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1/90. 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. ( info)

2/90. A case of hyperosmolar nonketotic coma occurring during chemotherapy using cisplatin for gallbladder cancer.

    A 61 year-old woman was admitted to our hospital because of an abdominal tumor. She was diagnosed with recurrent gallbladder cancer, and treated with cisplatin (CDDP). On day 6, after the 1st cycle of chemotherapy, she developed confusion and suddenly became comatose. She was diagnosed as having hyperosmolar nonketotic coma (HNC) on day 7. She had no history of diabetes mellitus. She recovered from HNC after 3 days of treatment with continuous infusion of 0.45% saline and moderate amounts of insulin. HNC may be a complication of CDDP chemotherapy in patients with malignancy. early diagnosis and appropriate treatment is necessary for HNC occurring during chemotherapy for malignant disease. ( info)

3/90. Elevated serum creatine kinase activity in a patient with acute pancreatitis.

    A 62-year-old man presented with a five-day history of a 'flu-like' illness, epigastric pain and a state of increasing confusion. His serum values for amylase and glucose were grossly elevated, as was the creatine kinase (CK) activity, being 23 times above the upper limit of normal. CK-MB was less than 5% of his total CK activity. There was no past history of diabetes or recent history of intramuscular injections or injury. A diagnosis of acute pancreatitis complicated by hyperosmolar non-ketotic (HONK) diabetic pre-coma was made. The patient was treated with intravenous fluids, insulin and subcutaneous heparin. Normal values for serum amylase and CK activity were recorded with convalescence. This case indicates a possible association of a rise in total CK activity with acute pancreatitis complicated by HONK diabetic pre-coma. This observation was made in the absence of clinically evident muscle pathology. ( info)

4/90. Reversible tetraplegia due to polyneuropathy in a diabetic patient with hyperosmolar non-ketotic coma.

    critical illness polyneuromypathy has not previously been reported as a complication of diabetic coma. We describe a patient with hyperosmolar non-ketotic coma (HONK) complicating gram-negative sepsis in whom persistent coma and profound tetraplegia caused considerable concern. Although, initially, it was feared that the patient had suffered a central neurological complication such as stroke or cerebral oedema, a diagnosis of critical illness motor syndrome (CIMS) was subsequently confirmed neurophysiologically. Profound limb weakness associated with HONK is not necessarily due to a catastrophic cerebral event, rather it may be a result of CIMS, which has an excellent prognosis for full neurological recovery. ( info)

5/90. suicide of a diabetic by inducing hyperglycemic coma.

    Deaths due to hyperglycemic and hyperosmolar coma in diabetics are usually disease-related. In the exceptional case reported here there was evidence for an intentional ingestion of a sugar solution, the person was a diabetic and known to be depressive suggesting a suicidal intention. The autopsy findings were inconspicuous and only further laboratory findings led to the final diagnosis. ( info)

6/90. Hyperosmolar nonketotic coma: prevention, diagnosis, and treatment.

    With the multi-faceted approach to head and neck cancer today, maintaining caloric intake by long-term enteral hyperalimentation is commonplace. Along with the tremendous advantages of this form of nutrition, the disadvantage of hyperosmolar nonketotic diabetic acidotic coma is present. mortality rates are quoted from 40% to 70% according to the literature reviewed. Therefore, prevention is the best form of treatment. The cause, diagnosis, and treatment will be discussed. ( info)

7/90. Hyperosmolar nonketotic syndrome with hypernatremia: how can we monitor treatment?

    We report the case of a 62 year-old symptomatic patient with severe hyperglycemic hyperosmolality associated with hypernatremia. During treatment, the progressive decrease in serum tonicity, which resulted in the amelioration of the neurological symptoms, followed the decrease in serum glucose and mainly the corrected serum sodium levels rather than the decrease in the uncorrected serum sodium levels. The case illustrates the usefulness of glucose - corrected serum sodium levels to monitor treatment in such conditions in order to avoid neurological consequences caused by the decrease in serum osmolality. ( info)

8/90. Olanzapine-lnduced hyperglycemic nonketonic coma.

    OBJECTIVE: To report a case of olanzapine-induced hyperglycemia leading to a hyperosmolar, hyperglycemic, nonketonic coma. CASE SUMMARY: A 51-year-old, 85.5-kg (ideal body weight 79.9 kg), white man presented to a veterans Affairs hospital with a serum glucose concentration of 1596 mg/dL. Soon thereafter, he went into a hyperosmolar, hyperglycemic, nonketonic coma. Olanzapine therapy had been instituted less than six months prior to this event; approximately two months before this event, his blood glucose was 108 mg/dL. Eight days after stopping olanzapine, the glucose concentration returned to normal, and the patient no longer required insulin nor any other glucose-lowering agents. DISCUSSION: The insulin resistance caused by olanzapine is normally attributed to the weight gain associated with the drug. In this patient, it appears that olanzapine caused hyperglycemia by a mechanism other than weight gain. CONCLUSIONS: This case report and others from the literature suggest that olanzapine therapy may induce hyperglycemia in some patients. ( info)

9/90. 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. ( info)

10/90. Hyperosmolar diabetic non-ketotic coma, hyperkalaemia and an unusual near death experience.

    Generally, cardiac arrest due to pulseless electrical activity has a poor outcome, except when reversible factors such as acute hyperkalaemia are identified and managed early. Hyperosmolar diabetic non-ketotic coma may lead to acute hyperkalaemia. Hyperosmolar diabetic non-ketotic coma is a metabolic emergency usually seen in elderly non-insulin dependent diabetics, characterized by severe hyperglycaemia, volume depletion, altered consciousness, confusion and less frequently neurological deficit. Cerebrovascular accident or transient ischaemic attack may be mistakenly diagnosed, particularly if the patient has no history of diabetes mellitus. Delays in diagnosis and management of glycaemic emergencies presenting as a constellation of neurological abnormalities can be avoided by routine early measurement of blood glucose. Hyperosmolar diabetic non-ketotic coma should be considered in any patient with altered consciousness or neurologic deficit in conjunction with hyperglycaemia. As hyperosmolar diabetic non-ketotic coma results in severe fluid depletion, electrolyte disturbance, profound hyperglycaemia and an altered mental state, the guiding principles of therapy include aggressive rehydration, insulin therapy, correction of electrolyte abnormalities and treatment of any underlying illnesses. Treatment of acute hyperkalaemia includes calcium ions, insulin with dextrose, salbutamol and haemodialysis. ( info)
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