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• W4255777783 abstract "The nonketotic hyperglycemic syndrome is rare during childhood and may occur as the initial manifestation of insulin-dependent diabetes mellitus or during an episode of gastroenteritis. In this article, we report an unusual case of this syndrome in a female infant who had atypically severe hyperglycemia in association with gastroenteritis. In addition, we provide a review of the literature and summarize the pathophysiologic mechanisms of the nonketotic hyperglycemic syndrome. The nonketotic hyperglycemic syndrome is rare during childhood and may occur as the initial manifestation of insulin-dependent diabetes mellitus or during an episode of gastroenteritis. In this article, we report an unusual case of this syndrome in a female infant who had atypically severe hyperglycemia in association with gastroenteritis. In addition, we provide a review of the literature and summarize the pathophysiologic mechanisms of the nonketotic hyperglycemic syndrome. A 12-month-old previously healthy female infant was brought to a local emergency department because of a 6-day history of emesis and severe diarrhea. Her diet had been changed to clear liquids that contained only apple and pineapple juices. A saphenous cutdown had to be performed to obtain venous access. The initial plasma glucose concentration was 1,446 mg/dL; a second specimen was 1,972 mg/dL. The venous pH was 6.85. Laboratory studies yielded the following results: serum sodium, 151 mEq/L; potassium, 3.6 mEq/L; chloride, 114 mEq/L; bicarbonate, 5 mEq/L; and serum creatinine, 3.8 mg/dl.. She received 20 mL/kg of Ringer's lactate and an intravenous dose of 1.5 U/kg of insulin, followed by a continuous infusion of 0.1 U/kg of insulin per hour and half-normal saline. The patient was transported to our institution. On arrival, she was febrile (40.5°C). She had tachycardia (220 beats/min) and tachypnea (48 respirations/min), and her blood pressure was 80/50 mm Hg. She was somnolent but responsive to stimuli. No papilledema was found. The initial clinical impression was new-onset diabetes. At admission, laboratory studies yielded the following results: plasma glucose, 877 mg/dl.; serum sodium, 152 mEq/L; potassium, 3.4 mEq/L; chloride, 122 mEq/L; and creatinine, 2.0 mg/dL. An arterial blood gas study showed a pH of 7.06, a base deficit of -23, and a bicarbonate of 5 mEq/L. The anion gap, representing the difference between unmeasured cations and unmeasured anions, was 20 mEq/L [determined by Na – (CI + HCO3); normal, 12 ± 2 mEq/L]. The calculated effective osmolality was 351 mOsm/kg (normal, 275 to 295), estimated on the basis of the following formula: 2 × Na (mEq/L) + glucose (mg/dL)/18. The complete blood cell count was remarkable for leukocytosis with 19.8 × 109/L leukocytes. The cerebrospinal fluid contained 569 mg/dL of glucose, 435 mg/dL of protein, and 4,909 erythrocytes and 42 leukocytes/uL. Urinalysis showed 4 to 10 erythrocytes, 4 to 10 leukocytes, a large amount of glucose, but no ketones. Blood test results (which were delayed for several hours) included absent serum ketones, β-hydroxybutyrate of 0.1 mmol/L (normal overnight fasting value, less than 0.4), and serum lactate of 5.0 mmol/L (normal, 0.93 to 1.65). The serum amylase and lipase levels were normal. We administered 20 mL/kg of Ringer's lactate per hour for 2 hours. Thereafter, half-normal saline with 20 mEq/L of potassium phosphate and 20 mEq/L of potassium acetate was given at 2,900 mL/m2 per day for 42 hours. During the first 3 hours of treatment, she also received 1 U/kg of insulin intravenously per hour; this dosage was decreased to 0.25 U/kg or less per hour for the next 13 hours. The plasma glucose concentration decreased rapidly (from 877 mg/dL to 171 mg/dL in 150 minutes), and the hypernatremia resolved after 10 hours. No neurologic complications occurred. The glycosylated hemoglobin concentration was 5.6% on admission (normal, 4.0 to 7.0%) and remained normal (5.7%) when tested 3 months later. No islet cell antibodies were detected. A stool specimen was reported to contain rotavirus antigen. Before dismissal of the patient, we performed a glucagon challenge test. The baseline plasma glucose value was 87 mg/dL, serum insulin was 6 μU/mL (normal value in adults, 0 to 20), and C-peptide was 1,500 pg/mL (normal value in adults, 500 to 2,500). Six minutes after the intravenous injection of 0.03 mg/kg of glucagon, the plasma glucose concentration was 132 mg/dL, serum insulin was 54 μU/mL, and C-peptide was 6,600 pg/ml, a demonstration of brisk insulin secretion in response to glucagon. Results of a glucose tolerance test were normal in both parents. The patient's most recent follow-up at age 4.4 years showed normal intellectual development, growth and weight gain at the 95th percentiles for age, and a fasting glucose concentration of 70 mg/dL. The nonketotic hyperglycemic syndrome (NKHS) was first described in the medical literature in 19241Umber-Berlin F Stoffwechselkrankheiten. II. Der Diabetes mellitus: 6. Das Coma diabeticum.Munchen Med Wochenschr. 1924; 71: 1324-1326Google Scholar and is synonymous with the hyperglycemic hyperosmolar syndrome or coma. It is defined as hyperglycemia (plasma glucose, 600 or more mg/dL) and hyperosmolarity (330 or more mOsm/kg) with absent or minimal urine ketones.' This syndrome is rare in children but occurs frequently in elderly, neglected, and debilitated patients, often with diabetes. In adult patients, its incidence seems to have remained unchanged during the past 2 decades; previously undiagnosed diabetes mellitus is found more often in men than in women.3Wright AD Hale PJ Singh BM Kilvert JA Nattrass M FitzGerald MG Changing sex ratio in diabetic ketoacidosis.Diabet Med. 1990; 7: 628-632Crossref PubMed Scopus (15) Google Scholar In children, the most frequent precipitating factors are gastroenteritis and new-onset insulin-dependent diabetes mellitus, whereas in older patients, infections, inadequate insulin therapy or noncompliance, and concomitant cardiovascular disease are most frequent4Berger W Keller U Treatment of diabetic ketoacidosis and non-ketotic hyperosmolar diabetic coma.Baillieres Clin Endocrinol Metab. 1992; 6: 1-22Abstract Full Text PDF PubMed Scopus (29) Google Scholar. Other conditions that occasionally lead to NKHS in adults and children are extensive burns, hypothermia, heat stroke, severe infections, acute pancreatitis, thyrotoxicosis, acromegaly, peritoneal dialysis or hemodialysis, and administration of corticosteroids, thiazides, diazoxide, phenytoin, propranolol, and cimetidine.2Ellis EN Concepts of fluid therapy in diabetic ketoacidosis and hyperosmolar hyperglycemic nonketotic coma.Pediatr Clin North Am. 1990 Apr; 37: 313-321PubMed Google Scholar Mortality rates of 40 to 70% have been reported. As with diabetic ketoacidosis (DKA), the most severe complication is cerebral edema. Appropriate treatment of NKHS consists primarily of careful restoration of the intravascular volume, rehydration, and identification and management of precipitating illnesses.4Berger W Keller U Treatment of diabetic ketoacidosis and non-ketotic hyperosmolar diabetic coma.Baillieres Clin Endocrinol Metab. 1992; 6: 1-22Abstract Full Text PDF PubMed Scopus (29) Google Scholar, 5Siperstein MD Diabetic ketoacidosis and hyperosmolar coma.Endocrinol Metab Clin North Am. 1992 Jun; 21: 415-432PubMed Google Scholar, 6Levine SN Sanson TH Treatment of hyperglycaemic hyperosmolar non-ketotic syndrome.Drugs. 1989; 38: 462-472Crossref PubMed Scopus (21) Google Scholar Twenty-two well-documented pediatric cases of NKHS that have been published in the English-language medical literature beginning in the 1960s are listed in Table 1. Most of the patients were either less than 2 years of age or neurologically impaired before the onset of NKHS. Of the latter group, six of eight (75%) died.Table 1Reported Cases of Nonketotic Hyperglycemic Syndrome*DS = Down syndrome; KS = Kearns-Sayre syndrome; NR = not reported.CaseReferenceAgeNeurologically intact†Before onset of syndrome.CauseGlucose (mg/dL)Sodium (mEq/L)Seizure with treatmentFatal outcome17Boulware SD Tamborlane WV Not all severe hyperglycemia is diabetes.Pediatrics. 1992; 89: 330-332PubMed Google Scholar22 moYesGastroenteritis614139NoNo28Heggarty H Trindade P Bryan EM Hyperglycaemia in hyperosmolar dehydration.Arch Dis Child. 1973; 48: 740-741Crossref PubMed Scopus (10) Google Scholar11 wkYesGastroenteritis620174NoNo38Heggarty H Trindade P Bryan EM Hyperglycaemia in hyperosmolar dehydration.Arch Dis Child. 1973; 48: 740-741Crossref PubMed Scopus (10) Google Scholar8 moYesGastroenteritis670151YesNo4Current case12 moYesGastroenteritis1,446151NoNo59Ehrlich RM Bain HW Hyperglycemia and hyperosmolarity in an eighteen-month-old child.N Engl J Med. 1967; 276: 683-684Crossref PubMed Scopus (19) Google Scholar18 moYesNew-onset diabetes1,750139YesNo610Rubin HM Kramer R Drash A Hyperosmolality complicating diabetes mellitus in childhood.J Pediatr. 1969; 74: 177-186Abstract Full Text PDF PubMed Scopus (34) Google Scholar15 moYesNew-onset diabetes750147NoNo710Rubin HM Kramer R Drash A Hyperosmolality complicating diabetes mellitus in childhood.J Pediatr. 1969; 74: 177-186Abstract Full Text PDF PubMed Scopus (34) Google Scholar18 moNo (DS)New-onset diabetes1,480137NoNo811Fernandez F Hughes ER Nonketotic hyperosmolar diabetic coma in an infant [letter].J Pediatr. 1974; 84: 606-607Abstract Full Text PDF PubMed Scopus (12) Google Scholar12 moYesNew-onset diabetes1,725146YesNo912Goldman SL Hyperglycemic hyperosmolar coma in a 9-month-old child.Am J Dis Child. 1979; 133: 181-183PubMed Google Scholar9 moYesNew-onset diabetes2,400126YesNo1013Yamashiro Y Yamamoto T Mayama H Nonketotic hyperosmolar coma in two diabetic children.Acta Paediatr Scand. 1981; 70: 337-340PubMed Google Scholar9yrYesNew-onset diabetes2,628116NoNo1114Vernon DD Postellon DC Nonketotic hyperosmolal diabetic coma in a child: management with low-dose insulin infusion and intracranial pressure monitoring.Pediatrics. 1986; 77: 770-772PubMed Google Scholar3.5 yrYesNew-onset diabetes2,424122NoNo1215Ginsberg-Fellner F Primack WA Recurrent hyperosmolar nonketotic episodes in a young diabetic.Am J Dis Child. 1975; 129: 240-243PubMed Google Scholar16 moYesNew-onset diabetes1,160144YesNo1313Yamashiro Y Yamamoto T Mayama H Nonketotic hyperosmolar coma in two diabetic children.Acta Paediatr Scand. 1981; 70: 337-340PubMed Google Scholar12 yrYesPreviously diagnosed diabetes1,300144NoNo1410Rubin HM Kramer R Drash A Hyperosmolality complicating diabetes mellitus in childhood.J Pediatr. 1969; 74: 177-186Abstract Full Text PDF PubMed Scopus (34) Google Scholar2.5 yrNoGastroenteritis820149?Yes? New-onset diabetes1510Rubin HM Kramer R Drash A Hyperosmolality complicating diabetes mellitus in childhood.J Pediatr. 1969; 74: 177-186Abstract Full Text PDF PubMed Scopus (34) Google Scholar6.9 yrNo (DS)? New-onset diabetes1,350123?Yes1610Rubin HM Kramer R Drash A Hyperosmolality complicating diabetes mellitus in childhood.J Pediatr. 1969; 74: 177-186Abstract Full Text PDF PubMed Scopus (34) Google Scholar3.9 yrNo? New-onset diabetes820185?Yes1716Belmonte MM Colle E Murphy DA Wiglesworth FW Nonketotic hyperosmolar diabetic coma in Down's syndrome.JPediatr. 1970; 77: 879-881Abstract Full Text PDF PubMed Scopus (15) Google Scholar2.4 yrNo (DS)? New-onset diabetes1,100156NoYes1810Rubin HM Kramer R Drash A Hyperosmolality complicating diabetes mellitus in childhood.J Pediatr. 1969; 74: 177-186Abstract Full Text PDF PubMed Scopus (34) Google Scholar6 wkYes? New-onset diabetes894149?Yes1917Bachynski BN Flynn JT Rodrigues MM Rosenthal S Cullen R Curless RG Hyperglycemic acidotic coma and death in Kearns-Sayre syndrome.Ophthalmology. 1986; 93: 391-396PubMed Scopus (21) Google Scholar10 yrNo (KS)Prednisone>500NR?Yes2017Bachynski BN Flynn JT Rodrigues MM Rosenthal S Cullen R Curless RG Hyperglycemic acidotic coma and death in Kearns-Sayre syndrome.Ophthalmology. 1986; 93: 391-396PubMed Scopus (21) Google Scholar12 yrNo (KS)Prednisone968148?Yes2118Balsam MJ Baker L Kaye R Hyperosmolar nonketotic coma associated with diazoxide therapy for hypoglycemia.J Pediatr. 1971; 78: 523-525Abstract Full Text PDF PubMed Scopus (16) Google Scholar13 moNoDiazoxide2,000128?No2219Hoffman WH Fernados SS Hyperglycaemic hyperosmolar non-ketotic coma in a non-diabetic child [letter].Diabetologia. 1983; 25: 531Crossref PubMed Scopus (6) Google Scholar10 yrYesAdrenaline1,279128YesNo* DS = Down syndrome; KS = Kearns-Sayre syndrome; NR = not reported.† Before onset of syndrome. Open table in a new tab Seven of the reports in Table 1 (cases 5 through 12) describe NKHS in patients with newly diagnosed insulin-dependent diabetes mellitus.9Ehrlich RM Bain HW Hyperglycemia and hyperosmolarity in an eighteen-month-old child.N Engl J Med. 1967; 276: 683-684Crossref PubMed Scopus (19) Google Scholar, 10Rubin HM Kramer R Drash A Hyperosmolality complicating diabetes mellitus in childhood.J Pediatr. 1969; 74: 177-186Abstract Full Text PDF PubMed Scopus (34) Google Scholar, 11Fernandez F Hughes ER Nonketotic hyperosmolar diabetic coma in an infant [letter].J Pediatr. 1974; 84: 606-607Abstract Full Text PDF PubMed Scopus (12) Google Scholar, 12Goldman SL Hyperglycemic hyperosmolar coma in a 9-month-old child.Am J Dis Child. 1979; 133: 181-183PubMed Google Scholar, 13Yamashiro Y Yamamoto T Mayama H Nonketotic hyperosmolar coma in two diabetic children.Acta Paediatr Scand. 1981; 70: 337-340PubMed Google Scholar, 14Vernon DD Postellon DC Nonketotic hyperosmolal diabetic coma in a child: management with low-dose insulin infusion and intracranial pressure monitoring.Pediatrics. 1986; 77: 770-772PubMed Google Scholar, 15Ginsberg-Fellner F Primack WA Recurrent hyperosmolar nonketotic episodes in a young diabetic.Am J Dis Child. 1975; 129: 240-243PubMed Google Scholar At the time of initial examination, remarkably increased plasma glucose concentrations (mean, 1,789 mg/dL) and normal or low serum sodium concentrations (mean, 134.6 mEq/L) were typically found. In the children with gastroenteritis and NKHS (cases 1 through 3), plasma glucose concentrations were lower (mean, 634 mg/dl), and serum sodium levels were higher (mean, 154.7 mEq/L).7Boulware SD Tamborlane WV Not all severe hyperglycemia is diabetes.Pediatrics. 1992; 89: 330-332PubMed Google Scholar, 8Heggarty H Trindade P Bryan EM Hyperglycaemia in hyperosmolar dehydration.Arch Dis Child. 1973; 48: 740-741Crossref PubMed Scopus (10) Google Scholar In contrast to gastroenteritis with fully developed NKHS, mild to moderate hyperglycemia with gastroenteritis is common.8Heggarty H Trindade P Bryan EM Hyperglycaemia in hyperosmolar dehydration.Arch Dis Child. 1973; 48: 740-741Crossref PubMed Scopus (10) Google Scholar, 20Roberts W Alimentary hyperglycaemia simulating diabetic ketosis [letter].Lancet. 1964; 2: 754Abstract PubMed Scopus (5) Google Scholar, 21Burman D Glaspole DW Alimentary hyperglycaemia simulating diabetic ketosis [letter].Lancet. 1964; 2: 208-209Abstract PubMed Scopus (5) Google Scholar, 22Stevenson RE Bowyer FP Hyperglycemia with hyperosmolal dehydration in nondiabetic infants.J Pediatr. 1970; 77: 818-823Abstract Full Text PDF PubMed Scopus (43) Google Scholar, 23Rabinowitz L Joffe BI Abkiewicz C Shires R Greef MC Seftel HC Hyperglycaemia in infantile gastroenteritis.Arch Dis Child. 1984; 59: 771-775Crossref PubMed Scopus (16) Google Scholar, 24Mandell F Fellers FX Hyperglycemia in hypernatremic dehydration.Clin Pediatr. 1974; 13: 367-369Crossref PubMed Scopus (13) Google Scholar Our patient (case 4) had confirmed rotavirus infection. This situation differs from those of previously described patients in that our patient had the pronounced hypernatremia commonly associated with gastroenteritis but with an initial plasma glucose concentration (1,446 mg/dL) in a range previously verified only in patients with diabetes. The cause of nonketotic hyperglycemia is not completely understood. Insulin secretion and action are impaired by hyperosmolality and acidosis.25Bratusch-Marrain PR DeFronzo RA Impairment of insulin-mediated glucose metabolism by hyperosmolality in man.Diabetes. 1983; 32: 1028-1034Crossref PubMed Google Scholar Gluconeogenesis is enhanced by the lack of insulin and increased levels of stress hormones; however, the absence of ketosis is the most intriguing factor. Free fatty acid (FFA) levels have consistently been reported to be lower in patients with NKHS than in those with DKA26Gerich J Penhos JC Gutman RA Recant L Effect of dehydration and hyperosmolarity on glucose, free fatty acid and ketone body metabolism in the rat.Diabetes. 1973; 22: 264-271Crossref PubMed Scopus (34) Google Scholar Early studies claimed that lipolytic hormones such as cortisol, glucagon, growth hormone, and catecholamines are lower in NKHS than in DKA,27Gerich JE Martin MM Recant L Clinical and metabolic characteristics of hyperosmolar nonketotic coma.Diabetes. 1971; 20: 228-238Crossref PubMed Scopus (158) Google Scholar, 28Arieff AI Carroll HJ Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria and the effects of therapy in 37 cases.Medicine. 1972; 51: 73-94Crossref PubMed Scopus (208) Google Scholar Since then, several clinical reports have shown conflicting results, including one of the previously mentioned reports (case 11) in which strikingly increased glucagon and catecholamine levels were found.14Vernon DD Postellon DC Nonketotic hyperosmolal diabetic coma in a child: management with low-dose insulin infusion and intracranial pressure monitoring.Pediatrics. 1986; 77: 770-772PubMed Google Scholar Possibly, hyperosmolarity per se has an antilipolytic effect.26Gerich J Penhos JC Gutman RA Recant L Effect of dehydration and hyperosmolarity on glucose, free fatty acid and ketone body metabolism in the rat.Diabetes. 1973; 22: 264-271Crossref PubMed Scopus (34) Google Scholar Nonetheless, with comparable levels of hyperosmolarity in DKA and NKHS, the absence of ketosis in NKHS remains unclear. Current hypotheses, supported by experiments in rats, emphasize the importance of an “insulinized liver,” in which adequate portal vein insulin concentrations with peripheral insulinopenia inactivate the intrahepatic oxidation of FFAs and route the FFA metabolites toward production of triglycerides.29Joffe BI Goldberg RB Knit LH Seftel HC Pathogenesis of nonketotic hyperosmolar diabetic coma.Lancet. 1975; 1: 1069-1071Abstract PubMed Scopus (14) Google Scholar Another explanation may be the portal vein glucagon-to-insulin ratio. Insulin seems incapable of inhibiting gluconeogenesis in the presence of a high glucagon concentration.29Joffe BI Goldberg RB Knit LH Seftel HC Pathogenesis of nonketotic hyperosmolar diabetic coma.Lancet. 1975; 1: 1069-1071Abstract PubMed Scopus (14) Google Scholar In our patient, we hypothesize that the combination of severe dehydration and treatment with high-carbohydrate-containing fluids led to volume restriction, decreased renal function, acidosis, and hyperosmolality. This situation impaired insulin action and function in an otherwise healthy infant. An episode of illness-related hyperglycemia or NKHS does not seem to be a prognostic factor for the development of insulin-dependent diabetes mellitus in the absence of an abnormal glucose tolerance test result, islet cell anti-bodies, and HLA-DR3/DR4 heterozygosity.30Vardi P Shehade N Etzioni A Herskovits T Soloveizik L Shmuel Z et al.Stress hyperglycemia in childhood: a very high risk group for the development of type I diabetes.J Pediatr. 1990; 117: 75-77Abstract Full Text PDF PubMed Scopus (36) Google Scholar, 31Schatz DA Kowa H Winter WE Riley WJ Natural history of incidental hyperglycemia and glycosuria of childhood.J Pediatr. 1989; 115: 676-680Abstract Full Text PDF PubMed Scopus (38) Google Scholar, 32Herskowitz-Dumont R Wolfsdorf JI Jackson RA Eisenbarth GS Distinction between transient hyperglycemia and early insulin-dependent diabetes mellitus in childhood: a prospective study of incidence and prognostic factors.J Pediatr. 1993; 123: 347-354Abstract Full Text PDF PubMed Scopus (56) Google Scholar Our 12-month-old patient had unusually severe metabolic abnormalities during a course of rotavirus-induced gastroenteritis. Severe dehydration led to decreased renal function, and treatment with high-carbohydrate-containing fluids seems to have been responsible for the development of NKHS. During a 3.5-year follow-up period, the patient's plasma glucose concentration has remained normal. She has no family history of diabetes. In retrospect, we failed to diagnose NKHS immediately. Most likely, we could have corrected the metabolic disturbances without administration of insulin and thereby avoided the rapid decrease of plasma glucose and serum osmolality. For optimal treatment, we recommend slow rehydration for 48 hours; serum sodium and osmolality changes are used as guidelines to avoid rapid intracerebral fluid shifts.33Gullans SR Verbalis JG Control of brain volume during hyperosmolar and hypoosmolar conditions.Annu Rev Med. 1993; 44: 289-301Crossref PubMed Scopus (263) Google Scholar" @default.
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• W4255777783 title "An Unusual Case of the Nonketotic Hyperglycemic Syndrome During Childhood" @default.
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