1/26. Surgical treatment for severe diabetic macular edema with massive hard exudates.PURPOSE: Massive diabetic macular exudates respond poorly to conventional laser treatment. The purpose of this study was to analyze the surgical results of eyes with massive hard exudates secondary to diabetic macular edema treated with combined pars plana vitrectomy, posterior hyaloid removal, focal endolaser treatment, and panretinal photocoagulation. methods: The author retrospectively analyzed the surgical outcome of 13 consecutive eyes (11 patients) with massive diabetic macular exudates. All patients had had at least one session of focal and/or grid laser treatment without any effect. Pars plana vitrectomy, posterior hyaloid removal, focal macular endolaser treatment, and intraoperative panretinal photocoagulation were performed. Postoperative visual acuity, evolution of macular edema, and hard exudates were recorded. RESULTS: All 13 eyes showed significant decreases in macular edema and hard exudates, a process that became clinically obvious 3 months after the operation. Eleven eyes had improved vision of at least two lines during an average follow-up period of 14.8 months. Intraoperative and postoperative complications included angle closure glaucoma (one eye), persistent vitreous hemorrhage (two eyes), choroidal detachment (one eye), intravitreal fibrin formation (one eye), epiretinal membrane formation (one eye), and neovascular glaucoma (one eye). CONCLUSION: Combined surgery may offer an opportunity for improvement of vision and reduction of massive macular exudates in patients with severe diabetic macular edema.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
2/26. A DIDMOAD syndrome family with juvenile glaucoma and myopia findings.We present here two DIDMOAD syndrome cases (diabetes mellitus, diabetes insipidus, optic atrophy, deafness) in a Turkish family. In the examination of the propositus who had consanguineous parents, diabetes mellitus, diabetes insipidus, optic atrophy, and deafness were observed in addition to myopia, juvenile glaucoma, posterior polar cataract, and dilatation of the urinary tract. diabetes mellitus, diabetes inspidus, optic atrophy, deafness, myopia, and ventricular septal defect were observed in his elder brother. Juvenile onset diabetes mellitus, congenital glaucoma, deafness, and heart disease were the other remarkable findings observed in relatives to this family. Juvenile glaucoma, posterior polar cataract observed in our propositus, and myopia in both our DIDMOAD syndrome cases are the first ophthalmic manifestations described in the DIDMOAD syndrome.- - - - - - - - - - ranking = 3.5keywords = coma (Clic here for more details about this article) |
3/26. Marked hyperthermia as a manifestation of hypoglycemia in long-standing diabetes mellitus.Hyperthermia has recently been recognized as a manifestation of hypoglycemia. We describe two episodes of hypoglycemia associated with nausea, vomiting, chills, and impaired consciousness which were followed by marked hyperthermia. We suggest that the hyperthermia may result from excessive reaction to preceding hypothermia caused by the hypoglycemia. We would like to alert the clinician to the possibility of a previous, severe hypoglycemic episode in any diabetic patient with hyperthermia and coma.- - - - - - - - - - ranking = 0.5keywords = coma (Clic here for more details about this article) |
4/26. Spontaneous expulsive suprachoroidal hemorrhage.PURPOSE: To present a 90-year-old patient with spontaneous expulsive suprachoroidal hemorrhage (SESCH). This unique case suggests a mechanism of SESCH, which is still under debate. methods: The patient, who had corneal inflammatory disease and diabetes mellitus, atherosclerosis, and glaucoma, presented with active ocular bleeding and expulsion of intraocular tissues. Almost the entire cornea was absent, except for several small and irregular areas in its periphery. Histopathologic evaluation of the eviscerated contents was performed. RESULTS: Clinicopathologic evaluation revealed acute inflammation of the corneal remains as well as intraocular inflammation. Inflammatory necrosis of choroidal vessels was evident. CONCLUSION: The findings point to the assumption that choroidal bleeding, secondary to vascular inflammatory necrosis, was the initial event in this case of spontaneous expulsive suprachoroidal hemorrhage. Presumedly, the intraocular pressure level was very high owing to continuous bleeding, which could result in a very large, rather than localized, tearing of the peripherally inflamed cornea.- - - - - - - - - - ranking = 0.5keywords = coma (Clic here for more details about this article) |
5/26. Postoperative hypoglycaemic coma associated with chlorpropamide.A 72-year-old male being treated with chlorpropamide for diabetes mellitus had an emergency operation for a perforated gastric ulcer. Hypoglycaemic coma occurred after the operation.- - - - - - - - - - ranking = 2.5keywords = coma (Clic here for more details about this article) |
6/26. Fatality from olanzapine induced hyperglycemia.A case history of a 31-year-old male schizophrenic patient is presented. The man was treated with olanzapine for three weeks before he died. After one week on a 10 mg daily dose of olanzapine, his fasting blood glucose was elevated to 11.3 mmol/L (203 mg/dL). In order to treat more aggressively his psychosis, the olanzapine dose was raised to 20 mg daily resulting in his fasting blood glucose climbing to 15.8 mmol/l (284 mg/dL). On the days preceding his death, he became progressively weaker, and developed polydipsia with polyuria. He had no personal or family history of diabetes mellitus and he was on no other medication at the time of his death. Postmortem blood, vitreous humor, and urine glucose concentrations were 53 mmol/L (954 mg/dL), 49 mmol/L (882 mg/dL), and 329 mmol/L (5922 mg/dL), respectively. Drug screen on urine and blood indicated only a small amount or olanzapine and no alcohols. Peripheral blood olanzapine concentration was within therapeutic limits, 45 ng/mL. Analysis of vitreous humor and urine revealed severe dehydration with small amounts of ketones. death was attributed to hyperosmolar nonketotic diabetic coma, and olanzapine was felt most likely to be the cause. Another atypical neuroleptic, clozapine, has also been associated with the development and exacerbation of diabetes mellitus or diabetic ketoacidosis. We recommend including vitreous glucose and beta-hydroxybutyrate analysis as part of postmortem toxicology work up when the drug screen reveals the presence of either olanzapine or clozapine.- - - - - - - - - - ranking = 0.5keywords = coma (Clic here for more details about this article) |
7/26. Acute hypertensive encephalopathy with widespread small-vessel disease at MRI in a diabetic patient: pathogenetic hypotheses.We report unusual magnetic resonance imaging (MRI) findings in a diabetic patient with neglected hypertension and hyperglycemia, presenting with seizures and coma. Outcome was fatal despite intensive care. The MRI findings included bilateral insular and temporo-occipital grey and white matter involvement, and numerous, scattered, lacunar-like lesions involving the peripheral and deep white matter, basal ganglia grey matter, and brainstem. Lesions had a low apparent diffusion coefficient, and some enhanced following contrast injection. hypertensive encephalopathy with widespread and severe acute small-vessel disease was considered. Pathophysiology is discussed.- - - - - - - - - - ranking = 0.5keywords = coma (Clic here for more details about this article) |
8/26. Drug-induced immunodeficiency associated with nodal Kaposi's sarcoma.A 40-year-old male showed a syndrome of acquired immunodeficiency after a prolonged use of antidiabetic sulfamides. The lesions were revealed by the biopsic examination of inguinal lymph nodes. Immunodeficiencies are usually associated with malignant lymphoma: our case was, however, associated with Kaposi's sarcoma.- - - - - - - - - - ranking = 2.5keywords = coma (Clic here for more details about this article) |
9/26. hypoglycemia: causes, neurological manifestations, and outcome.During a 12-month prospective study there were 125 visits to the Harlem Hospital Emergency Room for symptomatic hypoglycemia. Sixty-five patients had obtundation, stupor, or coma; 38 had confusion or bizarre behavior; 10 were dizzy or tremulous; 9 had had seizures; and 3 had suffered sudden hemiparesis. diabetes mellitus, alcoholism, and sepsis, alone or in combination, accounted for 90% of predisposing conditions; others included fasting, terminal cancer, gastroenteritis, insulin abuse, and myxedema. Average blood glucose levels were lower among comatose than among obtunded patients, but overlap was considerable, and overall there was little correlation among cause, blood glucose levels, and symptoms. Although mortality was 11%, only one death was attributable to hypoglycemia per se, and only four survivors had focal neurological residua.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
10/26. Severe acidosis from acetazolamide in a diabetic patient.An insulin-dependent diabetic patient with nephropathy developed severe acidosis after treatment with acetazolamide for glaucoma. A renal tubular abnormality may have allowed the usually self-limiting acidosis of acetazolamide to progress. It is suggested that the plasma electrolytes of patients at risk should be monitored.- - - - - - - - - - ranking = 0.5keywords = coma (Clic here for more details about this article) |
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