1/14. Bilateral basal ganglion haemorrhage in diabetic ketoacidotic coma: case report.We report bilateral oedema and haemorrhagic transformation in the basal ganglia of a 59-year old woman with severe diabetic ketoacidosis. Lack of cerebral vascular autoregulation, followed by blood-brain barrier disruption due to the so-called breakthrough mechanism is presumed to be the cause.- - - - - - - - - - ranking = 1keywords = ketoacidosis (Clic here for more details about this article) |
2/14. Reversal of foetal hydrops and foetal tachyarrhythmia associated with maternal diabetic coma.Foetal hydrops is always a challenge for the clinician. We report a case of tachycardia associated with hydrops and hydramnios in a pregnancy complicated with diabetic coma at 28 weeks gestation. Normal foetal heart rate was recorded immediately after correction of maternal acidotic status and hydrops eventually disappeared. The woman was delivered at 32 weeks and the baby had an uncomplicated postnatal course. We hypothesise that maternal ketoacidosis has been the precipitating factor of tachycardia and congestive heart failure and that this case is conceptually similar to the "late death" phenomenon, reported in cases of poorly controlled maternal diabetes.- - - - - - - - - - ranking = 1keywords = ketoacidosis (Clic here for more details about this article) |
3/14. Recurrent hyperosmolar nonketotic episodes in a young diabetic.A 15-month-old girl was successfully treated for substantial hyperosmolarity in the absence of ketosis at the onset of permanent insulin-requiring diabetes mellitus. hypotonic solutions containing small amounts of glucose and subcutaneous administration of low doses of insulin were empolyed. Potassium was added to the hydrating solutions during the second hour of treatment. In the next three months, two recurrences of this syndrome were verified and successfully treated in a similar manner.- - - - - - - - - - ranking = 2.4340010333998keywords = ketosis (Clic here for more details about this article) |
4/14. Profound hypokalemia in diabetic ketoacidosis: a therapeutic challenge.OBJECTIVE: To describe profound hypokalemia in a comatose patient with diabetic ketoacidosis. methods: We present a case report, review the mechanisms for the occurrence of hypokalemia in diabetic ketoacidosis, and discuss its management in the setting of hyperglycemia and hyperosmolality. RESULTS: A 22-year-old woman with a history of type 1 diabetes mellitus was admitted in a comatose state. Laboratory tests revealed a blood glucose level of 747 mg/dL, serum potassium of 1.9 mEq/L, pH of 6.8, and calculated effective serum osmolality of 320 mOsm/kg. She was intubated and resuscitated with intravenously administered fluids. Intravenous administration of vasopressors was necessary for stabilization of the blood pressure. Intravenous infusion of insulin was initiated to control the hyperglycemia, and repletion of total body potassium stores was undertaken. A total of 660 mEq of potassium was administered intravenously during the first 12.5 hours. Despite such aggressive initial repletion of potassium, the patient required 40 to 80 mEq of potassium daily for the next 8 days to increase the serum potassium concentration to normal. CONCLUSION: Profound hypokalemia, an uncommon initial manifestation in patients with diabetic ketoacidosis, is indicative of severe total body potassium deficiency. Under such circumstances, aggressive potassium repletion in a comatose patient must be undertaken during correction of other metabolic abnormalities, including hyperglycemia and hyperosmolality. Intravenously administered insulin should be withheld until the serum potassium concentration is (3)3.3 mEq/L.- - - - - - - - - - ranking = 7keywords = ketoacidosis (Clic here for more details about this article) |
5/14. Cerebral oedema complicating diabetic ketoacidosis.Four children presented with cerebral oedema secondary to diabetic ketoacidosis, each of whom had a different clinical picture and time of onset of neurological deterioration. No single factor emerged as the cause of the cerebral oedema, but disturbances in brain water balance appeared to be already operative at the time of presentation with ketoacidosis. Irregularities in treatment may exacerbate these disturbances, leading to frank cerebral oedema. diagnosis of this dangerous complication of diabetic ketoacidosis depends on clinical awareness; the diagnosis may be confirmed by CT scan. Management remains empirical.- - - - - - - - - - ranking = 7keywords = ketoacidosis (Clic here for more details about this article) |
6/14. Coexisting bacterial pyelonephritis and bilateral ureteral fungus balls in a diabetic patient. Case report.Bacterial pyelonephritis is a common precipitating factor in the development of diabetic ketoacidosis. Prompt diagnosis and appropriate antimicrobial therapy usually result in resolution of constitutional symptoms and adequate control of serum glucose. However, occasional cases of presumed bacterial pyelonephritis may not respond to appropriate empiric antibiotic therapy, then causes should be sought such as obstruction or untreated fungal infections of the urinary tract. In this case a diabetic patient with classical pyelonephritis was found to have bilateral ureteral fungus balls as the underlying cause of refractory infection.- - - - - - - - - - ranking = 1keywords = ketoacidosis (Clic here for more details about this article) |
7/14. Cerebral edema complicating nonketotic hyperosmolar coma.Cerebral edema as a complication of the therapy of diabetic coma has been described for over 50 years, although modern awareness dates to about 1967. Almost all cases have occurred in patients with diabetic ketoacidosis (DKA). Although a few cases of cerebral edema have been reported in patients with nonketotic hyperosmolar coma (NKHC), these are in general not well documented by either autopsy data of cat scans. Over a period of 9 years, I have encountered 5 patients who developed cerebral edema as a complication of the therapy of NKHC. The initial plasma glucose in these patients was 1,496 /- (SD) 296 mg/dl and plasma osmolality was 382 /- 29 mosm/kg. All had depression of sensorium to at least a stupor (stage I coma or greater). All were treated with intravenous insulin and either 77 or 154 mM NaCl, and plasma glucose fell at a mean rate of 38 mg/dl/h. In all patients, plasma glucose fell below 250 mg/dl (mean of 18 /- 66 mg/dl) and all patients experienced increased depression of sensorium, elevated csf pressure, and brain swelling as diagnosed by cat scanning. Therapy with various combinations of glucose, mannitol and steroids were without effect. In 1 patient, insertion of a subdural intracranial screw lowered intracranial pressure from 24 to 3 cm of H2O. Three of the 5 patients died and 2 remain in a persistent vegetative state, 1 of whom is also quadriplegic.(ABSTRACT TRUNCATED AT 250 WORDS)- - - - - - - - - - ranking = 1keywords = ketoacidosis (Clic here for more details about this article) |
8/14. Hyperglycemic hyperosmolar coma in a 9-month-old child.Hyperglycemic hyperosmolar coma is a life-threatening emergency with a mortality much higher than that of other forms of hyperosmolarity such as hypernatremia or diabetic ketoacidosis. Despite the differences in the three conditions, present evidence suggests that correction of hyperosmolarity should proceed slowly to avoid the seizures that may occur in all three conditions. This report describes a 9-month-old diabetic child who initially had hyperglycemic hyperosmolar coma and who is one of the youngest survivors of this syndrome in the American literature. This case report points out the limited understanding of the pathophysiology of this syndrome and the consequent problems of therapy.- - - - - - - - - - ranking = 1keywords = ketoacidosis (Clic here for more details about this article) |
9/14. Nonketotic hyperosmolar coma in two diabetic children.Two diabetic children with nonketotic hyperosmolar coma were treated successfully. In one of the patients, plasma-free fatty acids, insulin, c-peptide and two lipolytic hormones (growth hormone and cortisol) were measured serially during the coma. Free fatty acids, insulin, c-peptide, growth hormone and cortisol levels were within normal ranges and subsequently these levels did not change significantly. The results suggest that the normal levels of lipolytic hormones may account for the normal plasma free fatty acids and the absence of ketosis found in children with nonketotic hyperosmolar coma, in contrast to the elevated levels of lipolytic hormones and ketone bodies in ketoacidotic diabetic coma.- - - - - - - - - - ranking = 2.4340010333998keywords = ketosis (Clic here for more details about this article) |
10/14. Constant low-dose insulin infusion in severe diabetes mellitus.Eight patients with diabetic ketoacidosis and two patients with hyperosmolar non-ketotic coma have been treated with a constant low-dose insulin infusion technique (2-4 units/hour). In all cases a rapid, smooth control of blood glucose levels was obtained in conjunction with a similar improvement in clinical status and remedying of other biochemical defects. At no stage of therapy did hypoglycaemia or hypokalaemia occur. In the majority of cases control of the patient's metabolic state was achieved within eight to 12 hours. The insulin regime is simple to institute and maintain.- - - - - - - - - - ranking = 1keywords = ketoacidosis (Clic here for more details about this article) |
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