1/57. leukostasis followed by hemorrhage complicating the initiation of chemotherapy in patients with acute myeloid leukemia and hyperleukocytosis: a clinicopathologic report of four cases.BACKGROUND: Pulmonary and cerebral leukostasis, or parenchymal hemorrhage in these organs, are well-known early complications developing in patients with acute myeloid leukemia (AML), particularly when myelomonocytic features, hyperleukocytosis, and/or a coagulation disorder are initially present. Commonly, these complications arise during increasing leukocyte counts (WBCs). methods: The authors describe four patients with AML and hyperleukocytosis who developed leukostasis followed by parenchymal hemorrhage. RESULTS: Bleeding in all patients occurred while their WBCs were decreasing following cytosine-arabinoside chemotherapy, and in the absence of disseminated intravascular coagulation or severe thrombocytopenia. Radiologic and histopathologic findings underscoring possible mechanisms are presented in the article. CONCLUSIONS: Alterations of cell adhesion associated with chemotherapy-induced blast lysis or cellular differentiation are possible factors contributing to this particular sequence (cytosine arabinoside-based chemotherapy, leukostasis, and subsequent hemorrhage). Prophylactic measures for managing this early complication of AML treatment include leukapheresis to reduce the WBC prior to the initiation of chemotherapy.- - - - - - - - - - ranking = 1keywords = cerebral (Clic here for more details about this article) |
2/57. 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 = 11.532228610087keywords = haemorrhage (Clic here for more details about this article) |
3/57. Nontraumatic acute spinal subdural hematoma: report of five cases and review of the literature.Acute subdural spinal hematoma occurs rarely; however, when it does occur, it may have disastrous consequences. The authors assessed the outcome of surgery for this lesion in relation to causative factors and diagnostic imaging (computerized tomography [CT], CT myelography), as well as eventual preservation of the subarachnoid space. The authors reviewed 106 cases of nontraumatic acute subdural spinal hematoma (101 published cases and five of their own) in terms of cause, diagnosis, treatment, and long-term outcome. Fifty-one patients (49%) were men and 55 (51%) were women. In 70% of patients the spinal segment involved was in the lumbar or thoracolumbar spine. In 57 cases (54%) there was a defect in the hemostatic mechanism. spinal puncture was performed in 50 patients (47%). Late surgical treatment was performed in 59 cases (56%): outcome was good in 25 cases (42%) (in 20 of these patients preoperative neurological evaluation had shown mild deficits or paraparesis, and three patients had presented with subarachnoid hemorrhage [SAH]). The outcome was poor in 34 cases (58%; 23 patients with paraplegia and 11 with SAH). The formation of nontraumatic acute spinal subdural hematomas may result from coagulation abnormalities and iatrogenic causes such as spinal puncture. Their effect on the spinal cord and/or nerve roots may be limited to a mere compressive mechanism when the subarachnoid space is preserved and the hematoma is confined between the dura and the arachnoid. It seems likely that the theory regarding the opening of the dural compartment, verified at the cerebral level, is applicable to the spinal level too. Early surgical treatment is always indicated when the patient's neurological status progressively deteriorates. The best results can be obtained in patients who do not experience SAH. In a few selected patients in whom neurological impairment is minimal, conservative treatment is possible.- - - - - - - - - - ranking = 1keywords = cerebral (Clic here for more details about this article) |
4/57. Gingival bleeding, epistaxis and haematoma three days after gastroenteritis: the haemorrhagic lupus anticoagulant syndrome.A 3 year and 9 month-old girl presented with gingival bleeding, epistaxis, and multiple haematomas 3 days after an acute episode of gastroenteritis. prothrombin time and activated partial thromboplastin time were prolonged with reduced clotting activity of factor II (< 10%), VIII (<1%), IX (3%), XII (10%) and evidence of a high titre inhibitor. Prothrombin (factor II) level was below the detection limit, both in a functional and immunological assay. It did not increase after administration of vitamin K or fresh frozen plasma. Further studies revealed presence of a strong lupus anticoagulant and a specific IgG antibody against prothrombin. factor viii antigen levels also were reduced (31%), but to a lesser extent than functionally determined factor viii (<1%). blood coagulation normalised following clinical recovery 6 weeks after admission. The pathophysiology of this acquired inhibitor phenomenon (accelerated clearance of complexes of clotting factors and phospholipids) is discussed. CONCLUSION: The haemorrhagic lupus anticoagulant syndrome (acquired hypoprothrombinaemia lupus anticoagulant syndrome) is a rare presentation of acquired bleeding diathesis in childhood. Since most cases in post-infectious children are asymptomatic, it might be underdiagnosed. In children with newly appearing bleeding symptoms or unclear prolonged prothrombin time or activated partial thromboplastin time, one has to consider this syndrome which could lead to relevant bleeding.- - - - - - - - - - ranking = 2.9600643052058keywords = haematoma (Clic here for more details about this article) |
5/57. Surreptitious bleeding in surgery: a major challenge in coagulation.Apart from inadequate surgical haemostasis, postoperative bleeding can be related to acquired disorders of platelet number, platelet function or coagulation proteins (e.g. vitamin k deficiency, DIC or liver injury). We highlight our experience with three patients who suffered life-threatening bleeding in the postoperative setting. The three patients - a 47-year-old man and 70- and 74-year-old women -- all had negative histories for excessive bleeding with prior surgeries, and all had normal preoperative PT and aPTT tests. Surgeries were resection of ischaemic bowel, cholecystectomy and coronary artery bypass grafting. All patients experienced unexpected bleeding within the first few postoperative days requiring multiple red cell transfusions and surgical re-explorations. Evaluations within the first 4--7 days after surgery revealed that these three patients had developed prolonged aPTT due to demonstrable factor viii antibodies initially at low titre. One patient was treated with high doses human factor viii, corticosteroids, intravenous gammaglobulin and plasma exchanges. The inhibitor was no longer demonstrable after 6 weeks of such therapy, and he has remained in remission without therapy. The second patient was initially treated with high-dose human factor viii infusions. Five months later, prednisone and 6-mercaptopurine were begun for worsening inhibitor titre and diffuse purpura and subcutaneous haematomas. The factor inhibitor remitted, but the patient died from liver failure related to post-transfusion hepatitis. The third patient was initially managed with high-dose human factor viii. Two months later, worsening inhibitor titre and tongue haematoma was treated with activated prothrombin complex, corticosteroids and cyclophosphamide. Eight years later, she is on no therapy, demonstrates a mild bleeding tendency and has a stable low-titre inhibitor. There have been a few case reports of inhibitors to coagulation factors including factor viii becoming manifest in the postoperative setting but surgery has not been widely recognized as an underlying cause for acquired haemophilia. This paper speculates on pathogenesis and reviews treatment options. This syndrome is remarkable for its abrupt onset in the first few postoperative days and for its substantial morbidity. The problem is potentially reversible with immunosuppressive therapy. Clinicians should be aware of this syndrome, considering acquired haemophilia in patients with unexpected postoperative bleeding.- - - - - - - - - - ranking = 1.1840257220823keywords = haematoma (Clic here for more details about this article) |
6/57. 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 = 5.7661143050436keywords = haemorrhage (Clic here for more details about this article) |
7/57. 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 = 1.0063605446612keywords = cerebral, brain (Clic here for more details about this article) |
8/57. 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 = 27.208547247463keywords = haemorrhage, haematoma (Clic here for more details about this article) |
9/57. 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 = 5.7724748497048keywords = haemorrhage, brain (Clic here for more details about this article) |
10/57. Cerebral vein thrombosis and prothrombin gene (G20210A) mutation.Recently, prothrombin gene mutation G20210A has been associated with elevated thrombosis risk and rarely with cerebral vein thrombosis (CVT). Three patients are described who had this genetic predisposition and who developed CVT in an unusual constellation with other factors. In the first patient, the intake of valproic acid (VPA) may have played an aggravating role in the development of CVT; in the second patient diagnosis of coagulation disorder was made during pregnancy consultation 6 years after CVT; in the third patient the CVT occurred at the age of 78 years. In patients with CVT, coagulation-examinations should include tests for the prothrombin gene (G20210A) mutation.- - - - - - - - - - ranking = 1keywords = cerebral (Clic here for more details about this article) |
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