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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four cases of diabetic ketoacidosis presenting with abdominal pain are reported. Case 1: a 14-year-old boy suffered from sudden onset of mid-abdominal pain, then migrating to the right lower quadrant. Nausea and vomiting occurred subsequently. Appendectomy was performed under the impression of acute appendicitis in an outside surgical clinic. The patient became comatose the next day and then was transferred to our hospital. Diabetic ketoacidosis was diagnosed after the detection of hyperglycemia, glycosuria, and ketonuria on the day of admission. Unfortunately, he expired on the same day in spite of vigorous resuscitation. Case 2: a 9-year-old boy complained of abdominal pain for 10 days. There was no specific finding in the physical examination. Diabetic ketoacidosis was confirmed four days later when conscious disturbance, dehydration, and tachypnea were noticed. Case 3: a 10-year-old girl presented with a history of intermittent abdominal pain for one month. The character of the abdominal pain was nonspecific. Glycosuria was detected in a pediatric clinic. Diabetic ketoacidosis was confirmed after her referral to our hospital. Case 4: a 5-year-old girl suffered from acute abdominal pain for four hours. She was found to have tachypnea, lethargy, and ill-looking. Diabetic ketoacidosis was diagnosed after serial examinations. The abdominal pain in diabetic ketoacidosis may lead the pediatrician into diagnostic error. Therefore, when a child presented with non-specific abdominal pain, a routine urine sugar should be checked in order not to miss the possibility of diabetic ketoacidosis.
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PMID:[Abdominal pain in diabetic ketoacidosis: report of four cases]. 212 98

Among 287 cases of diabetic ketoacidosis, 212 patients were alert, 48 drowsy, 10 stuporous and 17 comatose. The mean blood hydrogen ion concentrations in these 4 groups of patients were 50.0; 72.8; 106.8 and 109.9 nmol/l, respectively. Increased blood hydrogen ion concentration seems to be an important factor in lowering the level of consciousness in diabetic ketoacidosis.
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PMID:The influence of blood hydrogen ion concentration on the level of consciousness in diabetic ketoacidosis. 310 57

A patient with a history of diabetes mellitus and congestive heart failure was taking furosemide and metolazone as diuretics. Diabetic ketoacidosis developed, and the patient became lethargic and confused. Initial biochemical determinations showed an alkalemic pH, serum and urine ketones with an anion gap, and hyperventilation. The hyperventilation was appropriate for the degree of ketoacidosis but it was grossly inappropriate for the alkalemia. This could be explained by a direct effect of ketones on the respiratory center or a sudden increase in hydrogen ion concentration superimposed on previously chronic alkalemic pH due to the potent combination of furosemide and metolazone.
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PMID:Alkalemia in diabetic ketoacidosis. 643 81

To evaluate the efficacy of low-dose insulin therapy in cases of severe diabetic ketoacidosis (DKA), we examined admission clinical and biochemical parameters and responses to therapy in 48 diabetic patients who presented with DKA and were randomized to receive either high- or low-dose insulin. There were no differences in the initial clinical and biochemical parameters of the patients, regardless of assignment to low or high dose; however, a subgroup of 13 patients who were classified as severe DKA (based on their presentation in a comatose or stuporous state) had, as expected, more marked clinical and biochemical abnormalities than their alert cohorts. The responses to therapy (rate of glucose decrement and control of acidosis) were comparable in the high-dose and low-dose groups of comatose/stuporous patients and were not significantly different from the noncomatose cohorts. These data indicate that low-dose insulin therapy in severely ill comatose patients is as effective as high-dose.
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PMID:Efficacy of low-dose insulin therapy for severely obtunded patients in diabetic ketoacidosis. 677 27

Rhino-orbital-cerebral mucormycosis is a disease that is frequently fatal. A 39-year-old man with diabetic ketoacidosis was referred to the authors' ophthalmic service with fever, orbital apex syndrome in the right eye, lethargy, and a black eschar in the palate. He was treated with systemic and local (intraconal) amphotericin B and his ketoacidosis was controlled; exenteration was not performed. Biopsy of the palate proved mucormycosis. Eighteen months later the patient was still alive and had a blind, anatomically preserved right eye with ptosis and intact extraocular muscle function without proptosis or pain. The authors propose this alternative means of treatment to achieve higher doses of the drug at the site of infection and better cosmetic and psychological results.
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PMID:Intraconal amphotericin B for the treatment of rhino-orbital mucormycosis. 885 37

Permanent neonatal diabetes mellitus (PNIDDM) is a rare form of IDDM with unclear etiology and pathogenesis. We determined the incidence and prevalence rates and studied the clinical and biochemical features of PNIDDM in the Sultanate of Oman. The mean incidence rate during the study period from January 1989 to December 1994 was 1.788 +/- 0.82 per 100,000 live births per year. At the end of December 1994 the prevalence rate was 2.4 per 100,000 children below the age of 5 years. They constituted 41.6% of all cases of IDDM in this age group. Diarrhoea, fever, lethargy, poor feeding and failure to thrive were the most common presenting symptoms. Dehydration and tachypnoea were the most common signs. All patients who developed IDDM during the neonatal period had intrauterine growth retardation and 4.5 presented with diabetic ketoacidosis (plasma glucose 37 +/- 9 mmol/L, pH 7.12 +/- 0.1). Hypertriglyceridemia was a constant feature (19.4 +/- 4.8 mmol/L). They were products of consanguineous marriage with significantly high prevalence of IDDM and NIDDM in their family members. None of the infants had clinical or immunological evidence of congenital viral infection. Three of the five children had HLA-DR2, the diabetes resistance alleles. C-peptide secretion was absent during and after metabolic control of hyperglycemia in all the studied infants and none had circulating islet cell antibody at presentation or during the first year after diagnosis. Despite marked growth retardation at birth, there was a significant improvement of growth after initiating insulin therapy. Four of the 5 patients had normal developmental milestones, one had mild developmental delay following a severe and prolonged attack of hypoglycemia. None of the patients had exocrine pancreatic deficiency. In summary, the very high rate of parental consanguinity, occurrence in both sexes and in two siblings in the same family, absence of islet cell antibodies and the presence of HLA-DR2 loci in 3/5 of patients suggest that PNIDDM is a different disease process to standard IDDM in childhood and an autosomal recessive mode of transmission.
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PMID:Permanent neonatal diabetes mellitus: epidemiology, mode of presentation, pathogenesis and growth. 1079 84

Emphysematous pyelonephritis is a rare life threatening infection in diabetes characterised by suppurative infection of renal parenchyma and perirenal tissues. It usually presents with fever, nausea, vomiting, abdominal pain, shock, lethargy, and confusion. Diabetic ketoacidosis is an uncommon presentation. In the present case, an elderly female presented with abdominal pain, fever, vomiting, and altered sensorium. She was diagnosed to have diabetic ketoacidosis with metabolic encephalopathy with right emphysematous pyelonephritis. She had an excellent response to medical treatment alone and was later discharged on oral hypoglycaemic agents.
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PMID:Emphysematous pyelonephritis: a rare presentation. 1085 76

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

A 63-year-old woman presented at the emergency department (ED) with a history of increasing lethargy and drowsiness. The electrocardiogram (ECG) showed tall peaked T waves with broadening of the QRS interval, suggestive of hyperkalaemia. This patient had an elevated serum potassium level due to diabetic ketoacidosis. She was treated with intravenous calcium chloride and insulin with 50% dextrose. The ECG changes associated with hyperkalaemia are discussed, with illustrations from a second 48-year-old male patient with renal failure who presented with malaise, lethargy and generalised weakness.
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PMID:Electrocardiographical case. A tale of tall T's. Hyperkalaemia. 1604 16

Cerebral edema is the most important complication of diabetic ketoacidosis in children. It has a high mortality rate of 20 to 90% in different series. Twenty to 40% of survivors suffer from neurologic sequelae. The pathogenetic mechanisms are still controversial and the risk factors which are thought to predict its occurrence do not consistently correlate with cerebral edema in various studies. Prevention and recognition of early warning signs, such as decreased arousal, lethargy after initial improvement, headache, vomiting, relative bradycardia and relative hypertension, are crucial. Therapeutic guidelines to prevent cerebral edema in diabetic ketoacidosis include slow rehydration over about 48 hours, avoidance of hypotonicity and of unnecessary alkali therapy. Early recognition of cerebral edema and prompt institution of hypertonic therapy with mannitol may prevent permanent neurological sequelae.
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PMID:Cerebral edema in diabetic ketoacidosis. 1695 33


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