1/32. theophylline intoxication mimicking diabetic ketoacidosis in a child.A 5-year-old boy presented with abdominal pain, nausea and vomiting of blood. Twelve hours after admission, "diabetic ketoacidosis" was diagnosed on the basis of elevated glycaemia, glycosuria, ketonuria and a low bicarbonate blood level, which led to treatment with fluids and regular insulin infusion. Over a 36-hour period, insulin was progressively decreased and finally stopped because of the rapid fall and normalization of blood glucose concentration. Drug poisoning was suspected on the basis of persistent tachycardia in the absence of other signs of dehydration. Salicylate intoxication was excluded, and theophylline was finally incriminated. This compound, used by adults in the child's home, had caused accidental theophylline poisoning, mimicking diabetic ketoacidosis. Pre-diabetic immune markers were repeatedly negative, and no diabetes has developed after four years of follow-up. Thus, the transient increase in blood glucose was not related to a pre-diabetic status. A diagnosis of masked theophylline poisoning should be considered in similar situations involving a rapid decrease of insulin requirements.- - - - - - - - - - ranking = 1keywords = ketoacidosis (Clic here for more details about this article) |
2/32. Post-transplant diabetic ketoacidosis--a possible consequence of immunosuppression with calcineurin inhibiting agents: a case series.Post-transplant diabetes mellitus, a complication due to corticosteroids and the calcineurin inhibitors, cyclosporine and tacrolimus (FK506), is commonly regarded as a form of type-2 (adult-onset) diabetes mellitus. diabetic ketoacidosis, which requires relative insulin deficiency to impair fatty acid metabolism, is a complication of type-1 diabetes mellitus. We report three patients who presented with diabetic ketoacidosis post-transplant. All three patients presented with severe hyperglycemia, significant ketosis and metabolic acidosis of variable severity. One patient was a renal transplant recipient on a cyclosporine-based regimen. The other two patients were liver transplant recipients receiving either cyclosporine or tacrolimus-based immunosuppression. Both of the liver transplant recipients were found to have moderate to high serum levels of calcineurin inhibitors on presentation. The liver recipient on cyclosporine (Neoral) had a 4 hour post-dose level of 388 ng/ml and the patient on tacrolimus was found to have a trough level of 21.2 ng/ml. Our experience suggests that post-transplant diabetes mellitus, in association with calcineurin inhibition, may result in ketoacidosis either secondary to relative beta cell dysfunction, peripheral insulin resistance, or a combination of the two effects. Post-transplant diabetes mellitus can be an atypical form of adult-onset diabetes with features of both type I and type II diabetes mellitus.- - - - - - - - - - ranking = 1.356719844098keywords = ketosis, ketoacidosis (Clic here for more details about this article) |
3/32. Ketotic hyperglycemia and epilepsia partialis continua.epilepsia partialis continua (EPC) may occur during nonketotic hyperglycemia but has not been described with diabetic ketoacidosis. The authors report a patient with EPC associated with ketotic hyperglycemia. brain MRI showed two areas of abnormal signal intensity in the left precentral gyrus and in the right cerebellar hemisphere. hyperglycemia may reduce seizure threshold because of the increase in gamma-aminobutyric acid metabolism and may trigger epileptic discharges.- - - - - - - - - - ranking = 0.16666666666667keywords = ketoacidosis (Clic here for more details about this article) |
4/32. Abrupt onset of diabetes during interferon-alpha therapy in patients with chronic hepatitis c.INTRODUCTION: interferon-alpha (IFN-alpha) is now widely used in the treatment of chronic hepatitis c. Few patients have been reported as developing impaired glucose tolerance or diabetes mellitus (DM) using this therapy. The explanation for the development of DM in chronic hepatitis c treated with IFN-alpha is unclear. We report two patients who developed an abrupt onset of diabetes during IFN-alpha for chronic hepatitis c. case reports: Two male middle-aged patients were admitted to our hospital for an abrupt onset of diabetes, in diabetic ketoacidosis, with a very short duration of hyperglycaemic symptoms. Their clinical course was similar. Case 1 never demonstrated any markers of pancreatic immunogenicity. Case 2 had high levels of decarboxylase glutamic acid autoantibodies (GADAb), before the IFN-alpha treatment that persisted. We compared initial beta-cell function and metabolic control with a group of middle-aged patients from our hospital who had recently been diagnosed with Type 1 diabetes mellitus (DM1). In contrast to these, the onset of the disease was particularly severe with beta-cell function substantially impaired and displaying unstable short-term metabolic control. CONCLUSIONS: Type 1 diabetes should be considered as a potential complication if IFN is administered to patients with chronic hepatitis c. Its onset may be severe and result in short-term difficulties in metabolic control.- - - - - - - - - - ranking = 0.16666666666667keywords = ketoacidosis (Clic here for more details about this article) |
5/32. Clonic focal seizure of the foot secondary to nonketotic hyperglycemia.Focal epileptic seizures can be the first manifestation of a diabetic disorder. Metabolic disturbances, including hyperglycemia, mild hyperosmolality, hyponatremia, and lack of ketoacidosis contribute to the development of partial focal seizures. A review of the medical literature for partial focal seizures is presented, followed by a case study of a patient who developed clonic seizures of the right foot secondary to hyperglycemia, hyponatremia, and hyperosmolality.- - - - - - - - - - ranking = 0.16666666666667keywords = ketoacidosis (Clic here for more details about this article) |
6/32. Severe degree of hyperglycaemia: insights from integrative physiology.We illustrate how the application of principles of integrative physiology at the bedside can reveal novel insights that have been largely overlooked to this day. In this didactic exercise, modern-day physicians seek an imaginary medical consultation with Professor Sir Hans Krebs because of an unusual finding in his area of expertise: a very severe degree of hyperglycaemia. Although Professor Krebs is restricted to data prior to world war ii, this does not prevent him from making novel discoveries. First, he illustrates how an occult factor, rapid absorption of glucose from the intestinal tract, was a critical feature in explaining the basis of the severe degree of hyperglycaemia without obvious ketoacidosis in a 16-year-old patient with type 1 diabetes mellitus in poor control. Second, by examining simple principles of renal and gastrointestinal physiology in a quantitative fashion, Professor Krebs speculates as to how cerebral oedema might occur before therapy in a patient with a severe degree of hyperglycaemia. We hope that readers and educators will appreciate the value of applying principles of integrative physiology in a quantitative fashion at the bedside.- - - - - - - - - - ranking = 0.16666666666667keywords = ketoacidosis (Clic here for more details about this article) |
7/32. 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 = 0.16666666666667keywords = ketoacidosis (Clic here for more details about this article) |
8/32. diabetic ketoacidosis and persistent hyperglycemia as long-term complications of L-asparaginase-induced pancreatitis.diabetic ketoacidosis (DKA) and pancreatic pseudocysts are rare complications following treatment of hematological malignancies with L-asparaginase (L-asp). Persistent hyperglycemia with recurrent DKA presenting as a long-term complication of L-asp-induced pancreatitis is even rarer. A 21-year-old man with pre-B-type acute lymphoblastic leukemia (ALL) developed pancreatic pseudocysts, DKA and persistent hyperglycemia after L-asp therapy. The patient was treated with oral hypoglycemic agents (OHA) for sugar control thereafter. Ten months later, another episode of DKA developed during relapsed ALL without having obvious precipitating factors. Insulin was then instituted for control of his blood sugar until death. The leukemic process may play some role in glucose homeostasis and may be considered as a precipitating factor for DKA. The patient finally died of disease progression of ALL and sepsis 2 years after the initial diagnosis of ALL.- - - - - - - - - - ranking = 0.83333333333333keywords = ketoacidosis (Clic here for more details about this article) |
9/32. Inpatient management of diabetes.hyperglycemia is common in hospitalized patients with diabetes and contributes to poor outcomes in this population. Use of intravenous insulin protocols for patients who are unable to eat, continuation of usual insulin regimens for those who are eating, pre-meal insulin supplements for hyperglycemia, and avoidance of sliding-scale insulin can help the clinician improve glycemic control. Careful attention to management of diabetes in the hospitalized patient decreases the risk of ketoacidosis, fluid and electrolyte abnormalities, and infection; in critically ill postoperative patients, tight glucose control with insulin administration decreases the risk of death.- - - - - - - - - - ranking = 0.16666666666667keywords = ketoacidosis (Clic here for more details about this article) |
10/32. Infective endocarditis and acute purulent pericarditis in a patient with hyperglycemia.A diabetic patient was admitted to our hospital for infective endocarditis with acute purulent pericarditis and diabetic ketoacidosis. echocardiography revealed attachment of vegetation to the chordae tendineae in the left ventricle and pericaridial effusion. The vegetation was enlarged and pendulated for a few days despite maximal antimicrobial therapy. Surgical resection was desirable to decrease the risk of embolic complications and cardiovascular collapse. We could not open the heart because of accumulation of purulent pericardial fluid, and right renal infarction was complicated. We believe that the immunocompromised and hypercoagulable state due to diabetes caused these conditions.- - - - - - - - - - ranking = 0.16666666666667keywords = ketoacidosis (Clic here for more details about this article) |
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