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11/57. Early acenocoumarol overanticoagulation among cytochrome P450 2C9 poor metabolizers.

    Cytochrome P450 2C9 (CYP2C9) is the enzyme that terminates the anticoagulant effect of warfarin. The heterozygous carriers of the two allelic variants CYP2C9*2 and CYP2C9*3 have been associated with impaired warfarin metabolism and a higher risk of haemorrhage. Only three CYP2C9 poor metabolizers (CYP2C9*3/CYP2C9*3) initiating warfarin treatment have so far been identified, all of them with a dramatic overdose occurring a few days after treatment initiation. acenocoumarol, another coumarinic anticoagulant, has recently been shown to be metabolized by CYP2C9. We report, for the first time, two cases of dramatic overanticoagulation occurring in patients starting acenocoumarol treatment while taking recommended doses (4 mg/day). In both cases, the overdose was discovered at the first INR control with values above 9. Genotyping revealed that the two patients were homozygous for the CYP2C9*3 allele. Our report highlights the need for CYP2C9 genotyping before starting oral anticoagulants in order to prevent early overanticoagulation episodes.
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ranking = 1
keywords = haemorrhage
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12/57. Spontaneous haematoma of the iliac psoas muscle: a case report and review of the literature.

    Spontaneous haematomas of the iliac psoas muscle are rare lesions seen in patients receiving anticoagulant agents or suffering from clotting disorders. We report the rare case of a spontaneous iliac psoas haematoma causing femoral neuropathy in a patient not undergoing anticoagulant treatment or suffering from a coagulopathy. After conservative treatment the patient was entirely asymptomatic, and magnetic resonance imaging demonstrated complete dissolution of the haematoma. Spontaneous iliac psoas haematomas should be considered in the differential diagnosis of leg pain in otherwise healthy patients.
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ranking = 0.82136819316721
keywords = haematoma
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13/57. Surgical treatment of spontaneous intracerebral hemorrhage in a full-term infant with coagulopathy--case report.

    An 11-week-old male infant presented with intracerebral hemorrhage associated with coagulopathy manifesting as left hemiparesis, lethargy, and vomiting. Computed tomography demonstrated extensive right frontoparietal intracerebral hemorrhage extending into the ventricular system. liver function tests revealed abnormal values of transaminases and bilirubin. blood coagulation studies showed prolonged prothrombin time (PT) and activated partial thromboplastin time (APPT). PT and APTT immediately normalized after the administration of vitamin K and fresh frozen plasma. Right parietal craniotomy and evacuation of the hematoma were performed because of the deterioration in consciousness and left hemiparesis. No vascular abnormality was observed in the hematoma cavity. After surgery, he became alert and the left hemiparesis improved. There is a risk of intracerebral hemorrhage due to vitamin k deficiency even if prophylactic administration of vitamin K was given. Surgical treatment should be considered for the treatment of infantile spontaneous intracerebral hemorrhage, especially if neurological deterioration is present.
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ranking = 2.290791493643
keywords = cerebral, intracerebral
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14/57. Late-onset homozygous protein c deficiency manifesting cerebral infarction as the first symptom at age 27.

    We report a 31-year-old female who had repeated thrombosis and was diagnosed as having congenital homozygous protein c deficiency based on decreased protein C antigen and activity, and the findings of family history. This patient had shown no symptom of thrombosis until the age of 27 years, when she had cerebral infarction as the first symptom. Low molecular weight heparin was useful for disseminated intravascular coagulation (DIC) that complicated protein c deficiency in this patient.
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ranking = 0.8671350818742
keywords = cerebral
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15/57. Fatal rodenticide poisoning with brodifacoum.

    The increased prevalence of rodents resistant to warfarin led to the development of the hydroxycoumarin anticoagulant brodifacoum. A 25-year-old man attempted suicide by consuming four boxes of d-CON Mouse-Prufe II; each box contains 42 g of bait that is 0.005% brodifacoum. He presented to a hospital nine days later with syncope, hematochezia, gross hematuria, epistaxis, anemia, and a severe coagulopathy. Radiographic studies were consistent with pleural, pericardial, and mediastinal hemorrhages. Vitamin K and fresh frozen plasma were given, and he was later discharged on oral phytonadione (vitamin K1). The patient's coagulopathy recurred, necessitating multiple plasma transfusions and prolonged treatment with oral phytonadione. Fifteen weeks after hospital discharge, he presented again with a history of additional brodifacoum ingestion. Neurologic status was initially normal, but in the emergency department he suddenly became comatose soon after emesis was induced with syrup of ipecac. Computed tomography of the brain revealed a subarachnoid hemorrhage that led to brain death less than 24 hours later. This case demonstrates the severe and prolonged coagulopathy that can result from ingestion of brodifacoum, a compound that has a toxic potency about 200-fold that of warfarin and a half-life as much as 60 times longer.
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ranking = 0.0022061805662158
keywords = brain
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16/57. Brain haemorrhage in five infants with coagulopathy.

    Most intracranial haemorrhages in infants after the neonatal period are secondary to non-accidental injury. Occasionally brain haemorrhages in non-mobile infants are due to an inherited coagulopathy. This may often be diagnosed with a coagulation screen on admission. Little is known about the neurological outcome of infants in the latter group. Five infants are described who presented with acute spontaneous brain haemorrhage secondary to an inherited coagulopathy (n = 3) and vitamin k deficiency in alpha(1) antitrypsin deficiency (n = 1) and Alagille's syndrome (n = 1). Despite the critical clinical presentation and the severe imaging findings, these five infants made a good neurological recovery. Infants presenting with spontaneous ICH due to a significant (inherited) coagulopathy are usually easy to differentiate from non-accidental shaking injury; their bleeding pattern within the brain seems different from non-accidental shaking injury and neurodevelopment outcome appears better.
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ranking = 7.0033092708493
keywords = haemorrhage, brain
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17/57. Management of coagulopathy with recombinant factor viia in a neonate with echovirus type 7.

    A 5-day-old newborn presented with neonatal enteroviral infection. The patient's hospital course was complicated by acute liver dysfunction, renal insufficiency, fluid overload, respiratory failure, hypertension, catheter related thrombosis, klebsiella pneumoniae sepsis, intracerebral and intraventricular hemorrhage, and disseminated intravascular coagulation (DIC). Administration of fresh frozen plasma (FFP) and cryoprecipitate failed to control the patient's hemostasis and led to significant fluid overload. Recombinant activated factor VII (rFVIIa, Novoseven NovoNordisk, Bagsvaerd, denmark) was given to the neonate as a bolus (rFVIIa at 60-80 microg/kg body weight), followed by a continuous infusion (2.5-16 microg/kg/hr). Recombinant activated factor VII controlled hemostasis, until the patient's liver function recovered. The patient's blood product requirement significantly decreased and his fluid overload resolved. Administration of rFVIIa appears to have stabilized the coagulation process. The patient appears to have fully recovered from the infection's complications.
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ranking = 0.28634893670537
keywords = cerebral, intracerebral
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18/57. Evaluation and management of transient ischemic attack and minor cerebral infarction.

    After immediate intervention for cerebral infarction or transient ischemic attack (TIA), the primary goal is secondary prevention of future cerebral ischemia and prevention of complications related to the initial ischemic event. The goals of the diagnostic evaluation are to (1) determine potential contributing mechanisms (cardioembolic, large-vessel disease of the extracranial and intracranial vessels, small-vessel disease, coagulation defects, and cryptogenic), (2) identify contributing risk factors (hypertension, hyperlipidemia, tobacco use, diabetes), and (3) complete the evaluation in a cost-effective and safe manner. We provide a sequential approach to the diagnostic evaluation of cerebral infarction or TIA to optimize diagnostic yield of testing, minimize cost and potential harm to the patient, and provide information that will change management. This systematic approach focuses on 6 important questions: (1) Are the symptoms consistent with a cerebral infarction or TIA (versus nonischemic pathology)? (2) Where does the ischemic event localize? (3) What etiologies and mechanisms of cerebral infarction and TIA are possible? (4) What is the prevalence of each potential etiology? (5) What treatments are available for this etiology? (6) What tests and studies are useful to evaluate this etiology?
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ranking = 1.5608431473736
keywords = cerebral
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19/57. Life-threatening envenoming by the Saharan horned viper (Cerastes cerastes) causing micro-angiopathic haemolysis, coagulopathy and acute renal failure: clinical cases and review.

    BACKGROUND: The desert horned vipers (Cerastes cerastes and C. gasperettii) are the most familiar snakes of the great deserts of North africa and the middle east, including the plains of iraq. They are responsible for many human snake bites. In Western countries, they are popular among exotic-snake keepers. AIM: To investigate mechanisms of life-threatening envenoming and treatment. DESIGN: Clinical investigation. methods: Clinical and laboratory studies with measurement of serum venom antigen concentrations by enzyme immunoassay. RESULTS: Two men bitten while handling captive Saharan horned vipers (Cerastes cerastes) in europe developed extensive local swelling and life-threatening systemic envenoming, characterized by coagulopathy, increased fibrinolysis, thrombocytopenia, micro-angiopathic haemolytic anaemia and acute renal failure. The clinical picture is explicable by the presence in C. cerastes venom of several thrombin-like, Factor-X-activating, platelet-aggregating, haemorrhagic and nephrotoxic components. In one case, prophylactic use of subcutaneous epinephrine may have contributed to intracranial haemorrhage. The roles in treatment of heparin (rejected) and specific antivenom (recommended) are discussed. DISCUSSION: Cerastes cerastes is capable of life-threatening envenoming in humans. Optimal treatment of envenoming is by early administration of specific antivenom, and avoidance of ineffective and potentially-dangerous ancillary methods.
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ranking = 1
keywords = haemorrhage
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20/57. cerebral infarction in young men with nephrotic syndrome.

    BACKGROUND AND PURPOSE: thrombosis is one of the main complications of nephrotic syndrome; however, cerebral infarction associated with nephrotic syndrome has been rarely reported. SUMMARY OF REPORT: We describe acute cerebral infarction in two young men with nephrotic syndrome. Both had a hypercoagulable state based on hemostatic studies. By retrospectively reviewing the medical records of the past 10 years at our hospital, we found an additional five cases of cerebral infarction with nephrotic syndrome. Two of the patients were found to have nephrotic syndrome during admission for stroke. CONCLUSIONS: Hypercoagulability may be the major contributing factor of cerebral infarction in patients with nephrotic syndrome.
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ranking = 0.69370806549936
keywords = cerebral
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