Cases reported "Thrombocytopenia"

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1/77. White-centred retinal haemorrhages (Roth spots).

    Roth spots (white-centred retinal haemorrhages) were classically described as septic emboli lodged in the retina of patients with subacute bacterial endocarditis. Indeed many have considered Roth spots pathognomonic for this condition. More recent histological evidence suggests, however, that they are not foci of bacterial abscess. Instead, they are nonspecific and may be found in many other diseases. A review of the histology and the pathogenesis of these white-centred haemorrhages will be provided, along with the work-up of the differential diagnosis.
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2/77. A fatal case of autoimmune thrombocytopenia with an IgM anti-GPIb/IX following one antigen mismatched unrelated donor bone marrow transplantation.

    We report the case of a 32-year-old patient with ALL who developed autoimmune thrombocytopenia 2 months following allogeneic bone marrow transplantation. An IgM autoantibody against the platelet glycoprotein Ib/IX complex was observed. Treatment with high-dose steroids and intravenous immunoglobulin g failed to produce any benefit and the thrombocytopenia led to fatal gastrointestinal haemorrhage. The possible factors contributing to post-allograft thrombocytopenia and potential management strategies are discussed.
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keywords = haemorrhage
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3/77. Disseminated nocardiosis as a complication of Evans' syndrome.

    Nocardiosis is an opportunistic infection caused by gram-positive, weakly acid-fast filamentous aerobic organisms. Three species cause infection in man: N. asteroides, N. brasiliensis, and N. caviae, the first one being the most common. With increased use of immunosuppressive therapy for various autoimmune diseases, opportunistic infection by nocardia has increasingly been reported. N. asteroides infections manifest in various ways; the lungs, skin, and brain are the organs most frequently involved. We describe a patient with Evans' syndrome, a disease requiring long-term immunosuppression, who acquired systemic nocardiosis. The infection was primarily pulmonary, misdiagnosed as tuberculosis, with subsequent hematogenous dissemination to the skin and central nervous system. The diagnosis of cerebral involvement was difficult to prove, as the patient presented with stroke-like episodes. After a positive blood culture was obtained, antibiotic therapy was introduced. The patient's condition deteriorated and the brain with infiltration of the meninges, lungs, skin, and kidneys. nocardia is an important but often overlooked opportunistic infectious agent in immunocompromised hosts, causing diagnostic and therapeutic problems. As the mortality of cerebral nocardiosis is greater than 80%, early diagnosis and appropriate therapy are crucial.
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keywords = brain
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4/77. Multiple major cerebral artery thromboses with profound thrombocytopenia in acute leukaemia.

    A child with acute lymphoblastic leukaemia complicated by prolonged gastrointestinal and skin haemorrhages due to profound thrombocytopenia finally died of thrombotic occlusions of major cerebral arteries due to mucormycosis. biopsy of any suspect lesion is needed urgently before prolonged therapy with amphotericin b is started. So far there have been no cures in childhood.
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5/77. Acute myeloid leukemia in TAR syndrome.

    TAR syndrome is a rare inherited autosomal recessive disorder with a mortality rate of 30-40% mainly as a result of haemorrhage, in the first year of life. Most of the infants recover from the effects of thrombocytopenia and associated haematological complications with the modern medical care. Very rarely, the outcome is fatal, with the occurrence of acute leukemias.
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keywords = haemorrhage
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6/77. Acute respiratory failure associated with catastrophic antiphospholipid syndrome.

    We present a case of multiple organ dysfunction syndrome with acute respiratory failure due to alveolar haemorrhage associated with antiphospholipid antibodies in a 42-year-old woman with a medical history of antinuclear antibody-negative systemic lupus erythematosus and antiphospholipid syndrome. Severe respiratory failure, circulatory shock and acute renal failure necessitated artificial ventilation, inotropic and vasopressor therapy, and continuous venovenous haemofiltration. A tentative diagnosis of haemorrhagic lupus pneumonitis or pulmonary manifestation of antiphospholipid syndrome was made. Lupus anticoagulant, IgG anticardiolipin and anti-beta2-glycoprotein I antibodies were positive. High-dose glucocorticoid, anticoagulation with heparin, plasmapheresis and cyclophosphamide improved her clinical condition. Despite this, the patient died several days later of spontaneous intracranial haemorrhage. This case illustrates the uncommon manifestation of acute respiratory failure associated with antiphospholipid syndrome.
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ranking = 0.64053074387383
keywords = intracranial haemorrhage, haemorrhage
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7/77. heparin-induced thrombocytopenia thrombosis after cardiac surgery. A case report.

    We report a rare case of cerebral infarct resulting in brain death due to heparin-induced thrombocytopenia thrombosis (HITT), manifested in the immediate postoperative period following aortic valve replacement in a 46-year-old woman whose only prior exposure to heparin was during catheterization four months prior to surgery. The diagnosis of HITT was suspected after a significant decrease of the platelet count and it was confirmed by a heparin-induced platelet activation assay showing platelet aggregation in the presence of heparin.
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keywords = brain
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8/77. quinine induced coagulopathy--a near fatal experience.

    A 67 year old man presented to his local dentist for restorative treatment. He stated he was fit and well and denied taking any medications. When he was given an inferior alveolar nerve block, excessive bleeding was noted at the injection site and the dentist advised the patient see an oral and maxillofacial surgeon. An appointment was made for the patient but he did not attend. Three days later, he presented with evidence of massive deep haemorrhage to the point of airway compromise. He underwent hospital admission, early intubation, intensive care for nine days and hospitalization for six weeks. The cause of his bleeding was a severe thrombocytopoaenia, induced by chronic ingestion of quinine. He was self-medicating with this to relieve muscular cramps. Despite this experience, the patient continued to deny that quinine was the cause of his problem and that he had failed in his obligations to advise the dentist of his drug history. dentists need to be alert to the risk that patients may not reveal their true medical history. There are, however, obligations on the dentist to ensure the accuracy of information the patient gives and to ensure that patients whom they believe are at risk follow their advice. Teamwork and skillful airway management prevented this patient's demise.
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keywords = haemorrhage
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9/77. Acute adrenocortical insufficiency due to heparin-induced thrombocytopenia with subsequent bilateral haemorrhagic infarction of the adrenal glands.

    A 56 year old male developed bilateral massive adrenal haemorrhage (BMAH) resulting in chronic adrenal insufficiency in the course of heparin-induced thrombocytopenia (HIT)-syndrome. thrombosis of the central adrenal vein (CAV) with subsequent adrenal haemorrhagic infarction is the most probable cause of the rare association of HIT and BMAH. The exorbitantly high catecholamine plasma levels within the CAV in addition to immunogenic platelet activation are discussed as possible underlying pathophysiological mechanisms.
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keywords = haemorrhage
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10/77. Assessment of prognostic factors in severe traumatic brain injury patients treated by mild therapeutic cerebral hypothermia therapy.

    This study analyzed the predictable factors of outcome such as neuro-parameters and systemic complications to elucidate the indications for therapeutic hypothermia. In our institute, 35 patients with severe head injury (Glasgow coma Scale 3-7) were treated with mild hypothermia therapy (33 degrees-35 degrees C). Twenty-two of these 35 patients underwent complete neuromonitoring and outcome assessments by glasgow outcome scale (GOS) at three months after injury. GOS of hypothermia group was significantly better than another patient group which was treated without mild hypothermia therapy. The hypothermia group was divided into two groups: good outcome (GOOD) (good recovery or moderate disability; n = 9, 40.9%) and poor outcome (POOR) (severe disability, vegetative state, or death; n = 13, 59.1%). The mean age (mean 30.2 years, range 9-46) was significantly lower in GOOD than in POOR (mean 45.2 years, range 17-62). patients aged over 50 years had poor outcome. CPP was significantly higher in GOOD during hypothermia. All patients with thrombocytopenia had poor outcome. hypothermia therapy can improve outcome in patients with traumatic brain injury who are younger than 50 years old, without severe brain damage, and if improvement of cerebral perfusion is expected. Systemic complications must be prevented as far as possible by combination with other therapies.
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keywords = brain
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