Diabetic ketoacidosis is a common, serious acute complication in children with diabetes mellitus. Diabetic ketoacidosis can accompany new-onset type 1 diabetes mellitus or it can occur with established type 1 diabetes mellitus during the increased demands of an acute illness or with decreased insulin delivery due to omitted doses or insulin pump failure. Additionally, diabetic ketoacidosis episodes in children with type 2 diabetes mellitus are being reported with greater frequency. Although the diagnosis is usually straightforward in a known diabetes patient with expected findings, a fair proportion of patients with new-onset diabetes present in diabetic ketoacidosis. The initial management of children with diabetic ketoacidosis frequently occurs in an emergency department. Physicians must be aware that diabetic ketoacidosis is an important consideration in the differential diagnosis of pediatric metabolic acidosis. This review will acquaint emergency medicine clinicians with the pathophysiology, treatment, and potential complications of this disorder.
Key words: pediatric diabetic ketoacidosis, DKA, type 1 diabetes mellitus, type 2 diabetes mellitus, insulin-dependent diabetes mellitus, insulin-resistant diabetes mellitus, cerebral edema
A 7-year-old girl presents to the ED with low-grade fever, vomiting, and abdominal pain. A review of systems reveals a 2-week history of increasing polyuria and polydipsia with a 2-pound weight loss. Vomitus is not bloody or bilious, and she has no headache. The family history is pertinent for a first cousin with type 1 diabetes. On physical exam, she is somewhat lethargic, but alerts fully and is oriented. Her GCS score is 14. There is no evidence of trauma. Vital signs include a heart rate of 122 beats/min, a respiratory rate of 32 breaths/min, and a blood pressure of 113/63 mm Hg. The oral mucosa is dry, and capillary refill time is 3 seconds. Pulses are equal and full. Lungs are clear to auscultation, and the cardiac exam is unremarkable. Her abdomen is soft and slightly tender in the epigastric area, and there is no guarding or rebound tenderness. There is no focal neurologic deficit. IV access is obtained; a point-of-care (bedside) glucose measurement is 625 mg/dL. Subsequent lab results obtained on presentation show the serum HCO3 is 12 mg/dL and venous pH is 7.22. Urinalysis shows large glucose and ketones. As you begin considering the differential diagnosis for this child, you ask yourself: What questions are most pertinent to ask the parents in determining the etiology? What lab tests should be initially obtained? What is the top initial priority in management? What parameters are most important to follow in this patient’s clinical course? What complications can occur during management?
Diabetic ketoacidosis (DKA) is the most common acute complication requiring hospitalization of children with type 1 diabetes mellitus.1-3 DKA is potentially fatal, accounting for 70% of diabetes-related deaths in children < 10 years of age.3,4 Most DKA fatalities are caused by cerebral edema.3-5
Successful emergency department (ED) management of DKA requires timely intervention, meticulous monitoring, and protocol-based hour-by-hour therapy adjustment aimed at ensuring tissue perfusion, correcting fluid and electrolyte depletion, arresting ketogenesis, and restoring normal cellular utilization and metabolism of glucose. To successfully manage the crucial initial phase of DKA, emergency clinicians must thoroughly understand the pathophysiology of DKA and the appropriate therapeutics and monitoring requirements of this complex disorder as well as maintain a keen awareness of potential complications as therapy proceeds. The purpose of this review is to discuss the pathogenesis, evaluation, and management of pediatric DKA in the outpatient setting.
A 12-year review of PubMed entries using the key word pediatric diabetic ketoacidosis revealed scant medical literature comparing the efficacy of various protocols for managing DKA. Most protocols are time honored and are intuitively based on well-defined pathophysiologic considerations. They share the aims of carefully restoring metabolic homeostasis through rehydration, replacing electrolyte and mineral deficits, insulin replacement to reverse ketogenesis, and diligent clinical monitoring.4
Since the most serious complication of DKA—cerebral edema—is uncommon, studies describing risk factors have been retrospective multicenter case series6 and case reports.7,8
Patients in moderate or severe DKA should be assumed to be 7% to 10% dehydrated, and although rehydration should proceed at a carefully calibrated, gradual pace, there should be no delay in administering IV fluid therapy.
The risk for cerebral edema increases with overly aggressive fluid supplementation (ie, volume and rate of administration). If the blood pressure is normal and peripheral perfusion is adequate, conservative rehydration is preferred.
DKA-related cerebral edema is a clinical diagnosis, and therapy to reduce intracranial pressure should commence prior to confirmatory imaging.
Total body stores of potassium are depleted with DKA. Hypokalemia should be anticipated with initiation of insulin replacement and correction of acidosis; therefore, potassium should be added to the IV fluids after the initial hour of rehydration.
A bolus of regular insulin during the first hour of therapy has been associated with increased risk for developing cerebral edema. Insulin should never be bolused and should not be administered prior to the second hour after NS rehydration. Hydration alone will cause the plasma glucose concentration to decrease rapidly.
The ECG is a reflection of the intracellular potassium level (which is distinct from the extracellular serum concentration [measured]) and can show signs of intracellular potassium deficiency when the measured serum potassium concentration is normal.
The insulin infusion should never be decreased for falling glucose levels; rather, the amount of glucose infused should be increased by providing 10% dextrose solution so as to continue inhibition of ketogenesis and prevent hypoglycemia.
The insulin infusion should never be discontinued; the half-life of insulin in the serum is only 6 minutes.
DKA is present only if there is metabolic acidosis.
DKA is not uncommon with type 2 diabetes; up to 25% of patients with new-onset type 2 diabetes can present in DKA.
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.
To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study will be included in bold type following the references, where available. The most informative references cited in this paper, as determined by the author, will be noted by an asterisk (*) next to the number of the reference.
March 1, 2013