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 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a rare case of hypothermia with acute renal failure in a patient suffering from diabetic nephropathy. A 71-year-old male who had been receiving insulin therapy for the treatment of diabetes mellitus complicated with advanced diabetic nephropathy since 1998 was malnourished with an extremely decreased muscle mass. Without any prolonged exposure to excessively low external temperatures or hypothyroidism, pituitary insufficiency, adrenal insufficiency, sepsis, hypoglycemia, and diabetic ketoacidosis, acute hypothermia appeared together with an aggravation of diabetic nephropathy. His skin temperature fell to below measurable levels and his rectal temperature fell to 30.0 degrees C. His consciousness was drowsy and the hypothermia was not accompanied by shivering. Skeletal muscle is known to play an important role as a center of heat production and shivering thermogenesis in skeletal muscle mainly operates on acute cold stress. Therefore, in this case, hypothermia may have occurred because the shivering thermogenesis could not fully act on the acute cold stress due to the dramatically reduced muscle mass. We should always keep in mind that older, malnourished diabetic patients can easily suffer from impairments of the thermoregulatory system.
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PMID:Hypothermia with acute renal failure in a patient suffering from diabetic nephropathy and malnutrition. 1080 30

A case of 5 year old diabetic girl with melioidosis was reported. She presented with the symptoms and signs of intraabdominal infection, septicemia and diabetic ketoacidosis. Abdominal ultrasonography showed multiple splenic and liver abscesses, melioidosis was suspected. Hemoculture and pus culture yielded Burkholderia pseudomallei which was susceptible to ceftazidime and cotrimoxazole. Correction of fluid and electrolyte combined with insulin therapy and proper antibiotics resulted in a good outcome in this patient.
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PMID:Diabetic ketoacidosis and melioidosis in a child. 1090 72

Although hypophosphatemia is relatively uncommon, it may be seen in anywhere from 20% to 80% of patients who present to the ED with alcoholic emergencies, diabetic ketoacidosis (DKA), and sepsis. Severe hypophosphatemia, as defined by a serum level below 1.0 mg/dL, may cause acute respiratory failure, myocardial depression, or seizures. Because hypophosphatemia is not as often treated by ED physicians, becoming familiar with a single intravenous phosphate solution and specific guidelines for phosphate repletion are essential. One mL of the most commonly available phosphate solution (K2PO4) contains 4.4 meq of potassium and 3 mmol (93 mgs) of phosphate. Administering K2PO4 at a rate of 1 mL per hour is almost always a very safe and appropriate treatment for hypophosphatemia. This article provides guidelines for phosphate therapy in hypophosphatemic ED patients including those in DKA, those presenting with alcohol-related complaints including alcoholic ketoacidosis and patients with acute exacerbation of asthma and chronic obstructive pulmonary disease.
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PMID:Hypophosphatemia in the emergency department therapeutics. 1091 39

Diabetic ketoacidosis and moderate degree of hyperglycemia can be managed by glucose-insulin-potassium (GIK) regimen. The GIK regimen is also useful in the treatment of acute myocardial infarction (AMI). But, the exact mechanism(s) of the beneficial action of GIK regimen is not known. I suggest that glucose-insulin can suppress the secretion and antagonize the harmful effects of tumor necrosis factor alpha (TNF alpha) and macrophage migration inhibitory factor (MIF). If this is true, it suggests that GIK regimen may be useful in septicemia and septic shock, and other inflammatory conditions such as ulcerative colitis, Crohn's disease, rheumatoid arthritis, systemic lupus erythematosus and cancer, conditions in which TNF alpha and MIF appear to play a major role.
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PMID:Newer uses of glucose-insulin-potassium regimen. 1120 54

Profound hypothermia (core temperature of less than 28 degrees C) is a life threatening state and a medical emergency associated with a high mortality rate. The prognosis depends on underlying diseases, advanced or very early age, the duration prior to treatment, the degree of hemodynamic deterioration, and especially, the methods of treatment, including active external or internal rewarming. This is a case study of an 80-year-old female patient with severe accidental hypothermia (core temperature 27 degrees C). She was found in her home lying immobile on the cold floor after a fall. The patient was in a profound coma with cardiocirculatory collapse, and the medical staff treating her was inclined to pronounce her deceased. On her arrival at the hospital, she was resuscitated, put on a respirator and actively warmed. Very severe metabolic disorders were found, including a marked metabolic acidosis composed of diabetic ketoacidosis (she had suffered from insulin treated type 2 diabetes mellitus) and lactic acidosis with a very high anion gap (42) and a hyperosmotic state (blood glucose 1202 mg/dl). There were pathognomonic electrocardiographic abnormalities, J-wave of Osborn and prolonged repolarization. Slow atrial fibrillation with a ventricular response of 30 bpm followed by a nodal rhythm of 12 bpm and reversible cardiac arrest were recorded. The pulse and blood pressure were unobtainable. Despite the successful resuscitation and hemodynamic and cognitive improvement, rhabdomyolysis (CKP 6580 u/L), renal failure and hepatic damage developed. She was extubated and treated with intravenous fluids containing dopamine, bicarbonate, insulin and antibiotics. Her medical condition gradually improved, and she was discharged clear minded, functioning very well and independent. Renal and liver tests returned eventually to normal limits. Progressive bradycardia, hypotension and death due to ventricular fibrillation or asystole commonly occur during severe hypothermia. Respiratory and metabolic, sometimes lactic, acidosis, lethargy and coma, hypercoagulopathy, hyperosmolar state, acute pancreatitis and renal and hepatic failure are frequent complications of hypothermia. Underlying predisposing causes of hypothermia are diabetic ketoacidosis, cerebrovascular disease, mental retardation, hypothyroidism, pituitary and adrenal insufficiency, malnutrition, acute alcoholism, liver damage, hypoglycemia, sepsis, hypothalamic dysfunction, sepsis and polypharmacy, and especially, the use of sedative and narcotic drugs. Our case demonstrates once again that CPR once begun should continue until the successful rewarming because "no one is dead until warm and dead".
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PMID:[Severe accidental hypothermia in an elderly woman]. 1175 73

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.
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PMID:Diabetic ketoacidosis and persistent hyperglycemia as long-term complications of L-asparaginase-induced pancreatitis. 1243 31

Zygomycosis caused by Rhizopus species is an aggressive and rapidly progressive opportunistic fungal infection in immunocompromised patients. It comprises mucocutaneous, rhinocerebral, pulmonary, urological and disseminated infections. Predisposing factors are immunosuppression owing to severe diseases, immunological defects or metabolic disturbances like diabetic ketoacidosis. Rhizopus infections are characterized by angioinvasive growth, necroses of infected tissue and perineural invasion. The histopathologic demonstrable invasion of blood vessels is remarkable for a fungal infection. The mortality of zygomycosis is very high, especially for disseminated disease and when immunosuppression cannot be corrected. We report about two cases of pulmonary zygomycosis, caused by Rhizopus spp.: patient 1, female 73 years old: Delayed clinical course according to hip arthroplasty infection and infection of a femoropopliteal bypass of the right leg, eventually exarticulation of the right hip joint, Pseudomonas pneumonia, severe sepsis caused by staphylococci, acute respiratory distress syndrome (ARDs), acute renal failure and multiple use of antibiotics. Subsequently detection of Rhizopus spp. in the bronchoalveolar lavage and treatment with amphotericin B for this reason. Patient 2, male 68 years old: transplantation of kidney in past medical history, presenting with acute renal failure and with quite a few infections before. In the sequel development of abscessing pneumonia on the right side with a pleural empyema. Rhizopus spp. were detected by microbiological testing in the empyema fluid. These findings required surgical intervention, resection of the lower lobe of the right lung and within the same operation of the renal graft because of rejection. The patient was treated with caspofungin. The further course was delayed by several septic phases. Both patients died later on in spite of all efforts. The very rarely seen pulmonary zygomycosis caused by infection with Rhizopus spp. developed in both patients owing to immunosuppression, in one patient iatrogenically induced by immunosuppressive drugs after organ transplantation, in the other as a result of prolonged severe sepsis. In comparison with other mycoses treatment of Rhizopus infections remains difficult. The affinity to blood vessels, where the fungi multiply, and their feature of vascular invasion with thrombosis and infarction complicate therapeutic efforts.
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PMID:[Pulmonary zygomycosis--a rare angioinvasive fungal infection]. 1582 97

The main objective of this study was to assess the relationship of standard base excess (SBE) to delta strong ion difference effective (DeltaSIDe) in critical illness. Critical illness is characterized by variable plasma nonvolatile weak acid components (DeltaA(-)), and SBE becomes discordant with DeltaSIDe. The author hypothesized that both acid-base models are equivalent when SBE and DeltaSIDe are corrected for DeltaA(-). A retrospective chart review was performed to assess this hypothesis by looking at changes in SBE, DeltaSIDe, and DeltaA(-) in 30 coronary artery bypass graft surgery patients, 30 severe sepsis patients, and 15 diabetic ketoacidosis patients. SBE equals the sum of the DeltaSIDe and DeltaA(-). The SBE quantifies the magnitude of the metabolic acid-base derangement, the DeltaSIDe quantifies the plasma strong cation/anion imbalance, and the DeltaA(-) quantifies the magnitude of the hypoalbuminemic alkalosis. The partitioning of SBE into physicochemical components can facilitate analyses of complex acid-base disorders in critical illness.
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PMID:Comparative quantitative acid-base analysis in coronary artery bypass, severe sepsis, and diabetic ketoacidosis. 1628 Apr 4

Diabetes mellitus is a heterogeneous disorder that may occur at any age. Neonatal diabetes mellitus, defined as hyperglycaemia presenting within the first 6 weeks of life in term infants, is a rare disorder that may result in permanent or transient diabetes mellitus. Although reported in paediatric diabetes literature, there are no reports of this condition in emergency medicine journals and these children may present to emergency departments with a picture mimicking sepsis. We report the case of a 5-week-old infant with diabetes mellitus who presented with diabetic ketoacidosis and review the literature surrounding this rare condition.
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PMID:Neonatal diabetes mellitus: A rare but important diagnosis in the critically ill infant. 1709 Oct 57

The authors report a case with life-threatening hyperglycemia and acidosis in a patient with no previous diabetic history following treatment with olanzapine. A 35-year-old woman with a history of bipolar affective disorder treated with olanzapine presented with severe diabetic ketoacidosis. She had no prior history of diabetes or risk factors for diabetes. Glycosylated hemoglobin (HbA1c) on admission blood sample suggested that long-term glycemic control had been poor. The authors postulate that treatment with olanzapine precipitated hyperglycemia, an elevated creatine kinase level, and a high amylase level. A concurrent urinary tract infection precipitated an episode of sepsis, which combined to precipitate life-threatening diabetic ketoacidosis. During her stay in the intensive treatment unit and subsequently in the medical ward, her blood glucose concentration was intensively monitored. She remains on insulin therapy, and her antipsychotic medication was changed to risperidone. Newer atypical antipsychotic drugs such as olanzapine have been introduced with the benefit of fewer extrapyramidal side effects. A number of these have reported metabolic side effects of uncertain etiology such as diabetic ketoacidosis and elevated creatine kinase. The authors believe that the diabetic ketoacidosis occurred in this patient, who had no previous history of diabetes mellitus. Blood glucose should be monitored in patients taking olanzapine, especially in those patients with risk factors for diabetes mellitus.
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PMID:Life-threatening hyperglycemia and acidosis related to olanzapine: a case report and review of the literature. 1725 69


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