Cases reported "Thrombocytopenia"

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1/47. Clinical experience with combined treatment of thrombin inhibitors and GPIIb/IIIa inhibitors in patients with HIT.

    Despite the use of potent anticoagulants such as r-hirudin and argatroban, the morbidity/mortality of heparin-induced thrombocytopenia (HIT) patients remains high. In the last several months, we have treated three HIT-positive patients with a combined therapy of thrombin inhibitor and GPIIb/IIIa inhibitor when treatment with thrombin inhibitor alone failed to alleviate acute thrombosis. Combination therapies included r-hirudin (Refludan) with tirofiban (Aggrastat) or argatroban (Novastan) with ReoPro. A reduced dose of the thrombin inhibitor with the standard dose of the antiplatelet drug was the dosing regimen used. In all cases, there was no overt bleeding that required intervention and all patients had improved or fully recovered. This first report of the use of GPIIb/IIIa inhibitors with thrombin inhibitors in HIT patients with active thrombosis suggests that this combined therapy may be more effective than thrombin inhibitor treatment alone. The data from these three cases warrant testing of this therapeutic regimen in larger studies to determine optimal dosing strategies.
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keywords = morbidity
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2/47. Management of severe and complicated malaria in the intensive care unit.

    malaria remains today one of the major health problems in the tropics with increased morbidity and mortality. The most serious complications are caused by plasmodium falciparum, which, in contrast to the benign malarias, may progress to a life-threatening multi-system disease. Our case concerns a young woman in the 14th week of pregnancy, admitted to the ICU in a coma, with pulmonary oedema, haemolytic anaemia, renal failure and thrombocytopenia as complications of P. falciparum malaria. The case is discussed and possible explanations for the clinical picture and complications of P. falciparum malaria are given in the light of experiences from the literature.
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3/47. Neurologic complications in immune-mediated heparin-induced thrombocytopenia.

    OBJECTIVE: To evaluate neurologic complications in patients with immune-mediated heparin-induced thrombocytopenia (HIT) with respect to incidence, clinical characteristics, outcome, and therapy. methods: One hundred and twenty consecutive patients with immune-mediated HIT were recruited over a period of 11 years and studied retrospectively for the occurrence of neurologic complications. diagnosis of HIT was based on established clinical criteria and confirmed by detection of heparin-induced antibodies using functional and immunologic tests. RESULTS: Eleven of the 120 patients (9.2%) presented with neurologic complications; 7 suffered from ischemic cerebrovascular events, 3 from cerebral venous thrombosis, and 1 had a transient confusional state during high-dose heparin administration. Primary intracerebral hemorrhage was not observed. The relative mortality was much higher (Chi-square test, p < 0.01) in HIT patients with neurologic complications (55%) as compared to patients without neurologic complications (11%). The mean platelet count nadir in neurologic patients was 38 /- 25 x 10(9)/l on average, and was lower in patients with fatal outcome compared to those who survived (21 /- 13 x 10(9)/l versus 58 /- 21 x 10(9)/l; p < 0.05, Wilcoxon test). In three patients neurologic complications preceded thrombocytopenia. There was a high coincidence of HIT-associated neurologic complications with other HIT-associated arterial or venous thrombotic manifestations. CONCLUSION: Neurologic complications in HIT are relatively rare, but associated with a high comorbidity and mortality. HIT-associated neurologic complications include cerebrovascular ischemia and cerebral venous thrombosis. They may occur at a normal platelet count.
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keywords = morbidity
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4/47. heparin-bonded circuit with low systemic anticoagulation in a patient with heparin-induced thrombocytopenia: a case report.

    heparin-induced thrombocytopenia (HIT) in patients undergoing open heart surgery has been reported with increasing frequency. Several strategies have been suggested to approach this difficult problem. However, the syndrome is still associated with significant morbidity and mortality. We describe an 82-year-old male with HIT who underwent coronary artery bypass grafting utilizing a heparin-bonded cardiopulmonary bypass circuit with very low systemic anticoagulation. Only one unit of packed red blood cells was transfused. The patient recovered uneventfully. This strategy is safe and effective, and, therefore, should be considered in patients with HIT.
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keywords = morbidity
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5/47. ET gets HIT--thrombocytotic heparin-induced thrombocytopenia (HIT) in a patient with essential thrombocythemia (ET).

    Immune-mediated heparin-induced thrombocytopenia (HIT) is a relatively common complication in patients receiving heparin, and represents a strong risk factor for thromboembolic disease associated with high morbidity and mortality. The condition is commonly defined as a platelet count fall of greater than 30-50% to values below 150 x 10(9)/l. Despite this, several cases with platelet count nadirs in the normal range have been reported. This report describes a patient with status post-carotid thrombendarterectomy presenting with neurological symptoms and thrombocytosis (1235 x 10(9)/l), which in due course was diagnosed to be caused by essential thrombocythemia (ET). heparin therapy was established and symptoms resolved markedly. After 5 days of standard heparin therapy, serologically confirmed HIT with new neurological symptoms occurred. The platelet count nadir attributed to HIT was far above normal (633 x 10(9)/l), which nevertheless represented a substantial relative platelet count fall (49%). This is the first reported case of serologically confirmed HIT in a patient with ET. Furthermore, it represents the first published case of HIT being present in thrombocytosis. Clinicians should be aware that atypical HIT can even be present in thrombocytosis and, because of nomenclature, HIT with normal and elevated platelet count nadirs is likely to be largely underdiagnosed.
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keywords = morbidity
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6/47. 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.
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keywords = morbidity
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7/47. heparin-induced thrombocytopenia as the cause of gluteus muscle necrosis: a case study describing the benefits of multidisciplinary physical and psychosocial interventions.

    heparin-induced thrombocytopenia, an increasingly recognized aspect of heparin therapy, occurs in 0.6% to 30% of patients receiving heparin. Approximately 1% of those patients develop the more severe heparin-induced thrombocytopenia II, also called white clot syndrome, in which synchronous venous and arterial thrombi impede blood flow in central vessels. mortality (as high as 25%) and morbidity are related to the site and extent of thrombi formation. Following vascular surgery, one patient manifested an unusual consequence of heparin-induced thrombocytopenia II when thrombotic blockage of the vessels supplying the bilateral gluteus maximus and minimus muscles resulted in tissue ischemia and death. Supporting the patient through numerous complications and managing the extensive wound healing process required multidisciplinary skills and innovative technology, including use of vacuum-assisted closure therapy, platelet-derived growth factors, parenteral and enteral nutritional support, and spirit-restoring favorite foods. This article describes the patient's life-threatening and long-lasting effects from an allergic reaction to heparin therapy. In addition to information about the diagnosis of heparin-induced thrombocytopenia, this article also describes management of the wound and other aspects of care and comforting that occurred over a 9-month hospitalization.
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keywords = morbidity
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8/47. Polymerized human Hb use in acute chest syndrome: a case report.

    BACKGROUND: acute chest syndrome (ACS) is a complication of sickle cell disease that can cause significant morbidity. Transfusion therapy has been shown to significantly increase oxygenation in patients with ACS and RBC exchange is considered the standard of care in patients at high risk of respiratory failure. CASE REPORT: A patient with ACS and several high-risk features, including thrombocytopenia, profound anemia, bilateral pulmonary infiltrates, staphylococcal sepsis, and pulmonary embolism is presented. The patient refused transfusion on religious grounds and received 12 units of human polymerized Hb solution (poly SFH-P injection, PolyHeme, Northfield laboratories) over the course of 13 days. The patient's respiratory status improved and she was discharged home without receiving RBC transfusions. CONCLUSION: This is the first reported case that describes the use of PolyHeme in a patient with sickle cell disease, ACS, and sepsis. This therapy is thought to have been lifesaving for this patient.
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ranking = 1
keywords = morbidity
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9/47. heparin-induced thrombocytopenia with associated thrombosis in children after the Fontan operation: report of two cases.

    heparin-induced thrombocytopenia is a widely recognized clinical disorder. The spectrum of disease ranges from clinically insignificant to severe thrombosis (heparin-induced thrombocytopenia with associated thrombosis). overall, thrombosis occurs in approximately 33% of adults diagnosed with heparin-induced thrombocytopenia and has been associated with high morbidity and mortality rates. Diagnostic testing for this disorder is not standard in children with thrombocytopenia who are receiving heparin, despite the fact that children with congenital heart disease may be exposed to heparin frequently. There are few reported cases of heparin-induced thrombocytopenia with associated thrombosis in children; herein, we describe the cases of 2 children who developed this disorder after undergoing a Fontan operation.
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keywords = morbidity
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10/47. heparin-induced thrombocytopenia occurring after discontinuation of heparin.

    BACKGROUND: heparin-induced thrombocytopenia is caused by antibody formation to heparin-platelet factor 4 complexes. It typically develops 5 to 14 days after the initiation of heparin, but it can occur up to 3 weeks after the patient stops taking it. Early recognition by monitoring platelet counts during heparin therapy can decrease associated mortality and morbidity. methods: A case is described of a patient with severe morbidity as a result of heparin-induced thrombocytopenia. The medical literature was searched using the key words "heparin/adverse effects" and "thrombocytopenia." RESULTS AND CONCLUSIONS: The severe morbidity and potential mortality associated with heparin-induced thrombocytopenia are caused mainly by thrombosis. If it is suspected, all heparin products should be immediately stopped. Platelet counts usually return to normal after the heparin is discontinued. Approximately 50% of patients with heparin-induced thrombocytopenia develop thrombotic events. patients should receive anticoagulation with agents other than heparin or low molecular weight heparin. As early detection of heparin-induced thrombocytopenia seems to improve outcome, it is recommended that all patients on heparin should have frequent monitoring of platelet counts.
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ranking = 3
keywords = morbidity
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