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Metabolic Diseases chapter 16 Metabolic Diseases Nicole Glaser, MD Elka Jacobson-Dickman, MD Nathan Kuppermann, MD, MPH, FAAP Debra L. Weiner, MD, PhD, FAAP Objectives Chapter Outline Describe the 1 epidemiology, Introduction clinical features, Diabetic Ketoacidosis and emergency Hypoglycemia in Children With Diabetes management of Hypoglycemia in Nondiabetic Children diabetes mellitus (DM), Adrenal Insufficiency/Congenital Adrenal Hyperplasia adrenal insufficiency, Diabetes Insipidus syndrome of inappropriate secretion Syndrome of Inappropriate Secretion of Antidiuretic Hormone of antidiuretic Water Intoxication hormone (SIADH), Metabolic Disease of the Newborn and Young Child: Inborn water intoxication, and Errors of Metabolism diabetes insipidus (DI). Describe the fluid and 2 electrolyte problems associated with these conditions. Discuss the clinical 3 features and emergency management of metabolic diseases of the newborn and young child. Copyright © 2012 by the American Academy of Pediatrics and the American College of Emergency Physicians A 10-year-old boy presents to the emergency department (ED) with altered mental status and a 1 2-week history of polyuria and weight loss. He is experiencing abdominal pain. On examination, he has a respiratory rate of 36/min, a heart rate of 150/min, a systolic blood pressure of 80 mm Hg, and a temperature of 37.9°C (100.2°F). Pulse oximetry oxygen saturation is 97% on room air. On examination, he appears lethargic, has dry mucous membranes, has normal abdominal examination results, and has a nonfocal neurologic examination results. Bedside rapid glucose measurement is above the upper limit of the glucose meter (>500 mg/dL). 1. What therapeutic actions must be taken immediately? 2. What laboratory tests would you order? CASE SCENARIO SCENARIO CASE 3. What is the most important potential complication? Introduction Diabetic Ketoacidosis The emergency management of endocrine and Diabetic ketoacidosis (DKA) is the most impor- metabolic disorders presents diagnostic and tant complication of type 1 DM (Figure 16.1). therapeutic challenges. Many of these disor- Diabetic ketoacidosis occurs when insulin con- ders, such as congenital adrenal hyperplasia centrations are low relative to the concentrations (CAH) and inborn errors of metabolism, occur of counterregulatory hormones, particularly relatively infrequently. Nonetheless, rapid and glucagon. This imbalance results in hypergly- appropriate intervention is necessary to prevent cemia along with the breakdown of fat to form complications. Awareness of key clinical and ketone bodies, eventually resulting in acidosis. laboratory findings that differentiate endocrine Diabetic ketoacidosis occurs in 25% to 40% of and metabolic disorders from other entities with children with new onset of type 1 diabetes melli- similar presenting features is essential. tus (DM).1–3 Repeat episodes of DKA in children 16-3 Copyright © 2012 by the American Academy of Pediatrics and the American College of Emergency Physicians with known diabetes can occur during episodes causes of dehydration. Acidosis results in com- of illness or with diabetes mismanagement or pensatory tachypnea, and a characteristic fruity malfunction of diabetes care equipment (insulin (acetone) breath odor can often be detected. pumps). Presumed omission or incorrect ad- Because the hyperosmolar state allows for the ministration of insulin injections is the most relative preservation of intravascular volume, common cause of DKA in children with known some signs of dehydration can be less obvious DM (69%); bacterial infections are infrequently than in dehydrated patients with more normal present (13%).4 serum osmolality. Alterations in mental status can range from disorientation to depressed con- Clinical Features sciousness. This alteration of mental status can Diabetic ketoacidosis is characterized by hyper- glycemia and elevated serum ketone concentra- tions, resulting in acidosis. Inadequate insulin YOUR FIRST CLUE concentrations allow the partial oxidation of fatty acids to form ketone bodies. This process Signs and Symptoms of DKA then results in acidosis with an increased anion • History of polyuria, polydipsia, weight gap. Hyperglycemia results in osmotic diuresis loss, nausea, and vomiting with polyuria, polydipsia, and eventual dehy- • Signs of dehydration dration. Presenting features of DKA include • Breath with fruity odor a history of polyuria, polydipsia, nausea, and vomiting. Abdominal pain and intestinal ileus • Abdominal pain are common features and can mimic an acute • Tachypnea abdomen. In a patient with clinical signs of de- • Lethargy hydration, the presence of polyuria helps dif- ferentiate DKA from gastroenteritis and other Pathophysiology of Diabetic Ketoacidosis fatty acid oxidation gluconeogenesis glycogenolysis peripheral glucose uptake and metabolism Ketone Bodies Hyperglycemia Acidosis osmotic diuresis vomiting increased renal Na+ loss renal hyperkalemia insensible Dehydration Ca, phos, fluid losses Mg loss poor tissue perfusion renal K+ loss increased lactate Figure 16.1 Diabetic ketoacidosis. Behrman RE, Kliegman RM. Nelson Essentials of Pediatrics. 4th ed. Philadelphia, PA: WB Saunders; 2002:185. Reprinted with permission. 16-4 Metabolic Diseases Copyright © 2012 by the American Academy of Pediatrics and the American College of Emergency Physicians be due to acidosis and dehydration but can also are total body concentrations of sodium, phos- reflect more serious underlying intracranial dis- phate, calcium, and magnesium. Although total ease. Rarely, children with DKA present to the body sodium is depleted, the degree of deple- ED with clinically apparent cerebral edema,5 as tion is less than that suggested by the measured well as cerebral infarctions or thromboses. serum sodium concentration, which is artifi- cially depressed due to hyperglycemia. Blood Complications urea nitrogen (BUN) concentrations are usually The most frequent complications of DKA treat- elevated due to prerenal azotemia. The white ment include hypokalemia and hypoglycemia. blood cell count is often elevated and frequently Hypocalcemia, hypophosphatemia, and hypo- left-shifted as a result of the ketoacidotic state 4 magnesemia can also occur but are much less alone. It is generally unnecessary to search for common. Of the more serious complications of a source of infection beyond performing a care- DKA, clinically apparent cerebral edema is the ful physical examination unless fever or other most frequent, occurring in approximately 1% specific signs of infection are present. of DKA episodes. Cerebral edema is the most important diabetes-related cause of mortality in Differential Diagnosis children with type 1 DM.6,7 The presenting symptoms and signs of DKA Although cerebral edema can occur before can initially be confused with gastroenteritis or hospital treatment of DKA, this complication other gastrointestinal disorders that present with more typically occurs several hours after initia- vomiting and abdominal pain. Infections such as tion of therapy. The clinical presentation of ce- pneumonia, meningitis, and urinary tract infec- rebral edema can take different forms. Typically, tions also can present with metabolic acidosis, patients with cerebral edema experience head- tachypnea, and altered mental status or can be a ache and exhibit alterations in mental status. cause of the development of DKA. The history of Obtundation, papilledema, pupillary dilation polyuria despite clinical dehydration, absence of or anisocoria, blood pressure variability, brady- diarrhea, and presence of tachypnea with fruity cardia, and apnea can also occur in severe cases. breath odor should differentiate DKA from these Deep venous thromboses can occur in chil- other entities even before laboratory tests are or- dren with DKA, particularly when central ve- dered. Diabetic ketoacidosis must also be differ- nous catheters are used.8,9 Other complications entiated from hyperglycemic hyperosmolar state of DKA are rare but include cerebral infarctions (HHS) (formerly known as hyperglycemic hyper- or thrombosis, acute renal tubular necrosis lead- osmolar nonketotic coma), which presents with ing to renal failure, pulmonary edema, pulmo- severe hyperglycemia (serum glucose concentra- nary embolus, arrhythmia, pancreatitis, and tion >600 mg/dL and often >1,000 mg/dL) and intestinal necrosis. hyperosmolality (serum osmolality >330 mOsm), profound dehydration, and a depressed level of Diagnostic Studies consciousness, but mild or no ketosis.10 Hyper- Diabetic ketoacidosis is defined as hyperglyce- glycemic hyperosmolar state can in fact represent mia (serum glucose concentration >200 mg/dL), acidosis (venous pH <7.25 or serum bicarbon- ate concentration <15 mEq/L), and the presence THE CLASSICS of ketones in the serum or urine.6,7 Electrolyte abnormalities also occur as a result of urinary losses and shifts due to acidosis. High serum Laboratory Findings in DKA concentrations of potassium are often found at • Hyperglycemia the time of presentation of DKA, but normal • Metabolic acidosis or low concentrations can occur if the ketoaci- • Ketonemia or ketonuria dotic state is prolonged. Intracellular potassium concentrations are characteristically depleted, as Diabetic Ketoacidosis 16-5 Copyright © 2012 by the American Academy of Pediatrics and the American College of Emergency Physicians should not be compromised by theoretical con- WHAT ELSE? cerns associated with fluid administration. The average degree of dehydration in chil- dren with
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