1/27. Effect of haemofiltration on pathological fibrinolysis due to severe sepsis: a case report.Bleeding due to coagulopathy is a frequent complication of severe sepsis, especially in burn patients. The primary treatment is aimed at the underlying cause but additional supportive measures, consisting mainly of coagulation factor replacement, are frequently necessary. We describe the salutary effect of continuous veno-venous haemofiltration (CVVH) with predilution on diffuse haemorrhage in a patient with severe septic shock and renal failure. The diffuse haemorrhage was initially treated with replacement of coagulation factors. prothrombin time and partial thromboplastin time became normal while diffuse bleeding continued and the thrombelastogram showed evidence of fibrinolysis. A short period of CVVH lead to the cessation of bleeding which was reflected by a normal thrombelastogram.- - - - - - - - - - ranking = 1keywords = haemorrhage (Clic here for more details about this article) |
2/27. Spontaneous inhibitors to coagulation factors.Spontaneous inhibitors to coagulation factors are autoantibodies that usually appear in the elderly, but may also occur in patients with immunological disorders such as lupus, lymphoma, asthma or drug reactions. Most antibodies are directed against factor viii, but any coagulation protein may be affected. They should be suspected in individuals who previously had normal haemostasis, but who now begin to experience bleeding into the skin and muscles, or suffer haemorrhages after routine procedures such as insertion of vascular catheters, intramuscular injections, or minor surgery. The haemostasis laboratory is critical in identifying the particular inhibitor and quantitating its potency. factor viii inhibitors prolong the partial thromboplastin time (PTT) but not the prothrombin time (PT), and incubating mixtures of patient plasma and normal plasma enhances the prolongation of the clotting time. The Bethesda assay provides a rough assessment of inhibitor potency. Inhibitors of von willebrand factor prolong the bleeding time and impair ristocetin-induced platelet aggregation. Factor V inhibitors are associated with a prolonged PTT and PT, not correctable with normal plasma. patients will often have a history of exposure to bovine thrombin in fibrin glue. The antibodies most difficult to recognize are those that alter fibrin polymerization or stabilization. Abnormal clot retraction or clot solubility in urea solutions are an important clue. The management of these disorders depends on characterization of the inhibitor, and using appropriate clotting factor concentrates to control acute bleeding. For example, recombinant human factor viii or desmopressin may be effective for patients with low titre factor viii inhibitors, whereas porcine factor viii, recombinant factor Vlla, or prothrombin complex concentrates stem bleeding in those with high titres. Inhibitors of von willebrand factor may be amenable to desmopressin, cryoprecipitate, or von willebrand factor concentrates. Some patients with factor V inhibitors have responded to platelet transfusions, as the platelet factor V may be shielded from the autoantibody. Bleeding due to factor xiii inhibitors may be managed with fibrogammin, a factor xiii concentrate. All patients should be treated for underlying disorders and given drugs such as corticosteroids and cytotoxic agents to suppress inhibitor formation. Major advances in new immunosuppressive technologies, such as monoclonal B-cell antibodies, offer hope of more effective therapies for spontaneous inhibitors to coagulation factors.- - - - - - - - - - ranking = 0.5keywords = haemorrhage (Clic here for more details about this article) |
3/27. Thrombotic formations within the aortic arch as source of embolization in patients with coagulopathia.Thrombotic formations on atherosclerotic lesions of the thoracic aorta are potential sources of cerebral and systemic embolization. Especially younger patients without calcifications of atherosclerotic plaques or coagulation disorders have a higher risk for embolization. magnetic resonance imaging and transesophageal echocardiography are the diagnostic methods of choice. As an alternative to anticoagulation surgical therapy is indicated to prevent severe brain damage or multiorgan failure in patients with mobile thrombotic formations. Herein we describe two patients in whom successful surgical treatment was performed in deep hypothermic circulatory arrest by excision of the aortic arch atheroma.- - - - - - - - - - ranking = 0.00055154514155396keywords = brain (Clic here for more details about this article) |
4/27. Coagulopathy induced spinal intradural extramedullary haematoma: report of three cases and review of the literature.In a retrospective review of patients operated for coagulopathy induced spinal intradural-extramedullary haematoma the literature regarding coagulopathy induced spinal haemorrhage is reviewed and the etiology of these rare spinal subdural and subarachnoid haemorrhages is discussed. Spinal intradural haematomas are usually related to trauma or a previous lumbar puncture. A review of the literature revealed only a handful cases of spinal intradural haemorrhages occurring secondary to an underlying haematological disorder or an iatrogenic coagulopathy. Coagulopathy induced spinal haemorrhage should be included in the differential diagnosis of acute paraparesis in patients with co-existent haematological disorders or undergoing anticoagulation therapy. Due to the often mixed subdural and subarachnoid bleeding patterns we have termed this entity spinal intradural-extramedullary haematoma.- - - - - - - - - - ranking = 2keywords = haemorrhage (Clic here for more details about this article) |
5/27. Brain involvement in haemolytic-uraemic syndrome: MRI features of coagulative necrosis.We describe radiological demonstration of brain involvement in haemolytic-uraemic syndrome (HUS) in two siblings with a very different clinical course. While the brother presented with a mild, reversible encephalopathy, his sister developed high-signal lesions in the cortex, putamen and caudate nucleus on T1-weighted images, seen as dense areas on CT. biopsy revealed coagulative necrosis due to microthrombosis without haemorrhage, calcification or infection. These findings suggest a possible prognostic role for MRI in cases of encephalopathy due to HUS.- - - - - - - - - - ranking = 0.50055154514155keywords = haemorrhage, brain (Clic here for more details about this article) |
6/27. 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.- - - - - - - - - - ranking = 0.5keywords = haemorrhage (Clic here for more details about this article) |
7/27. 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.- - - - - - - - - - ranking = 0.0011030902831079keywords = brain (Clic here for more details about this article) |
8/27. 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.- - - - - - - - - - ranking = 3.7560329150777keywords = haemorrhage, intracranial haemorrhage, brain (Clic here for more details about this article) |
9/27. 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.- - - - - - - - - - ranking = 0.75437827965301keywords = haemorrhage, intracranial haemorrhage (Clic here for more details about this article) |
10/27. High titers of CA-125 may be associated with recurrent ischemic strokes in patients with cancer.In addition to etiologies common in the general population, strokes in cancer patients may be caused by hypercoagulable states, hyperviscosity, cardiogenic embolism, and neoplastic vessel infiltration. Intravascular mucins were reported in patients with recurrent thromboembolism. The authors report four patients with metastatic cancer, brain infarcts, and other thromboembolic disease with markedly elevated levels of the tumor marker CA-125 and explore possible associations between this mucinous protein and strokes.- - - - - - - - - - ranking = 0.00055154514155396keywords = brain (Clic here for more details about this article) |
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