Cases reported "Hypoglycemia"

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1/156. hypothermia--a sign of hypoglycemia.

    hypothermia may occur in association with hypoglycemia, and indeed may be the only sign. Two cases are presented. In one, the patient presented with hypoglycemic encephalopathy. In the insulin dependent diabetic, the condition is life-threatening. Subnormal temperature is a clue to hypoglycemia in the alcoholic. The mechanism of hypothermia has been extensively studied, but remains unclear.
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2/156. Recognizing factitious hypoglycemia in the family practice setting.

    BACKGROUND: Factitious hypoglycemia is a deliberate attempt to induce a low serum glucose level using either insulin or oral hypoglycemic agents. Sulfonylurea-induced hypoglycemia is more common than incidents of insulin abuse, and hypoglycemia caused by these oral agents is biochemically indistinguishable from insulinoma. methods: We describe a case of factitious hypoglycemia resulting from insulin abuse in an adult diabetic patient, review the essentials of glucose homeostasis, and describe diagnostic tests that allow a differential diagnosis. RESULTS AND CONCLUSION: Factitious hypoglycemia is associated with a higher incidence of suicide, depression, and personality disorders. Insulin-induced hypoglycemia can be detected by an insulin to c-peptide ratio that is greater than 1.0. In the absence of proof to the contrary, insulinoma should be considered the cause of hypoglycemia until another diagnosis is established. The generally poor prognosis for patients with factitious hypoglycemia underscores the importance of early recognition of factitious disorders.
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3/156. Evaluation of serum markers of neuronal damage following severe hypoglycaemia in adults with insulin-treated diabetes mellitus.

    BACKGROUND: Neurone-specific enolase (NSE) and protein s-100 (S-100) may be used as markers of acute neuronal damage in humans with neurological disorders. METHOD: To evaluate their use following a single episode of severe hypoglycaemia (defined as an episode requiring external assistance to aid recovery), serum concentrations of NSE and S-100 were measured following hypoglycaemia which had not caused persistent neurological impairment in 16 patients with insulin-treated diabetes (the 'hypo' subjects), and in three diabetic patients who died following severe hypoglycaemia. The serum proteins were also measured in 10 subjects with insulin-treated diabetes who had not experienced an episode of severe hypoglycaemia within the preceding year (the 'control' subjects). RESULTS: No differences in serum concentrations of NSE and S-100 were observed between the 'control' and the 'hypo' subjects at either 36 hours or seven days after the episode of severe hypoglycaemia (p>0.05). However, in two of the three subjects who died following hypoglycaemia, serum concentrations of the markers were markedly elevated. CONCLUSIONS: Any neuronal injury occurring during severe hypoglycaemia that is not associated with persistent neurological deficit is insufficient to provoke elevation of these serum markers. However, the measurement of serum concentrations of NSE and S-100 may have a prognostic role in evaluating clinical outcome following severe hypoglycaemia which is associated with neurological damage.
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4/156. The effect of maternal hypothermia on the fetal heart rate.

    Fetal bradycardia is a recognized response to maternal hypothermia but has not previously been reported in conjunction with diabetes. A 30-year-old insulin-dependent diabetic was admitted at 35 weeks gestation for control of her diabetes. She developed maternal hypothermia and hypoglycemia and the fetal heart rate fell to 100 beats per minute (b.p.m.). However, the fetal heart rate gradually returned to normal after rewarming the patient.
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5/156. Riding out a diabetic emergency.

    Acute complications of diabetes are like a runaway roller coaster. Diabetes or its treatment can rocket your patient's blood glucose level to dizzying heights or plunge it to life-threatening lows. hypoglycemia, the most common endocrine emergency, typically occurs in a known diabetic patient whose therapy with insulin or oral diabetes agents goes awry. At the opposite extreme, soaring blood glucose levels mark the acute conditions diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic nonketotic state (HHNS). These complications may send the patient to the emergency department (ED) before he even knows he has diabetes. In this article, I'll explain how these problems develop and spell out nursing measures to get your patient back on track.
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6/156. chlorpropamide toxicity with survival despite 27-day hypoglycemia.

    CASE REPORT: In the past 5 years at our institution, 12 cases involving the ingestion of chlorpropamide 3-15 g were fatal. We report a 23-year-old woman with an estimated ingestion of chlorpropamide 5-10 g. Initial cardiovascular collapse, attributed to the blockade of potassium channel transport, responded to intensive support including 3 days of cardiac pacing. Urinary excretion of chlorpropamide and hypoglycemia persisted until day 27. The toxic mechanisms and high risk of chlorpropamide are summarized. A fatal therapeutic dose ratio as low as 4:1 has made this antidiabetic agent obsolete.
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7/156. Adrenal crisis presenting as hypoglycemic coma.

    An 18-month-old male infant presented with hypoglycemic coma and clinical signs of bronchopneumonia. He was suspected of suffering from septic shock. The patient progressed to irreversible multiple organ failure before the diagnosis of adrenal crisis was established. plasma levels of ACTH and cortisol remained undetectable. renin and aldosterone were normal. An autopsy failed to demonstrate any adrenal gland cortical tissue. Immunohistochemical staining demonstrated the presence of all pituitary hormones except ACTH, establishing the diagnosis of isolated ACTH deficiency. intensive care clinicians should consider adrenal crisis in non-diabetic children with hypoglycemia and rapid circulatory deterioration.
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8/156. Normal pressure hydrocephalus in diabetic patients with recurrent episodes of hypoglycemic coma.

    The pathophysiology of brain damage induced by severe hypoglycemia is still unknown. We experienced a case with type 1 diabetes and recurrent severe hypoglycemic coma who showed a central brain atrophy and an abnormal cerebrospinal fluid flow, suggesting normal pressure hydrocephalus. Following this case, the CSF flow was studied using 111In-DTPA cisternography in six consecutive diabetic patients admitted for repeated episodes of hypoglycemic coma. All the patients showed the central brain atrophy on computed tomography and four of them (67%) had the ventricular reflux, with delayed clearance of 111In-DTPA. Two patients with abnormal CSF flow showed cognitive dysfunction by WAIS or WAIS-R. In contrast, none of five randomly selected diabetic patients, without hypoglycemic coma showed abnormal CSF flow. Our results suggest the presence of normal pressure hydrocephalus in diabetic patients with recurrent hypoglycemic coma. It may associate with the cognitive dysfunction.
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9/156. Reversal of hypoglycemia unawareness in a long-term type 1 diabetic patient by improvement of beta-adrenergic sensitivity after prevention of hypoglycemia.

    The purpose of this study was to assess the effect of strict avoidance of hypoglycemia on beta-adrenergic sensitivity in a type 1 diabetic patient with hypoglycemia unawareness and a diabetes duration of 55 yr. beta-Adrenergic sensitivity was determined by an isoproterenol test and was expressed as the lowest dose of isoproterenol that increases the heart rate by 25 beats/min (IC25). plasma epinephrine and symptom responses to hypoglycemia were determined during a 3-h hypoglycemic (3 mmol/L) clamp. Initially, the patient had a near-normal counterregulatory plasma epinephrine response to hypoglycemia but reduced beta-adrenergic sensitivity (IC25, 2 microg) compared to 10 hypoglycemia aware, type 1 diabetic patients (0.65 /- 0.14 microg) and 10 normal control subjects (1.13 /- 0.21 microg). After 1 yr of strict avoidance of blood glucose levels below 4 mmol/L, the IC25 decreased to 0.25 microg, reflecting improved beta-adrenergic sensitivity. In conclusion, the reduced beta-adrenergic sensitivity in this patient was probably the reason for hypoglycemia unawareness and was reversed by strict avoidance of hypoglycemia.
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10/156. The care of students with insulin-treated diabetes mellitus living in university accommodation: scope for improvement?

    Concern has been expressed about the welfare of young adults with Type 1 diabetes mellitus who leave home to attend university or college for tertiary education. This has been highlighted by the local experience in Edinburgh of two male students with Type 1 diabetes, both of whom died from metabolic complications of diabetes during their first term at universities distant from their homes. One student died following the development of cerebral oedema secondary to diabetic ketoacidosis, which was probably precipitated by prolonged coma after an episode of severe hypoglycaemia. Another student, who was found 'dead in bed', had a history of previous severe hypoglycaemia. At a Fatal Accident Inquiry in Edinburgh, held following the death of the first student, recommendations were made to improve the care and personal safety of students with diabetes living in university accommodation. Despite the report being circulated to all Scottish universities, the second student died within three years of the inquiry. Further efforts to protect the welfare of students with Type 1 diabetes who are attending centres for tertiary education away from their home environment may require the more active participation by diabetes healthcare professionals.
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