Cases reported "Acute Disease"

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1/51. Apparent hemolysis in an AIDS patient receiving trimethoprim/sulfamethoxazole: case report and literature review.

    OBJECTIVE: To describe a case of acute hemolysis associated temporally with administration of trimethoprim/sulfamethoxazole (TMP/SMX) in a patient with AIDS, review the available literature on TMP/SMX-induced hemolytic anemia, and discuss possible drug- and disease-related factors that may have contributed to the episode of hemolysis. CASE SUMMARY: A precipitous decrease in red blood cell count, hemoglobin, and hematocrit occurred shortly after a black woman with AIDS received a single intravenous dose of TMP/SMX for pneumocystis carinii pneumonia. Following drug discontinuation and repeated transfusions, the patient's hematologic indices returned to baseline. literature SOURCES: References were obtained using medline searches, the bibliographies of articles identified during the searches, review articles, and standard textbooks. DATA SYNTHESIS: Of the two different mechanisms of TMP/SMX-induced hemolytic anemia, the reaction is most likely to occur via dose-related oxidative disruption of the erythrocyte membrane in subpopulations deficient in glucose-6-phosphate dehydrogenase (G6PD) activity. In the US, G6PD deficiency most frequently is encountered among blacks. The potential for hemolysis may be further increased in G6PD-deficient AIDS patients, who also appear to lack adequate intracellular glutathione, which is essential for protecting the erythrocyte membrane from oxidative damage. Although an assay for G6PD activity was not conducted, the case circumstances were consistent with TMP/SMX-induced hemolysis in a G6PD-deficient patient. CONCLUSIONS: Black patients with AIDS who are receiving relatively high (greater than or equal to 50 mg/kg/d) dosages of TMP/SMX should be monitored closely for signs and symptoms of hemolytic anemia.
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2/51. Hypocalcemic tetany in a toddler with undiagnosed rickets.

    A 17-month-old black girl presented to the pediatric emergency department with sudden onset of her hands and feet "drawing up." A diagnosis of vitamin d deficiency rickets with tetany was made on a history of exclusive breast-feeding, low serum calcium, phosphorus, and 25-hydroxyvitamin D levels, and bone radiographs. Nutritional rickets should be considered in the differential diagnosis of acute hypocalcemia.
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3/51. nitric oxide successfully used to treat acute chest syndrome of sickle cell disease in a young adolescent.

    OBJECTIVES: To report a case of acute chest syndrome (ACS) of sickle cell disease treated successfully with nitric oxide and to review the physiologic effects of nitric oxide and its potential ability to improve outcome in ACS. DESIGN: Descriptive case report. SETTING: Eighteen-bed pediatric intensive care unit in a university children's hospital. PATIENT: A 15-yr-old black male with sickle cell disease, bilateral pulmonary infiltrates, refractory hypoxemia, and unstable hemodynamics. INTERVENTION: In addition to exchange transfusion, invasive hemodynamic monitoring, and aggressive ventilatory support, inhaled nitric oxide was administered in the gas mixture in a concentration of 20 ppm for 72 hrs. MEASUREMENTS AND MAIN RESULTS: cardiac output, pulmonary arterial pressure, pulmonary artery occlusion pressure, systemic vascular resistance, pulmonary vascular resistance, shunt fraction, and alveolar-arterial oxygen gradient were compared with and without inhaled nitric oxide. Marked reductions in pulmonary arterial pressure and pulmonary vascular resistance were noted. cardiac output improved, and shunt fraction and alveolar-arterial oxygen gradient were markedly reduced. The patient required decreased ventilator and hemodynamic support and rapidly made a complete recovery. CONCLUSIONS: nitric oxide may be beneficial for patients with ACS because of its ability to ameliorate pulmonary hypertension and ventilation/perfusion mismatch. nitric oxide may confer some protection against polymerization of sickle hemoglobin and exert a reversible antiplatelet effect that may be beneficial in ACS. Further study is necessary to determine the safety and efficacy of inhaled nitric oxide as a treatment for ACS.
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4/51. Black esophagus: a view in the dark.

    A 73-year-old man had a low anterior resection for a villous adenoma in the rectosigmoid. On the 4th day after surgery, he suddenly developed severe interscapular pain. Aortic dissection was ruled out, but endoscopy showed black mucosa of the entire esophagus. With conservative treatment, including proton pump inhibition, he recovered completely. We hypothesize that a transient gastric outlet obstruction and massive gastroesophageal reflux played a significant role in the etiology of this rare and alarming, but, in this case, completely reversible, syndrome.
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5/51. Secondary myeloid/natural killer cell acute leukemia following T-cell lymphoma.

    A 56-year-old woman was treated with combination chemotherapy and radiation therapy for peripheral T-cell lymphoma. Following complete remission for a period of 6 months, she returned again with marked leukocytosis. Leukemic cells were characterized by scanty cytoplasm with fine azurophilic granules, and were highly positive for myeloperoxidase and sudan black-B. Immunophenotypic analysis revealed that blast cells were positive for myeloid antigens (CD13, CD33), and natural killer (NK) cell antigen (CD56), but negative for T-cell antigens (CD2, CD5, CD7), B-cell antigens (CD19, CD20), CD34, and HLA-DR. The case was diagnosed as secondary myeloid/NK cell acute leukemia following non-Hodgkin's lymphoma. Despite aggressive chemotherapy against leukemia, she died of multiorgan failure 7 months following onset of leukemia. We present, to the best of our knowledge, the first published report of what seems to be a secondary myeloid/NK cell acute leukemia following T-cell lymphoma.
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6/51. Acute necrotizing bacterial tonsillitis with clostridium perfringens.

    Bacterial infection with clostridium perfringens in children less than 2 years of age is frequently associated with meningitis, necrotizing gastrointestinal infection, and postoperative infections. However, a review of the literature reveals no reports of these bacteria infecting the tonsils. A 9-month old black female was found unresponsive at the baby-sitter's and was rushed to the hospital. Shortly after admission to the emergency department death was pronounced. An autopsy performed on this otherwise healthy infant revealed shock and acute necrotizing bacterial tonsillitis. The initial report of this infant's death was questionable sudden infant death syndrome and questionable smothering. Postmortem cerebrospinal fluid, blood, and lung cultures grew pure colonies of C. perfringens. The necrotizing tonsil revealed no significant gross lesions. Microscopically, large numbers of gram-positive rods were easily recognized and were compatible with C. perfringens. Because the oropharynx is a common portal of entry for infectious agents, it is essential to sample tissues of Waldeyer's ring and especially the tonsils to find infectious diseases that may become systemic.
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7/51. Superior branch palsy of the oculomotor nerve caused by rhinocerebral mucormycosis.

    A 75-year-old woman presented with fever and right temporal, periorbital and facial pain for 7 days. physical examination revealed an ipsilateral paresis of the superior division of the oculomotor nerve with mild exophthalmos. She also had hyperglycemia. CT scan of the paranasal sinuses showed acute sinusitis. Rhinoscopy demonstrated black necrotic tissue in the nasal septum. KOH preparation of tissue biopsy specimen revealed large, non septate hyphae with right angle branching, diagnostic of rhinocerebral mucormycosis. She was treated with amphotericin b, surgical debridement and insulin therapy. Surgical tissue specimen also confirmed mucormycosis. She improved after treatment, but 4 months later, ptosis and upward palsy still persisted.
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8/51. Acute scleral thinning after pterygium excision with intraoperative mitomycin C: a case report of scleral dellen after bare sclera technique and review of the literature.

    PURPOSE: To describe a patient with scleral dellen after pterygium excision with intraoperative mitomycin C. methods: Case report and medline review of the medical literature on scleral dellen after bare sclera technique. RESULTS: A 48-year-old man had a left nasal pterygium excised by the bare sclera technique with intraoperative mitomycin C. Eight days after surgery, the patient noticed a small black spot in the bare sclera area with mild irritation. Slit-lamp examination revealed a focal area of extreme thinning, centered on the nonepithelialized bare sclera, surrounded by edematous conjunctiva. The ciliary body was visible through the thin and dry scleral lesion. After topical lubricant therapy, the scleral lesion appeared normal thickness and white in color 3 days later. Therapy was continued until the sclera epithelialized. CONCLUSIONS: Scleral dellen is an early postoperative complication of bare sclera technique owing to delayed conjunctival wound closure. Hydration of the thinned sclera will rapidly thicken it. However, medical therapy should be continued until the surrounding conjunctiva has flattened and the sclera has epithelialized. Surgical wound closure is an alternative management and may be the way to prevent scleral dellen formation after bare sclera technique. All patients after bare sclera surgery should be followed up until the conjunctival wound has healed. If delayed healing is found, frequent artificial tears, patching, or surgical intervention is necessary.
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9/51. Postmortem revelation of sickle cell disease following fatal episode of acute bronchial asthma.

    A 19-year-old black male with previous history of mild bronchial asthma presented sudden dyspnea and died in a state of respiratory distress in spite of resuscitation attempts. autopsy showed typical lesions of acute bronchial asthma in a context of long-standing asthma associated with a massive and disseminated intravascular sickling. Hemoglobin electrophoresis diagnosed heterozygous sickle cell disease. This rare case raises the problem of the accuracy of death certificate, especially the difficulties to distinguish postmortem lesions as the underlying cause of death or the contributory cause of death.
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10/51. Acute mercury intoxication with lichenoid drug eruption followed by mercury contact allergy and development of antinuclear antibodies.

    A 31-year-old black man was examined for evaluation of a suspected occupational disease. Three years earlier he had been suffering from acute mercury intoxication during work in a mercury recycling factory. skin symptoms then had been a lichenoid drug eruption, patchy alopecia and stomatitis, which had all disappeared rapidly after systemic glucocorticosteroid treatment. The examination revealed positive patch test reactions to metallic mercury and inorganic mercury compounds, an elevated titre of serum antinuclear antibodies and normal IgE levels. The induction of antinuclear antibodies by mercury has been shown in animal experiments. It can be hypothesized that this patient, who may have had an increased individual susceptibility, became allergic to mercury by the mercury intoxication.
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