1/10. peritoneal dialysis in an infant with type 1 diabetes and hyperosmolar coma.Hyperosmolar coma which is characterized by severe hyperglycemia in absence of chetosis is very rare in pediatric age with only 11 cases reported in the literature. The outcome of the condition is usually poor with mental retardation being the most common event. Here a case of hyperosmolar coma is described in a female of three months of age who was treated with peritoneal dialysis 11 hours after admittance to hospital. This female patient has been receiving insulin from three months of age and today at the age of 10 years she leads a normal life despite being on insulin therapy. A very low level of c-peptide (<0.3 ng/ml) clearly confirms she is affected by Type 1 diabetes. To our knowledge this is the first case report of hyperosmolar coma in a neonate with Type 1 diabetes who survived this condition without late neurological consequences.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
2/10. Prognostic value of evoked potentials and sleep recordings in the prolonged comatose state of children. Preliminary data.OBJECTIVES: sleep recordings and evoked potentials (EPs) were used in five comatose children to evaluate their predictive value for outcome following a severe comatose state. methods AND SUBJECTS: The protocol included EEG, Brainstem Evoked Responses (BERs), Somatosensory evoked potentials (SEPs) and polysomnography. From 10 to 15 days post-coma (D10 to D15), EEG and clinical examinations were carried out every second day, then one day in four from 15 to 30 days post-coma (D15 to D30), and one day in seven from D30 to six months (M6). evoked potentials and polysomnography were recorded on D10-D15 or D30 in the second month (M2) and in M6. Of the five children, three were in anoxic coma and two in traumatic coma. All had extensive lesions and a glasgow coma scale (GCS) score of less than five. The results of the EEG, polysomnographic and EP recordings were compared to the clinical outcome. RESULTS AND CONCLUSION: In the three anoxic comas we observed BER abnormalities and the absence of SEP N20 associated with wide cortical lesions with brainstem extension. sleep recordings showed major alterations of the wake-sleep cycle without any improvement in M6. Abnormalities included loss of the normal REM-sleep pattern associated with alteration of NREM sleep and periods of increase in motor activity without EEG arousal. This sleep pattern appeared to be associated with involvement of the brainstem. In the two traumatic comas, alterations of the early cortical SEP responses were less severe and the BERs were normal. Some sleep spindles were observed as well as the persistence of sleep cycles in the first weeks post-coma. The combined use of EEG, EPs and polysomnography improved the outcome prediction in comparison with the use of just one modality. EPs and sleep recordings were far superior to clinical evaluation and to GCS in the appreciation of the functional status of comatose children. The reappearance of sleep patterns is considered to be of favorable prognosis for outcome of the coma state, as is the presence of sleep spindles in post-trauma coma. This study showed that EPs and sleep recordings help to further distinguish between patients with good or bad outcomes.- - - - - - - - - - ranking = 2.2857142857143keywords = coma (Clic here for more details about this article) |
3/10. 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 = 0.14285714285714keywords = coma (Clic here for more details about this article) |
4/10. A case of diabetic non-ketotic hyperosmolar coma with an increase with plasma 3-hydroxybutyrate.We have seen a case of "diabetic non-ketotic hyperosmolar coma" with ketosis. An 84-year-old man was brought into the hospital in a deeply comatous and dehydrated state. The initial blood glucose level was 1252 mg/dl with plasma osmolarity of 435 mOsm/l, but no ketonuria was detected by the nitroprusside method (Ketostix). However, the plasma 3-hydroxybutyrate (3-OHBA) level was 5 mM in a newly developed bedside film test. The serum ketone bodies were later found to be 5.56 and 0.82 mmol/l for 3-OHBA and acetoacetate (AcAc), respectively. A marked increase in glucagon, cortisol and ADH with renal dysfunction (creatinine 5.0 mg/dl) were noted. An abnormal electrocardiogram, occular convergence and chorea like movement disappeared after correction of metabolic disturbances. The moderate level of IRI (14 microU/ml) on admission and a good response to glucagon 2 months after admission also indicate that the present case is a typical hyperosmolar non-ketotic coma. Because of a preferential increase in 3-OHBA, ketonuria seemed to be absent in the regular nitroprusside test. Marked dehydration is thought to cause renal dysfunction, and the increase in ADH may have helped to prevent further aggravation of ketoacidosis. We propose to change the term hyperosmolar non-ketotic coma (HNC) to diabetic hyperosmolar coma (DHC), because sometimes patients with hyperosmolar non-ketotic diabetic coma are ketotic, as seen in the present case. Determination of 3-OHBA or individual ketone bodies in blood is important and essential for the differential diagnosis of diabetic coma. The diagnosis of either ketoacidotic or hyperosmolar coma should be made depending on the major expression of ketoacidosis or hyperglycemic hyperosmolarity.- - - - - - - - - - ranking = 1.7142857142857keywords = coma (Clic here for more details about this article) |
5/10. survival with severe hypernatremia.In a 74-year-old woman, excessive insensible water loss developed secondary to a period of hot, humid weather, associated with an underlying inability to obtain adequate water replacement. On admission to the hospital she was comatose, clinically dehydrated, and had laboratory values consistent with a water deficit of approximately 30% (9 L) of body water. serum sodium concentration was 202 mEq/L. serum osmolality was 430 mOsm/L. The patient remained comatose for seven days, during which time she was vigorously treated with fluids, and she gradually recovered. This case represents what we believe is a unique report in the literature of the severity of hypernatremia developing via this pathogenic mechanism and survival in an adult with this degree of disturbance of sodium and water homeostasis.- - - - - - - - - - ranking = 0.28571428571429keywords = coma (Clic here for more details about this article) |
6/10. Uncommon extensive juxtacortical necrosis of the brain.A previously healthy woman in middle age, vacationing in spain, is treated with a massive dose of insulin for minimal hyperglycemia following an apparent gastrointestinal disease. This results in rapid coma and, 20 days later, in death. At autopsy, the main finding consists in a remarkable and uncommon ribbon-like juxtacortical necrosis of the white matter in both hemispheres of the telencephalon. There is also a microscopic focal necrosis in the pons cerebri. The grey matter of cortex and basal nuclei, and the subcortical arcuate fibers are spared. The detailed autopsy fails to reveal other essential changes. We have not been able to find reports on an identical case. Hypoglycemic coma usually causes cerebral lesions different from those seen in the present case. A brief analysis of the differential diagnosis is made. In the absence of unequivocal signs of infection, vascular disease or degenerative marks, the findings are tentatively related to complex interactions between fluid loss, hypoglycemic coma, hypoxia and other metabolic disturbances.- - - - - - - - - - ranking = 0.42857142857143keywords = coma (Clic here for more details about this article) |
7/10. Hyperosmolar non-ketotic coma in diabetic stroke patients.Hyperosmolar non-ketotic coma in diabetes is a life-threatening condition. We describe three patients, aged 59-67 years, who developed hyperosmolar coma during the first ten days after admission for stroke. Common to all three were normal plasma osmolality and slightly elevated plasma creatinine levels on admission, treatment with diuretics, parenteral dextrose administration before and low urinary glucose output during the coma. In the five days preceding the coma, total fluid deficits were 3.8, 6.5 and 9.4 1, respectively. In one patient the rate of glucose delivery had clearly exceeded utilization during adequate insulinization, in another a marked reduction in urinary glucose output preceded extreme hyperglycaemia and coma. Two of the three patients died, both from extensive thrombus formation in cerebral arteries and multiple emboli to the lungs. We conclude that enhanced endogenous glucose production and reduced renal clearance of glucose may contribute to precipitate hyperosmolar non-ketotic coma. A close monitoring of fluid and dextrose administration seems mandatory in diabetic stroke patients, in particular if renal function is impaired or if diuretics are given. insulin treatment should be considered in all diabetic patients during the first days after a stroke.- - - - - - - - - - ranking = 1.4285714285714keywords = coma (Clic here for more details about this article) |
8/10. Patch grafts of dehydrated cadaveric dura mater for tube-shunt glaucoma surgery.Human donor sclera is commonly used in glaucoma surgery with a tube-shunt (eg, Molteno, Baerveldt, Shocket, Krupin-Denver) to cover the external portion of the silicone tube and prevent its erosion through the overlying conjunctiva. Common problems with this technique include immune-mediated melting of the graft and the potential for infectious disease transmission by the grafted material. A case is presented of a patient in whom a low-grade iridocyclitis was associated with the gradual melting of a scleral patch graft; the scleral patch was then replaced with commercially available, dehydrated human dura mater. The practical and theoretical advantages of cadaveric human dura mater in tube-shunt glaucoma surgery are discussed.- - - - - - - - - - ranking = 0.85714285714286keywords = coma (Clic here for more details about this article) |
9/10. peritoneal dialysis in hypernatraemic, ketoacidotic diabetic coma.Hypertonic dehydration in a 13-year-old boy with ketoacidotic diabetic coma has been treated successfully with peritoneal dialysis and isotonic fluids. Modes of treatment with either hypotonic or isotonic fluids are discussed, as is the feasibility of peritoneal dialysis. We recommend isotonic solutions composed of equal parts of 5.5% glucose and 0.9% sodium chloride combined with peritoneal dialysis in order to secure a relatively slow correction of the hypertonic state.- - - - - - - - - - ranking = 0.71428571428571keywords = coma (Clic here for more details about this article) |
10/10. Hypocalcemic coma following two pediatric phosphate enemas.Coma, tetany, dehydration, hypotension, tachycardia, and hyperpyrexia developed in a 2 1/2-year-old girl following two hypertonic phosphate pediatric enemas. She had marked hyperphosphatemia, hypocalcemia, hypernatremia, and acidosis. hypocalcemia due to hyperphosphatemia can explain all of these findings. Calculations indicate that about one third of the phosphorus and sodium contents of the enema were absorbed. physicians should be aware of the potentially lethal complication of this treatment, which is part of everyday practice.- - - - - - - - - - ranking = 0.57142857142857keywords = coma (Clic here for more details about this article) |
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