1/29. 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.- - - - - - - - - - ranking = 1keywords = ketoacidosis (Clic here for more details about this article) |
2/29. 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.- - - - - - - - - - ranking = 1keywords = ketoacidosis (Clic here for more details about this article) |
3/29. hypoglycemia and resistance to ketoacidosis in a subject without functional insulin receptors.humans with congenital absence of the islets of langerhans and mice rendered null for the insulin receptor rapidly develop severe hyperglycemia and ketoacidosis and, if untreated, die in the early neonatal period. In contrast, children with homozygous or compound heterozygous mutations of the insulin receptor gene, although hyperglycemic postprandially, survive for many months without developing ketoacidosis. Paradoxically, they often develop hypoglycemia. The rarity of the condition and the difficulties of undertaking metabolic studies in ill infants have limited the physiological information that might explain the clinical features. We studied a boy with Donohue's syndrome who represents a further example of the null phenotype, with two different and novel nonsense mutations in the alpha-subunit of the receptor. He survived for 8 months without developing ketoacidosis, and fasting hypoglycemia was a frequent problem. Despite the complete absence of insulin receptors, evidence for persistent insulin-like effects on fat and liver was seen; fasting plasma beta-hydroxybutyrate and nonesterified fatty acid levels were low, fell further during the early postprandial period, and failed to rise in response to hypoglycemia. The inverse relationships between plasma insulin and insulin-like growth factor-binding protein-1 levels were maintained, suggesting persistent hepatic effects of insulin. GH levels measured over a 6.5-h period were low throughout. Thus, the differences between congenital insulin deficiency vs. insulin receptor deficiency in humans may be explained by persistent insulinomimetic activity of the grossly elevated plasma insulin presumably being mediated through the type 1 insulin-like growth factor receptor. As GH plays a critical role in the regulation of ketogenesis during insulinopenia in humans, but not in rodents, this may contribute to the distinct phenotype of human vs. mouse insulin receptor knockouts.- - - - - - - - - - ranking = 7keywords = ketoacidosis (Clic here for more details about this article) |
4/29. Effect of growth hormone treatment on hypoglycemia in a patient with both hepatic glycogen synthase and isolated growth hormone deficiencies.A 7 year-old boy presenting with growth retardation, fasting hypoglycemia and ketoacidosis was diagnosed as having both idiopathic growth hormone (GH) deficiency and hepatic glycogen synthase (GS) deficiency caused by a homozygous mutation in exon 5 of the liver glycogen synthase gene (GYS-2). After four years of treatment with recombinant human GH, height increased from -4.9 SDS to -2.05 SDS which is near his target height of -1.6 SDS. The GH treatment, however, did not prevent the fasting hypoglycemia. blood glucose levels were only normalized after avoiding fasting intervals of more than five hours and the frequent feeding of protein-rich meals according to the guidelines for treatment of hepatic GS deficiency.- - - - - - - - - - ranking = 1keywords = ketoacidosis (Clic here for more details about this article) |
5/29. Reversible amnesia in a Type 1 diabetic patient and bilateral hippocampal lesions on magnetic resonance imaging (MRI).AIMS: Intensive insulin therapy of Type 1 diabetes limits its chronic complications, but is associated with an increased risk of severe hypoglycaemia and its neuroglycopenic consequences. methods: Case report. RESULTS: A 24-year-old male with 15 years' history of Type 1 diabetes, who was missing for 48 h, was found at home in ketoacidosis coma. intensive care permitted a rapid improvement revealing an unexpected severe anterograde amnesia, confirmed by neuropsychological testing. MRI performed 4 days after admission showed abnormal bilateral hyperintensity signals on T2-weighted images in the hippocampus. Three months later, the patient had nearly completely recovered and resumed work. MR images and neuropsychological testing returned to normal. CONCLUSIONS: The most likely course of events favours an initial prolonged hypoglycaemic coma following insulin overdose. The hippocampal injury may be a result of hypoglycaemia. Neuropsychological testing and MRI abnormalities were completely reversible. This case underlines the potential risks of intensive insulin therapy.- - - - - - - - - - ranking = 1keywords = ketoacidosis (Clic here for more details about this article) |
6/29. Neonatal hypoglycaemia in severe succinyl-CoA: 3-oxoacid CoA-transferase deficiency.Succinyl-CoA: 3-oxoacid CoA-transferase (SCOT) deficiency is an inborn error of ketone body utilization, characterized by intermittent ketoacidotic crises and persistent ketosis. The diagnosis was suspected in a patient who presented with hypoglycaemia, ketoacidosis and coma at 4 days of age. The hypoglycaemic tendency was only observed during the first month of life. A novel macromolecular labelling assay in cultured skin fibroblasts using D-3-hydroxy[3-14C]butyrate supported the diagnosis. Subsequently, 9% residual SCOT activity and undetectable cross-reactive protein were noted in fibroblasts and the patient was found to be homozygous for the G324E SCOT gene mutation. By 7 years of age, recurrent episodes of ketoacidosis superimposed on persistent hyperketonaemia had resulted in over 25 hospitalizations requiring intravenous fluid, glucose and sodium bicarbonate therapy. He has had normal growth but developmental delay and attention deficit-hyperactivity disorder. A continuous intravenous glucose infusion at 38 microlmol (6.8 mg)/kg per min reduced plasma total ketone levels from greater than 1.5 mmol/L to less than 0.5 mmol/L after 48 h. This indicates that patients with SCOT deficiency do not always manifest ketosis with administration of a sufficient amount of carbohydrates, but that even under such conditions hyperketonaemia is difficult to eliminate completely. The presence of hypoglycaemia does not exclude the diagnosis of SCOT deficiency in infancy.- - - - - - - - - - ranking = 5.7040713706939keywords = ketosis, ketoacidosis (Clic here for more details about this article) |
7/29. The diagnosis of mitochondrial HMG-CoA synthase deficiency.Deficiency of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase, the only disorder exclusively affecting hepatic ketogenesis, is a cause of hypoglycemic coma. We report that the diagnosis can be made by typical laboratory findings (hypoketosis, elevated free fatty acids, normal acylcarnitines, specific urinary organic acids) during acute episodes.- - - - - - - - - - ranking = 1.8520356853469keywords = ketosis (Clic here for more details about this article) |
8/29. Alcohol induced ketoacidosis, severe hypoglycemia and irreversible encephalopathy.BACKGROUND: Severe hypoglycemia leading to permanent brain damage is rare in non-diabetic population. We present one such case where chronic alcoholism combined with prolonged fasting lead to such a state and patient ended in a persistent vegetative state. CASE REPORT: A 50 year old Asian woman with past history of chronic alcoholism and hepatitis c was found unresponsive in her house after drinking alcohol consecutively for 2 days. Finger-stick glucose done by paramedics was <20 mg/dl. She was given 50 ml of 50% dextrose without any neurological response. On arrival in the emergency department patient was found to be comatose with only withdrawal response to deep painful stimuli and a negative babinski's sign. Computed tomogram of the head revealed mild cerebral atrophy. After an extensive work up a diagnosis of alcoholic ketoacidosis with hypoglycemia related encephalopathy was made. CONCLUSIONS: Alcohol induced ketoacidosis is usually associated with normal blood glucose. The probable etiology of low blood sugar in our patient was alcohol-induced inhibition of gluconeogenesis along with starvation. The prolonged hypoglycemia caused cortical damage simulating ischemic brain damage. Ten months in to follow-up patient is still in persistent vegetative state with no noticeable neurological recovery.- - - - - - - - - - ranking = 6keywords = ketoacidosis (Clic here for more details about this article) |
9/29. A case of autoimmune hypoglycemia complicated with diabetic ketoacidosis.Autoimmune hypoglycemia is characterized by hyperinsulinemia, fasting hypoglycemia, and the presence of insulin auto- antibodies without previous exposure to exogenous insulin. We experienced a case of autoimmune hypoglycemia without diabetes mellitus or any evidence of insulinoma. The insulin auto-antibody and insulin receptor auto-antibody were present. We diagnosed the patient as having autoimmune hypoglycemia and treated with glucocorticoid. After treatment, the hypoglycemic symptoms were resolved. However, four months later, the patient was readmitted with transient diabetic ketoacidosis. After recovery, he showed no signs of diabetes mellitus. We believe that insulin auto-antibodies may play a role in autoimmune hypoglycemia and diabetic ketoacidosis, but its role and mechanism are not precisely known. Further studies are needed to define the action mechanisms and the functions of insulin auto-antibodies: here we present case with a relevant literature.- - - - - - - - - - ranking = 6keywords = ketoacidosis (Clic here for more details about this article) |
10/29. diabetic ketoacidosis secondary to growth hormone treatment in a boy with prader-willi syndrome and steatohepatitis.A 13 year-old boy with prader-willi syndrome and steatohepatitis presented with diabetic ketoacidosis 4 weeks after the initiation of growth hormone (GH) treatment. He did not have signs or symptoms of type 2 diabetes mellitus (DM2) before the initiation of GH treatment. hyperglycemia resolved 2 months after discontinuation of GH. He redeveloped DM2 6 months later associated with excessive weight gain. diabetic ketoacidosis as a rare complication of GH therapy emphasizes the importance of screening for carbohydrate intolerance before and during GH treatment in patients with prader-willi syndrome. Steatohepatitis may be the only manifestation of insulin resistance and warrants further evaluation.- - - - - - - - - - ranking = 6keywords = ketoacidosis (Clic here for more details about this article) |
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