Cases reported "Cerebral Hemorrhage"

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1/76. Fatal haemorrhagic infarct in an infant with homocystinuria.

    Thrombotic and thromboembolic complications are the main causes of morbidity and mortality in patients with homocystinuria. However, it is unusual for thrombosis and infarction to be the presenting feature leading to investigation for homocystinuria and cerebrovascular lesions in the first year of life. We describe a previously healthy 6-month-old infant who presented with a large middle-cerebral-artery territory infarction and died of massive brain swelling. homocystinuria due to cystathionine beta-synthase (CBS) deficiency was diagnosed by metabolite analysis and confirmed by enzymatic activity measurement in a postmortem liver biopsy. homocystinuria should be considered in the differential diagnosis of venous or arterial thrombosis, regardless of age, even in the absence of other common features of the disease. We recommend systematic metabolic screening for hyperhomocysteinemia in any child presenting with vascular lesions or premature thromboembolism.
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2/76. Late-form hemorrhagic disease of the newborn: a fatal case report with illustration of investigations that may assist in avoiding the mistaken diagnosis of child abuse.

    Hemorrhagic disease of the newborn (HDN) is usually a self-limiting hemorrhagic disorder of childhood that occurs as a result of vitamin k deficiency. It may be defined as early or late form depending on the time of onset related to birth. HDN is recognized as one of several bleeding disorders that can mimic the findings of nonaccidental head injury and may lead to a mistaken diagnosis of child abuse. We present a single fatal case of late-onset HDN with illustration of hematologic assays that can be performed to assist the pathologist in making the correct diagnosis of HDN.
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3/76. Intracranial haemorrhage due to factor v deficiency.

    factor v deficiency is a rare coagulation disorder which is inherited autosomal recessively. factor v deficiency should be considered in infants with bleeding disorders and prolonged prothrombin and activated partial thromboplastin times if bleeding continues in spite of vitamin K injection. In this article, the case of an infant with an intracranial haemorrhage due to congenital factor v deficiency is reported.
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4/76. Intracranial haemorrhage due to vitamin k deficiency following gastroenteritis in an infant.

    Breastfed infants who are not given supplemental vitamin K after birth may develop vitamin k deficiency following gastroenteritis. Severe intracranial haemorrhage may occur.
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5/76. Intracranial hemorrhage in an infant owing to vitamin k deficiency despite prophylaxis.

    A 3-month-old male infant with intracranial hemorrhage attributable to a vitamin K deficiency is reported. Vitamin K2 was administered orally at birth and then at 5 days and I month of age. Oral antibiotics were also given 2 days before the onset of bleeding. Although the incidence of intracranial hemorrhage resulting from vitamin k deficiency has decreased since the introduction of vitamin K2 prophylaxis, spontaneous intracranial hemorrhages are still being reported in infants. We suggest that vitamin K prophylaxis is needed especially for breast-fed infants and for those undergoing antibiotic therapy.
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6/76. coccidioidomycosis meningitis with massive dural and cerebral venous thrombosis and tissue arthroconidia.

    To our knowledge we report the first case of meningitis from coccidioides immitis associated with massive dural and cerebral venous thrombosis and with mycelial forms of the organism in brain tissue. The patient was a 43-year-old man with late-stage acquired immunodeficiency syndrome (AIDS) whose premortem and postmortem cultures confirmed C immitis as the only central nervous system pathogenic organism. death was attributable to multiple hemorrhagic venous infarctions with cerebral edema and herniation. Although phlebitis has been noted parenthetically to occur in C immitis meningitis in the past, it has been overshadowed by the arteritic complications of the disease. This patient's severe C immitis ventriculitis with adjacent venulitis appeared to be the cause of the widespread venous thrombosis. AIDS-related coagulation defects may have contributed to his thrombotic tendency.
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7/76. Spontaneous epidural hematoma following a shunt in an infant with congenital factor x deficiency. Case report and literature review.

    The authors describe a case of an infant with congenital factor x deficiency. The patient presented with a central nervous system hemorrhage followed by hydrocephalus. He underwent a ventriculoperitoneal shunt and, during the postoperative period, developed a spontaneous epidural hematoma, which was evacuated. The clinical and pathophysiological aspects of this case are discussed based on a literature review.
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8/76. factor xi deficiency-related spontaneous primary intraventricular hemorrhage.

    factor xi deficiency (plasma thromboplastin antecedent deficiency) is a rare autosomal-dominant disorder. Neurologic complications in factor xi deficiency are even rarer. We propose that the factor xi deficiency in our patient contributed to a primary intraventricular hemorrhage.
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9/76. Isolated factor vii deficiency diagnosed after a life-threatening brain haemorrhage.

    A 65-year-old man was admitted to another hospital with a life-threatening brain haemorrhage, and laboratory examinations on admission revealed prolonged prothrombin time with normal activated partial thromboplastin time. To establish the cause of his abnormal coagulation, he was referred to our clinic. Neither the patient nor his family had any previous history of bleeding symptoms. His liver function was within normal limits but coagulation tests showed increased plasma activities of factors II, VIII, IX, X, with reduced activities of factors V and VII. The activity of factor VII was less than 2% but no inhibitor of factor VII was detected in the plasma. We concluded that the patient had a rare congenital isolated factor vii deficiency although he had not shown earlier bleeding problems, presumably because of compensation for the factor vii deficiency by enhanced activities of components of the extrinsic coagulation pathway, factors II, VIII, IX and X.
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ranking = 6
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10/76. Intracerebral hemorrhage associated with a novel antithrombin gene mutation in a neonate.

    Fatal cerebral hemorrhage involving the left thalamus in a neonate was attributed to deep cerebral vein thrombosis. Although antithrombin levels were at the lower end of the normal range, family and genetic studies showed constitutional type I antithrombin deficiency related to a novel missense mutation in the antithrombin gene.
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