Polio eradication

Over the 10 year period 1987-1996, 328 children with type 1 diabetes mellitus presented in the city of Birmingham, England, of whom 27% had diabetic ketoacidosis. Asian children under the age of 5 had an eightfold increased risk of presenting in diabetic ketoacidosis compared with non-Asian children of the same age.

     

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目的探讨儿童糖尿病酮症酸中毒并发脑水肿的临床特征及危险因素。方法对重庆医科大学附属儿童医院1993—2005年住院治疗的糖尿病酮症酸中毒并发脑水肿患儿的临床特征及病因进行分析,并与未并发者进行对照比较。结果在71例酮症酸中毒患儿中,有6例临床表现符合脑水肿的诊断标准,临床确定为并发脑水肿,并发率为8·4%。6例均为重型酮症酸中毒。与未发生脑水肿同等程度的重型酮症酸中毒患儿相比较,并发脑水肿患儿酸中毒更为严重,在治疗期间血钠上升缓慢及持续低钠血症,尿素氮水平升高。6例患儿中有5例应用碳酸氢盐治疗,用量大于未并发者。结论糖尿病儿童并发重型酮症酸中毒易发生脑水肿。严重酸中毒、血钠上升缓慢或持续低钠血症、血尿素氮升高及碳酸氢盐的使用有可能增加脑水肿发生的危险性。     

Ketoacidosis at the diagnosis of type 1 (insulin dependent) diabetes mellitus is related to poor residual beta cell function. Childhood Diabetes in Finland Study Group.

The determinants of the degree of metabolic decompensation at the diagnosis of type 1 (insulin dependent) diabetes mellitus (IDDM) and the possible role of diabetic ketoacidosis in the preservation and recovery of residual beta cell function were examined in 745 Finnish children and adolescents. Children younger than 2 years or older than 10 years of age were found to be more susceptible to diabetic ketoacidosis than children between 2 and 10 years of age (< 2 years: 53.3%; 2-10 years: 16.9%; > 10 years: 33.3%). Children from families with poor parental educational level had ketoacidosis more often than those from families with high parental educational level (24.4% v 16.9%). A serum C peptide concentration of 0.10 nmol/l or more was associated with a favourable metabolic situation. Low serum C peptide concentrations, high requirement of exogenous insulin, low prevalence of remission, and high glycated haemoglobin concentrations were observed during the follow up in the group of probands having diabetic ketoacidosis at the diagnosis of IDDM. Thus diabetic ketoacidosis at diagnosis is related to a decreased capacity for beta cell recovery after the clinical manifestation of IDDM in children.     

Ketoacidosis at the diagnosis of type 1 (insulin dependent) diabetes mellitus is related to poor residual beta cell function. Childhood Diabetes in Finland Study Group

The determinants of the degree of metabolic decompensation at the diagnosis of type 1 (insulin dependent) diabetes mellitus (IDDM) and the possible role of diabetic ketoacidosis in the preservation and recovery of residual beta cell function were examined in 745 Finnish children and adolescents. Children younger than 2 years or older than 10 years of age were found to be more susceptible to diabetic ketoacidosis than children between 2 and 10 years of age (< 2 years: 53.3%; 2-10 years: 16.9%; > 10 years: 33.3%). Children from families with poor parental educational level had ketoacidosis more often than those from families with high parental educational level (24.4% v 16.9%). A serum C peptide concentration of 0.10 nmol/l or more was associated with a favourable metabolic situation. Low serum C peptide concentrations, high requirement of exogenous insulin, low prevalence of remission, and high glycated haemoglobin concentrations were observed during the follow up in the group of probands having diabetic ketoacidosis at the diagnosis of IDDM. Thus diabetic ketoacidosis at diagnosis is related to a decreased capacity for beta cell recovery after the clinical manifestation of IDDM in children.     

儿童1型糖尿病的10年回顾及白介素-10在糖尿病酮症酸中毒中的临床意义

目的：回顾浙江大学医学院附属儿童医院10年来住院儿童 1 型糖尿病的发病状况并探讨白介素-10（IL-10）在儿童 1 型糖尿病酮症酸中毒（DKA）中的临床意义。方法：对1999年1月至2009年2月在该院住院的263例334例次1型糖尿病患儿的临床资料进行回顾性分析;并对其中48例1型糖尿病患儿进行血脂、细胞因子等检查,根据有无酮症酸中毒分为 DKA组和非DKA组,24例正常健康儿童作为对照组,比较各组间血脂、细胞因子等参数的差异。结果：儿童1型糖尿病患儿中,女性多见（56.3%）,发病年龄以6~11.9岁多见。32.7% 的患儿以酮症酸中毒为就诊表现。DKA组血脂、血糖及糖化血红蛋白均高于非DKA组,二分类logistic 回归分析示上述指标水平的升高均为酮症酸中毒的危险因素。IL-10水平在DKA组明显升高,余细胞因子在DKA组和非DKA组无明显差异。糖尿病组各细胞因子水平明显高于正常对照组。结论：1型糖尿病患儿酮症酸中毒发生率较高,糖、脂代谢紊乱是酮症酸中毒的危险因素。IL-10可能为酮症酸中毒的敏感指标。［中国当代儿科杂志,2010,12（11）：849-854］     

Factors predicting cerebral edema in young children with diabetic ketoacidosis and new onset type I diabetes

We have attempted to identify any characteristics which could be used to predict the development of cerebral edema in four children under 5 years of age with new onset insulin-dependent diabetes mellitus and diabetic ketoacidosis. We retrospectively analysed and compared the concentration of serum sodium (corrected for serum glucose value) and effective serum osmolality of these 4 children with values of 10 age-matched controls with new onset insulin-dependent diabetes mellitus who did not develop cerebral edema during treatment of diabetic ketoacidosis. The initial serum sodium values of the two groups were not statistically different. Patients who developed cerebral edema had lower initial serum glucose values and effective serum osmolality. During treatment, patients who developed cerebral edema had consistently lower mean serum sodium and osmolality than controls at each 4-h interval after the first 4 h of therapy. Serum sodium and osmolality declined progressively after the initiation of therapy in cerebral edema patients, while remaining stable in controls. These data suggest that children who develop cerebral edema during treatment for diabetic ketoacidosis initially may have a relatively normal serum osmolality and subsequently develop progressive hyponatremia and/or a trend of declining serum sodium before developing cerebral edema.     

Abnormalities of in vitro lymphocyte response to mitogens in diabetic children during acute ketoacidosis.

Cell-mediated immunity was evaluated in 11 children with diabetes mellitus; six children were evaluated during ketoacidosis and five were evaluated with ketonuria in the absence of acidosis. Five of the six ketoacidotic children had at least one positive delayed-hypersensitivity skin test. Lymphocytes from two ketoacidotic patients were unresponsive to phytohemagglutinin and pokeweed mitogen, and lymphocytes from these two patients plus a third patient were unresponsive to concanavalin A. Lymphocytes from all six patients responded to these three mitogens after one week of therapy. In the five diabetic children without ketoacidosis, lymphocyte responses were normal to all three mitogens. Similarly, the addition of glucose to normal plasma did not alter the lymphocyte transformations of three healthy nondiabetic controls. These data suggest that cell-mediated immunity may be transiently defective in children with acute diabetic ketoacidosis.     

Acute renal failure complicating diabetic ketoacidosis

Two previously healthy children, aged 13 and 14 years, respectively, presented with diabetic ketoacidosis. Both children developed acute renal failure, a rare complication of diabetic ketoacidosis and required dialysis.     

Ketoacidosis occurring in newly diagnosed and established diabetic children

A 6-y retrospective case note review was performed to determine the causes of ketoacidosis. 135 patients and 463 diabetic years were involved. Fifty-two ketoacidosis episodes occurred: 19 episodes in new patients and 33 episodes in 19 patients with established diabetes. 27% of newly diagnosed patients presented in ketoacidosis. They were similar in terms of age, sex and proportion living in single parent families to those presenting without ketoacidosis. The 33 ketoacidosis episodes occurring in established patients included 12 episodes in 3 children who were transferred to our care because of uncontrolled diabetes. Insulin omission was the cause of ketoacidosis in 9/19 (47%) patients, and was suspected in a further 5/19 (26%). Family and school problems were common and 14/19 patients came from single parent families. Established patients aged ≥11 y were predominantly female (10F, 2M), whereas patients aged ≥10y were predominantly male (6M, 1F). 7 patients with multiple ketoacidosis episodes were all ≥11 y and 6 were female. Families with ≥2 diabetic children appeared vulnerable, 4 cases coming from 3/7 such families.     

Immunologic changes in diabetic ketoacidosis]

We studied 13 children and adolescents during diabetic ketoacidosis; the duration of diabetes ranged from 1.4 to 6.0 years. A group of 13 diabetic sex, age and duration of disease-matched children served as control. Patients in ketoacidosis showed important abnormalities of T subset percentages (OKT3: 63.4 +/- 1.87% vs 72.1 +/- 3.4; p less than 0.001. OKT4: 37.18 +/- 1.85% vs 44.6 +/- 3.9; p less than 0.01. OKT8: 28.5 +/- 6.51% vs 28.1 +/- 1.9; p less than 0.04) and impaired neutrophil chemotaxis (53.10 +/- 3.3 vs 88.1 +/- 7.2; p less than 0.001). The patients showed normal levels of all classes of immunoglobulins. No correlation was observed between these abnormalities and the degree of ketoacidosis or glycaemia. When the patients were re-evaluated out of ketoacidosis, the values of the immunological parameters were normal and similar to those of the control group.     

Low-dose intravenous insulin infusion in patients with diabetic ketoacidosis: biochemical effects in children.

Twenty-five episodes of diabetic ketoacidosis in 20 children were treated with continuous low-dose intravenous insulin infusion. Stable serum immunoreactive insulin concentrations were produced, along with prompt falls in glucose, beta-hydroxybutyrate, and glucagon levels, and a steadily increasing bicarbonate level. Neither hypokalemia nor hypophosphatemia developed. Elevated serum alanine concentrations were found during ketoacidosis in contrast to the lowered concentrations found in adults, and were correlated inversely with plasma glucagon concentrations. The treatment regimen described is safe, easy to use, efficacious, and resulted in prompt correction of the observed biochemical alterations in children with diabetic ketoacidosis.     

Incidence and outcome of diabetic cerebral oedema in childhood: Are there predictors?

Objective: Information regarding cerebral oedema in diabetic children with ketoacidosis does not point to any causal factor or any predictor of outcome. Cases of diabetic ketoacidosis resulting in cerebral oedema at Royal Children's Hospital, Melbourne, over the last 20 years were reviewed.
Methodology: The study was divided into two 10-year periods during which different fluid protocols were used. During the earlier period dehydration was corrected rapidly (over six h) with a fluid isotonic for sodium. During the latter period rehydration was over 24 h using half-normal saline.
Results: A similar number of patients developed cerebral oedema in the two periods (six of 3134 vs six of 3373). Only half of the patients (six) developed cerebral oedema during their initial presentation of diabetes mellitus. The age range was similar (1 to 15 years) with eight males and four females. Survival from cerebral oedema (four of 12) was not predicted by demographic or biochemical findings, including initial biochemistry, age, duration of ketoacidosis and the management protocols.
Conclusions: This study suggests that the rate of salt and water replacement in diabetic ketoacidosis are not key determinants of the appearance of cerebral oedema. No factors predictive of survival from cerebral oedema have been identified, though this is a rare entity and case numbers were small. Nevertheless, current protocols at Royal Children's Hospital and most other centres utilize slow rates of rehydration with isotonic saline fluids. Further review in 5–10 years may determine whether this protocol is effective in reducing rates of cerebral oedema complicating diabetic ketoacidosis.     

Insulin dependent diabetes in children

We present our experience with twenty children with insulin dependent diabetes mellitus admitted during the past 2 1/2 years. Sixteen patients were admited with acute onset of ketoacidosis while four were having gradual onset. Active and symptomatic treatment was started in all diabetic ketoacidotic patients. One patient died during the acute stage. Eleven patients were followed for 3–6 months or more. Glycosylated hemoglobin was considered as a criteria for control. Three had good control, two fair and six poor control; six developed diabetic ketoacidosis and three developed hypoglycemia     

Ketoacidosis at onset of type 1 diabetes mellitus in children--frequency and clinical presentation

Abstract: Background: Since 1987, patients with newly diagnosed diabetes mellitus type 1 under 15 yr of age have been registered in Baden‐Wuerttemberg (BW), Germany. Aim: Our aim was to describe the frequency and the clinical presentation of diabetic ketoacidosis (DKA) at onset of type 1 diabetes mellitus in children. Methods: All 31 pediatric departments in BW and one diabetes center participated in this study. Hospital records of 2121 children below 15 yr of age were examined retrospectively. DKA was defined as glucose > 250 mg/dL, pH < 7.30 or bicarbonate < 15 mmol/L and ketonuria. Statistical analysis was done after logarithmic transformation. Results: 26.3% (n = 558) of all patients presented with DKA. The mean age of these patients was 7.9 yr. The frequency of DKA is higher in girls than in boys (28.9 vs. 23.8%; p = 0.0079). Those aged 0–4 yr suffered most frequently (p < 0.0001) from ketoacidosis (36.0%). The percentage of DKA in newly diagnosed cases was constant over 10 yr. 23.3% of all patients with DKA presented with an altered level of consciousness; 10.9% of these had clinical signs of coma. No deaths occurred. The proportion of ketoacidosis does not increase concurrently with the number of diabetes manifestations in winter. Conclusion: The proportion of DKA in children with newly diagnosed diabetes mellitus is significant. In particular, children < 5 yr and girls face an increased risk. DKA may be the result of a particularly aggressive subtype of diabetes.     

Stroke in a child with Adams-Oliver syndrome and mixed diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome

Diabetes mellitus complicated by mixed diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome presents a special challenge to physicians. There is no standard protocol for the management of mixed hyperglycemic hyperosmolar syndrome and diabetic ketoacidosis in children. The commonest cause of neurological deterioration during an episode of diabetic ketoacidosis is cerebral edema, whereas hyperosmolality often leads to thrombosis. The risks for these complications are further increased in diseases associated with vasculopathies. We present the first case of complex cerebral arteriovenous thrombosis leading to stroke in a child with Adams-Oliver syndrome, a genetic condition that is associated with abnormal vasculogenesis. He presented with new-onset double diabetes complicated by a combination of diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome. Magnetic resonance imaging, magnetic resonance angiography, and magnetic resonance venography provided evidence for an ischemic stroke. Children and adolescents who present with a combination of hyperglycemic hyperosmolar syndrome and diabetic ketoacidosis should be monitored for neurologic deficits and must be investigated for both stroke and cerebral edema in the event of neurological deterioration.     

Comparison of 2 modes of treatment of diabetic ketoacidosis in children

In two groups of children with diabetic ketoacidosis, the effects of intramuscular insulin injections associated with intensive rehydration and alkalisation were compared with low-dose continuous intravenous infusion associated with well-controlled fluid and electrolyte therapy. Although correction of ketoacidosis was as effective with both methods, the second appeared to offer several advantages: 1. More progressive normalization of metabolic parameters; 2. Reduced risks of hypoglycemia and hypokaliemia; 3. Easier control of the decrease in plasma glucose levels; 4. Better correction of hyponatremia; 5. More gradual increase in pH values. These results confirmed that low-dose continuous insulin infusion with proper monitoring of fluid and electrolyte replacement was a safe, simple and effective treatment of diabetic ketoacidosis in children.     

Glucagon suppression with low-dose intramuscular insulin therapy in diabetic ketoacidosis.

The effects of low-dose intramuscular insulin therapy on endogenous glucagon secretion in diabetic ketoacidosis were compared prospectively with a conventional regimen. Ten patients, 4 to 15 years of age, who had 13 episodes of diabetic ketoacidosis, were alternately assigned to either group. Either 0.1 unit/kg regular insulin was given every two hours im, or 1.0 unit/kg regular insulin was given, half subcutaneously and half intravenously, every 4 hours. In both groups, a significant and equal fall in both serum glucose and glucagon concentrations was observed. No complications were encountered. It is concluded that 0.1 unit/kg of regular insulin given im every two hours is as effective in correcting hyperglycemia and hyperglucagonemia of diabetic ketoacidosis as is conventional therapy, and avoids the risks of secondary hypoglycemia known to occur when the larger insulin dosages are employed.     

Increased cardiac troponin I concentration in diabetic ketoacidosis

OBJECTIVE: To examine the hypothesis that diabetic ketoacidosis may be associated with some degree of induced injury to heart muscle, related either to acidosis or hyperglycemia. METHODS: Nineteen diabetic patients with acute ketoacidosis and 19 healthy children were enrolled in this study. Cardiac troponin I (cTnI), creatine kinase (CK)-MB and myoglobin levels were analyzed soon after admission and after 24 h. Patients were subdivided into two groups according to blood pH. RESULTS: At the time of admission, the diabetic patients had significantly higher values than the controls for cTnI (0.193+/-0.008 vs 0.176+/-0.006 ng/dl; p <0.001), CK-MB (24.1+/-2.1 vs 22.7+/-1.2 U/l; p = 0.02), and myoglobin (85.5+/-7.4 vs 52.5 +/-8.3 microg/dl; p <0.001). The diabetic patients also had significantly higher values than the controls for CK-MB (24+/-2.1 vs 22.7+/-1.2 U/l; p = 0.02) and for myoglobin (78.5+/-2.5 vs 52.5+/-8.3 microg/dl; p <0.001) at 24 h. cTnI had normalized in patients at 24 h. All parameters were significantly different between patients with pH > or =7.0 and patients with pH <7.0. In addition, serum cTnI levels correlated negatively with blood pH (r = -0.57, p = 0.026) and HCO3- (r = -0.65, p = 0.008) in the patients with diabetic ketoacidosis on admission. CONCLUSION: Our findings suggest that diabetic ketoacidosis, particularly when severe, has a detrimental effect on the myocardium.