1/8. A dentoalveolar abscess in a pediatric patient with ketoacidosis caused by occult diabetes mellitus: a case report.oral health professionals are frequently asked to evaluate patients with routine odontogenic infections. These patients can sometimes present with systemic signs and symptoms, including fever, malaise, tachycardia, and dehydration. It is important for the astute clinician to understand the possible associated systemic diseases that may be contributing to odontogenic infections. We present here an interesting case of a pediatric patient with a routine canine space infection who exhibited classic clinical signs and symptoms of diabetic ketoacidosis.- - - - - - - - - - ranking = 1keywords = ketoacidosis (Clic here for more details about this article) |
2/8. Bilateral optic atrophy following diabetic ketoacidosis.diabetic ketoacidosis (DKA) can result in neuropathic abnormalities of the somatic and the autonomous nervous systems. We report the case of a 50-year-old man with Type 1 diabetes of 20-year duration who after severe DKA lost vision in his right eye and only retain partial vision in his left. This case demonstrates that optic neural tissue is vulnerable to haemodynamic and metabolic complications of DKA.- - - - - - - - - - ranking = 1keywords = ketoacidosis (Clic here for more details about this article) |
3/8. 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 = 0.2keywords = ketoacidosis (Clic here for more details about this article) |
4/8. Alcoholic ketoacidosis associated with multiple complications: report of 3 cases.We report 3 patients with alcoholic ketoacidosis (AKA). All had a history of excessive intake and abrupt termination of alcohol. They showed tachypnea, tachycardia, abdominal tenderness, and epigastralgia. Metabolic acidosis with an increased anion gap, decreased PaCO2 and ketonemia were present. One patient whose ratio of 3-hydroxybutyric acid to acetoacetic acid was 4.0 was associated with diabetic ketoacidosis. All patients were successfully hydrated with electrolyte, glucose and thiamine. Complications such as liver dysfunction, lactic acidosis, acute pancreatitis, Wernicke's encephalopathy, rhabdomyolysis and heart failure were present. attention should be paid to multiple complications in the treatment of AKA.- - - - - - - - - - ranking = 1.2keywords = ketoacidosis (Clic here for more details about this article) |
5/8. 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 = 0.4keywords = ketoacidosis (Clic here for more details about this article) |
6/8. 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 = 1.4keywords = ketoacidosis (Clic here for more details about this article) |
7/8. Acute pancreatitis with diabetic ketoacidosis associated with hypermyoglobinemia, acute renal failure, and DIC.We report a case of acute pancreatitis with diabetic ketoacidosis associated with increased serum myoglobin concentration, acute renal failure, and disseminated intravascular coagulation. A 49-year-old man suffering from diarrhea, vomiting, and somnolence was admitted to the hospital. He had had flu-like symptoms for 4 days prior to the onset of these symptoms. He was a habitual drinker and had been consuming 360 ml-900 ml of the drink "shochu" (distilled spirits containing 28% alcohol) daily for 30 years. Laboratory data on admission revealed elevated serum levels of pancreatic enzymes, including amylase, trypsin, lipase, pancreatic secretory trypsin inhibitor (PSTI), phospholipase A2 (PLA2), and elastase-1, as well as elevated levels of glucose (373 mg/dl), ketone bodies (3675 mumol/l), and myoglobin (229.8 ng/ml). Treatment with subcutaneous insulin and intravenous administration of electrolyte fluid and the systemic protease inhibitor, gabexate mesilate, was begun immediately. Early after the initiation of treatment, there was an increase in serum creatinine (4.9 mg/dl), and thromobocytopenia (15000/microliters) was observed. The patient completely recovered from renal failure and acute pancreatitis, but required insulin therapy. Alcohol ingestion and dehydration are thought to have played a major role in the triggering of the acute pancreatitis. We examined the relationship among acute pancreatitis, diabetic ketoacidosis, and hypermyoglobinemia in the literature.- - - - - - - - - - ranking = 1.2keywords = ketoacidosis (Clic here for more details about this article) |
8/8. Severe ketoacidosis complicated by 'ecstasy' ingestion and prolonged exercise.Ecstasy (3,4-methylenedioxymethamphetamine or MDMA) is used with increasing frequency as a recreational drug. Accumulated evidence over recent years indicates a growing demand for the drug with a corresponding increase in number of reports of adverse effects from its use. There are reported metabolic disturbances due to MDMA use. These, in addition to the prolonged exercise involved in dancing at 'raves' where MDMA may be used, may exacerbate ketoacidosis. We report two cases of ketoacidosis complicated by MDMA ingestion.- - - - - - - - - - ranking = 1.2keywords = ketoacidosis (Clic here for more details about this article) |