Diabetic ketoacidosis in the pediatric patient

Diabetic ketoacidosis is the major source of morbidity and mortality in patients with Type I diabetes mellitus. One population-based study noted that approximately 25% of newly diagnosed patients present with diabetic ketoacidosis.¹ Most of those hospitalized with diabetes ketoacidosis, however, are those with poor control of their pre-existing diabetes. Cerebral edema has been found to be present in only 1% of children with diabetic ketoacidosis, but accounts for 20% of all diabetes-related deaths.² Although the mortality rate has fallen dramatically over the course of the last century, the underlying mechanisms involved with the development of cerebral edema are still not clear. Several studies have shown specific risk factors to be associated with cerebral edema, but as of yet no reduction in the recent incidence of cerebral edema has been demonstrated. A discussion of these risk factors and a suggested protocol for treating diabetic ketoacidosis are included in this review.     

Diabetic ketoacidosis associated with olanzapine in an adolescent patient

Olanzapine (Zyprexa) is an atypical neuroleptic used in adult and pediatric patients for the management of schizophrenia. Common side effects include increased appetite and weight gain. An uncommon but severe adverse effect is the development of diabetic ketoacidosis, reported until now only in adults. We report a case of acute onset diabetic ketoacidosis presenting in a 16-year-old girl during olanzapine therapy.     

Reduced Vascular Reactivity in Diabetic Children and Its Relation to Diabetic Control

ABSTRACT. The vascular reactivity in response to ischaemia was studied by a non-invasive method of measuring transcutaneous oxygen tension used at 37^oC, in 28 children with type I diabetes mellitus. Postischaemic hyperaemia was significantly reduced in the diabetic children compared with 34 healthy children. The degree of reduction in vascular reactivity correlated to both short-term and long-term diabetic control. Among tested variables, urinary glucose excretion during the night preceding the test showed the highest coefficient of correlation to the peak of the postocclusive reactive hyperaemia ( r = - 0.59, p < 0.01). This peak was only weakly correlated to triglycerides and glycosylated haemoglobins and showed no significant correlation to fasting plasma glucose or to the duration of the disease. It was weakly correlated to the total daily insulin dosage but not to the dosage of insulin/kg body weight. Multiple linear regression analysis revealed that urinary glucose excretion, plasma glucose, haemoglobin A₁, serum triglyceride and serum cholesterol, duration of diabetes, and insulin dosage per kg body weight together explained 54 % of the variation in vascular reactivity. The reduced vascular reactivity found in diabetic children could not be explained by the usual parameters of carbohydrate control alone. This new non-invasive method is able to reveal a reduction in vascular function in diabetic children and should therefore be of value in attempts to find the causes of vascular dysfunction in diabetics.     

Diabetic nephropathy

It is estimated that about 50 per cent of all patients with Type I diabetes mellitus develop uremia during the course of their disease. Glomerular microvasculopathy is the most serious and predictable threat to longevity. Following a discussion of this disorder, the author outlines a plan for overall management of each phase of kidney disease so that the patient, his or her family, and all members of the medical team can achieve an understanding of what can be anticipated and accomplished.     

Diabetic ketoacidosis

Diabetic ketoacidosis (DKA) is a true pediatric and medical emergency. Diagnosis should be entertained and confirmed within 30 min of presentation. Any delay in making the diagnosis or instituting fluid and electrolyte correction is likely to increase morbidity and mortality. Slow and careful monitoring and correction of water, sodium and potassium levels should decrease DKA-associated problems with either continuous intravenous low-dose insulin or intramuscular insulin protocols designed to slowly bring the hyperglycemic and hyperosmotic state towards normal homeostasis. Special attention should be paid to potassium replenishment. Most patients do not require bicarbonate replacement. Cerebral edema, when it occurs, is associated with an approximately 50% morbidity and mortality; therefore, all attempts should be made at early recognition and prevention since treatment is less than ideal. Recurrent ketoacidosis is often related to omitted insulin and major psychosocial turmoil in the family, such as depression substance abuse, physical and/or sexual abuse. Prevention of recurrent DKA remains a major challenge for diabetologists and involves detailed assessment of family psychodynamics plus responsibility for home monitoring and insulin administration by a mature adult. Sick day guidelines should be taught and reviewed frequently in an effort to decrease ketoacidosis and metabolic decompensation during episodes of intercurrent illness. □ Cerebral edema, diabetic ketoacidosis, diabetes mellitus, DKA, sick day guidelines, sick day management, type 1 diabetes mellitus     

Diabetic microangiopathy

Microvascular complications of diabetes include retinopathy, nephropathy and neuropathy. The first signs of these complications may develop in children and adolescents, particularly if insulin treatment has been inadequate. The mechanisms by which diabetic microangiopathy develop are not known, but probably include genetic influences. Several biochemical changes may interact, one important change being increased protein glycation. Important functional changes are increased organ blood flow, increased vascular permeability, abnormal blood viscosity and abnormal platelet and endothelial function. The structural hallmark of diabetic microangiopathy is the thickening of the capillary basement membrane. These changes may lead to occlusive angiopathy and to tissue hypoxia and damage. Screening for microangiopathy should start in children and adolescents after 5-y duration of the disease and 10 y of age. The screening should include retinal examination through a dilated pupil or fundus photography, urinary albumin excretion rate, blood pressure measurement and neurological examination. Several intervention trials have shown that near normoglycaemia may reduce the risk of microangiopathy. There is a curvilinear association between the risk of development and progression of microangiopathy and mean blood glucose. Therefore, optimal insulin treatment is important in children and adolescents.     

Diabetic ketoacidosis

Diabetic ketoacidosis (DKA) is a true pediatric and medical emergency. Diagnosis should be entertained and confirmed within 30 min of presentation. Any delay in making the diagnosis or instituting fluid and electrolyte correction is likely to increase morbidity and mortality. Slow and careful monitoring and correction of water, sodium and potassium levels should decrease DKA-associated problems with either continuous intravenous low-dose insulin or intramuscular insulin protocols designed to slowly bring the hyperglycemic and hyperosmotic state towards normal homeostasis. Special attention should be paid to potassium replenishment. Most patients do not require bicarbonate replacement. Cerebral edema, when it occurs, is associated with an approximately 50% morbidity and mortality; therefore, all attempts should be made at early recognition and prevention since treatment is less than ideal. Recurrent ketoacidosis is often related to omitted insulin and major psychosocial turmoil in the family, such as depression substance abuse, physical and/or sexual abuse. Prevention of recurrent DKA remains a major challenge for diabetologists and involves detailed assessment of family psychodynamics plus responsibility for home monitoring and insulin administration by a mature adult. Sick day guidelines should be taught and reviewed frequently in an effort to decrease ketoacidosis and metabolic decompensation during episodes of intercurrent illness.     

Diabetic ketoacidosis

In the past decade, considerable advances have occurred in our understanding of the pathophysiology of this disorder, its metabolic sequelae, and its management, particularly with respect to continuous low-dose insulin infusion and the potential benefits of phosphate. This article reviews these advances as they pertain to children.     

Diabetic ketoacidosis and cerebral edema

Cerebral edema is the leading cause of death in children presenting in diabetic ketoacidosis and occurs in 0.2 to 1% of cases. The osmolar gradient caused by the high blood glucose results in water shift from the intracelluar fluid (ICF) to the extracellular fluid (ECF) space and contraction of cell volume. Correction with insulin and intravenous fluids can result in a rapid reduction in effective osmolarity, reversal of the fluid shift and the development of cerebral edema. The goals for treatment should be a combination of intravenous fluid and insulin that results in a gradual reduction of the effective osmolarity over a 36- to 48-hour period, thereby avoiding rapid expansion of the ICF compartment and brain swelling.