Factors associated with brain herniation in the treatment of diabetic ketoacidosis

Duck, Stephen C.; Wyatt, David

doi:10.1016/s0022-3476(88)80521-3

Cited by 220 publications

(141 citation statements)

References 22 publications

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“…The rate of ␤-cell destruction is quite variable, as it is rapid in some individuals and slow in others (3). Some patients, particularly children and adolescents, may present with ketoacidosis at the first manifestation of the disease (4). Others have modest fasting hyperglycemia that can rapidly change to severe hyperglycemia and/or ketoacidosis in the presence of infection or other stress (5).…”

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Risk of Type 1 Diabetes Development in Children With Incidental Hyperglycemia

Lorini

Alibrandi²,

Vitali³

et al. 2001

Diabetes Care

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OBJECTIVE -The aim of our study was to determine whether children with incidental hyperglycemia are at an increased risk of developing type 1 diabetes. RESEARCH DESIGN AND METHODS-A total of 748 subjects, 1-18 years of age (9.04 Ϯ 3.62, mean Ϯ SD), without family history of type 1 diabetes, without obesity, and not receiving drugs were studied and found to have incidental elevated glycemia defined as fasting plasma glucose Ͼ5.6 mmol/l confirmed on two occasions. Subjects were tested for immunological, metabolic, and immunogenetic markers.RESULTS -Islet cell antibodies Ͼ5 Juvenile Diabetes Foundation units were found in 10% of subjects, elevated insulin autoantibody levels in 4.6%, GAD antibody in 4.9%, and antityrosine phosphatase-like protein autoantibodies in 3.9%. First-phase insulin response (FPIR) was Ͻ1st centile in 25.6% of subjects. The HLA-DR3/DR3 and HLA-DR4/other alleles were more frequent in hyperglycemic children than in normal control subjects (P ϭ 0.012 and P ϭ 0.005, respectively), and the HLA-DR other/other allele was less frequent than in normal control subjects (P ϭ 0.000027). After a median follow-up of 42 months (range 1 month to 7 years), 16 (2.1%) subjects (11 males and 5 females), 4.1-13.9 years of age, became insulin dependent. All had one or more islet autoantibodies, and the majority had impaired insulin response and genetic susceptibility to type 1 diabetes. Diabetes symptoms were recorded in 11 patients and ketonuria only in 4 patients. The cumulative risk of type 1 diabetes was similar in males and females, and it was also similar in subjects under or over 10 years, whereas the cumulative risk of type 1 diabetes was increased in subjects with one or more autoantibodies and in those with FPIR Ͻ1st centile.CONCLUSIONS -Children with incidental hyperglycemia have a higher-than-normal frequency of immunological, metabolic, or genetic markers for type 1 diabetes and have an increased risk of developing type 1 diabetes. Diabetes Care 24:1210 -1216, 2001T ype 1 diabetes results from cellmediated autoimmune destruction of ␤-cells in the pancreas (1). Multiple genes contribute to the predisposition of the disease, and major histocompatibility complex (MHC) is the most important one (1). Moreover, evidence suggests that environmental factors, which are still poorly defined, may play a role in either precipitating the disease and/or dominantly shaping its course (1). Various autoantibodies against ␤-cell components are present in the serum of newly diagnosed patients with type 1 diabetes (1). More importantly, these circulating autoantibodies may be present for months to years preceding the onset of clinical diabetes (2). The rate of ␤-cell destruction is quite variable, as it is rapid in some individuals and slow in others (3). Some patients, particularly children and adolescents, may present with ketoacidosis at the first manifestation of the disease (4). Others have modest fasting hyperglycemia that can rapidly change to severe hyperglycemia and/or ketoacidosis in the presence of infection ...

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Risk of Type 1 Diabetes Development in Children With Incidental Hyperglycemia

Lorini

Alibrandi²,

Vitali³

et al. 2001

Diabetes Care

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“…A maioria dos estudos mostra uma relação com alterações bruscas e acentuadas na pressão osmótica. Estudos retrospectivos mostraram que a administração excessiva de fluidos (acima de 4 litros/m 2 /dia), a diminuição rápida e acentuada da glicemia e a diminuição do sódio corrigido são fatores associados ao desenvolvimento de edema cerebral 15 .…”

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Diabetic ketoacidosis in children: review of pathophysiology and treatment with the use of the

Collett‐Solberg¹

2001

J Pediatr (Rio J)

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Objectives: To review diabetic ketoacidosis, including the two bags system, a method of administering liquids in order to provide a smoother correction of the hyperglycemic and ketotic states.Methods: Review of recent publications (last 7 years) from a Medline search and chapters published in pediatric textbooks that discuss the etiology, therapy, and complications of diabetic ketoacidosis. The management approach incorporates the findings of these publications as well as the clinical experience at the Childrens Hospital of Philadelphia and Duke University Medical Center. Results:The pathology of the type 1 Diabetes Mellitus involves the progressive destruction of the ß cells of the pancreas, causing insulin deficiency. Insulin is essential in the metabolism of carbohydrates, protein and fat. Insulin deficiency may lead to diabetic ketoacidosis which has three components: 1) hyperglycemia, which causes glycosuria and consequently dehydration; 2) lipolysis which, causes ketonemia/ketonuria; and 3) acidosis, that is caused by the dehydration and the high serum levels of ketones. Diabetic ketoacidosis is a serious condition and, if not treated appropriately, can cause coma and death. In children cerebral edema is the major complication of the therapy for diabetic ketoacidosis. Careful replacement of insulin, fluids, glucose and electrolytes is essential. Conclusions:The literature presents different ways to manage DKA in pediatrics, without a consensus on the cause of the most important complication (cerebral edema), and consequently without a consensus on the best approach.The use of the two saline bags in patients in DKA allows fast adjustments in the dextrose concentration of the infusion fluids, simplifying and reducing the costs of the treatment of diabetic ketoacidosis.J Pediatr (Rio J) 2001; 77(1): 9-16: diabetes mellitus, cerebral edema, diabetic ketoacidosis, fluid therapy. ResumoObjetivo: Rever vários aspectos da cetoacidose diabética, incluindo o sistema de duas soluções, um método de administrar líquidos que proporciona correção mais suave do estado de hiperglicemia e de cetose.Métodos: Revisão de publicações recentes (dos últimos 7 anos) referidas na base de dados da Medline e capítulos de livros de pediatria que abordam a etiologia, o tratamento e as complicações da cetoacidose diabética. O tratamento aqui apresentado utiliza a informação encontrada nestes artigos e a experiência clínica adquirida no Childrens Hospital of Philadelphia e no Duke University Medical Center.Resultados: A patologia do diabetes mellitus tipo 1 envolve a destruição das células ß do pâncreas, causando uma deficiência de insulina. A insulina é essencial para o metabolismo de carboidratos, proteínas e gorduras. A deficiência de insulina pode levar a um quadro de cetoacidose diabética que apresenta três componentes: 1) a hiperglicemia, que causa glicosúria e conseqüentemente desidratação; 2) a lipólise em excesso, que causa aumento nos níveis séricos e urinários de corpos cetônicos; e 3) a acidose metabólica, que é causa...

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“…The sudden development of cerebral edema, confirmed by computed tomography or on postmortem examination, during the first 24 hours of reasonable therapy for severe diabetic ketoacidosis remains poorly differentiated [1][2][3][4][5]. Contradictory reports have appeared that attempt to relate its occurrence to specific aspects of treatment, particularly to the overall fluid administration during the first 24 hours [3][4][5].We compared retrospectively two groups of patients treated with two different rehydration therapy protocols and administered by the same diabetic team at Suleimania Children's Hospital. Diagnosis of diabetic ketoacidosis was based on clinical findings (vomiting, abdominal pain, acidotic breathing, moderate to severe dehydration, torpor, or coma) and biological features (hyperglycemia > 15 mmol/L or 270 mg/dl) ketonuria, and metabolic acidosis (bicarbonate level, < 15 mmol/L).…”

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“…Intravenous fluids were given and initially consisted of normal saline when the corrected serum sodium level was below or equal to 140 mmol/L, ½ normal saline when the corrected serum sodium level was about 150 mmol/L, and ¼ normal D 5% when the blood glucose level reached 16.6 mmol/L (300 mg/dl). Corrected sodium was calculated by adding 2.75 mmol/L of sodium for each 5.55 mmol/L (100 mg/dl) of glucose above 5.55 mmol/L, i.e., 1 mmol sodium for 2 mmol of glucose [3,4]. Insulin therapy using continuous intravenous infusion of soluble insulin through a pump at a dose of 0.1 U/kg stat then 0.1 U/kg/hour then 0.05 U/kg/hour when blood glucose level reached 16.6 mmol/L (300 mg/dl) was similar for the two groups of patients.…”

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Fluid Therapy in Diabetic Ketoacidosis: Comparative Study

Salman

1991

Ann Saudi Med

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H Salman, Fluid Therapy in Diabetic Ketoacidosis: Comparative Study. 1991; 11(2): 235-237 To the Editor. A life-threatening emergency, diabetic ketoacidosis, is a unique state of hyperglycemic hypertonic dehydration accompanied by ketotic acidemia. Its incidence is not declining and represents 67.2% of our population of newly diagnosed diabetic children in Riyadh. Treatment remains difficult, and mortality reported in the literature is still high, particularly in young children below 5 years of age and those with new onset [1,2,5]. The sudden development of cerebral edema, confirmed by computed tomography or on postmortem examination, during the first 24 hours of reasonable therapy for severe diabetic ketoacidosis remains poorly differentiated [1][2][3][4][5]. Contradictory reports have appeared that attempt to relate its occurrence to specific aspects of treatment, particularly to the overall fluid administration during the first 24 hours [3][4][5].We compared retrospectively two groups of patients treated with two different rehydration therapy protocols and administered by the same diabetic team at Suleimania Children's Hospital. Diagnosis of diabetic ketoacidosis was based on clinical findings (vomiting, abdominal pain, acidotic breathing, moderate to severe dehydration, torpor, or coma) and biological features (hyperglycemia > 15 mmol/L or 270 mg/dl) ketonuria, and metabolic acidosis (bicarbonate level, < 15 mmol/L). We reviewed the medical records of 38 patients of both sexes admitted to Suleimania Children's Hospital between 1987 and 1989 with a comparable mean age of onset (6 years 5 months in Group 1, 5 years 8 months in Group 2). The patients were newly diagnosed diabetics and presented similarly at onset with moderate to severe diabetic ketoacidosis. In 52.6% (20/38), metabolic acidosis was severe with pH < 7.1. Laboratory investigations and monitoring in the first 24 hours were similar for both groups. Blood gas analysis (capillary) and Hemoglukotest (using Reflolux 11 M device) were done every half hour for the first three hours, then hourly for the next 3 hours, then every three hours. Serum urea and electrolyte concentrations were determined initially and after three hours, then every four to six hours. Random urine electrolyte analysis was done initially and after 3 hours. Urine was examined for glucose, and ketone was tested whenever urine was passed. Urine output was monitored in the initial 24 hours of treatment in all patients. The protocol used in the 15 patients who made up Group 1 consisted of rehydration using an initial volume of 20 to 40 ml/kg over the first 2 hours then 3 L/m 2 over the remaining 22 hours using initially normal saline then ¼ normal saline D 5 % when blood glucose level reaches 16.6 mmol/L (300 mg/dl). For protocol 2, which comprised 23 patients, 5 to 10 ml/kg of normal saline was infused rapidly only if signs of shock were present, until correction of oliguria, turgor time, and blood pressure. Over 24 hours, the volume of fluids infused was 1 .5 L/m 2 (in cases of mo...

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Factors associated with brain herniation in the treatment of diabetic ketoacidosis

Cited by 220 publications

References 22 publications

Risk of Type 1 Diabetes Development in Children With Incidental Hyperglycemia

Risk of Type 1 Diabetes Development in Children With Incidental Hyperglycemia

Diabetic ketoacidosis in children: review of pathophysiology and treatment with the use of the

Fluid Therapy in Diabetic Ketoacidosis: Comparative Study

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