present a very low birth weight infant with this syndrome who underwent four operations. A male baby (1179 g, 37 cm) was born at a gestational age of 28 weeks and 6 days by caesarean section. A large hemangioma, 7 x 8 cm in size, was recognized on the left thigh. As associated consumption coagulopathy (Kasabach-Merritt syndrome) was diagnosed with platelet count 5.1 +/- 10(4) mm-3 and fibrinogen 49 mg.dl-1. Despite treatment with liniac X-ray radiation, systemic steroid and component transfusion, coagulopathy became worse with extremely low platelet count of 1.1 x 10(4) mm-3. Infusion of dopamine and dobutamine was necessary for high output cardiac failure. On day 9, PDA ligation was performed. Cerebro-ventricular drainage, ventricuro-peritoneal shunt and shunt revision were required on day 15, 49 and 88, respectively, for hydrocephalus due to intraventricular hemorrhage. Main anesthetics used were fentanyl and sevoflurane. Major problems encountered by anesthetists were: bleeding tendency, water and electrolyte management, body temperature control, and immaturity and fragility of premature infant. Coagulopathy in Kasabach-Merritt syndrome must be a risk factor for intraventricular hemorrhage, which is a characteristic complication of a very low birth weight infant.
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PMID:[Anesthetic problems in a very low birth weight infant with Kasabach-Merritt syndrome]. 881 2


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