Pediatric Diabetic Ketoacidosis Management in the Era of Standardization

Ildiko H Koves; Catherine Pihoker

Expert Rev Endocrinol Metab. 2012;7(4):433-443.

Abstract and Introduction

Abstract

Up to 70% of children with new-onset Type 1 diabetes mellitus (T1DM) present with diabetic ketoacidosis (DKA), with most cases initially assessed by their primary care provider. DKA is the most common cause of death in children with T1DM, mainly related to cerebral edema that occurs at a frequency of 0.15–4.6%. Early recognition of DKA can be improved by increasing the awareness of early clinical symptoms such as enuresis, polyuria and polydipsia. Clinical acumen paired with early assessment of patients with suspected T1DM and known T1DM, particularly if risk factors for DKA are present, can prevent serious complications and fatal outcomes. Urgent referral to specialist centers for suspected new-onset T1DM/DKA is required. A standardized approach is recommended to be followed to ensure successful initial management of DKA, both in the nonspecialist setting before transfer and in the more specialized hospital setting. This article outlines such a management approach.

Inroduction

Type 1 diabetes mellitus (T1DM) is one of the most common chronic conditions in children. The overall worldwide incidence in children younger than 15 years of age is estimated to be approximately 65,000, with a global annual increase of 3%.^[1,2] Depending on the geographical location, 10–70% of these children present with diabetic ketoacidosis (DKA), a life-threatening complication of T1DM.

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Next Section

Abstract and Introduction
Definition
Pathophysiology
Differential Diagnosis
Epidemiology
Morbidity & Mortality Associated With DKA
Clinical Manifestations & Presentation
Risk & Protective Factors
Management
Fluid Therapy
Electrolytes
Insulin
The Two-bag System
Clinical & Biochemical Monitoring
Complications
Prevention
Costs
Expert Commentary & Five-year View
References
Sidebar

Table 1. Other complications of diabetic ketoacidosis.
Complication	Association	Treatment
Hypokalemia	Inadequate potassium replacement and ongoing potassium losses	Increase potassium replacement; may require concentrated potassium infusion at 0.1–0.3 mEq/kg/h
Hyperkalemia	Generally secondary to intracellular to extracellular shift; infrequently renal failure	Reduce/eliminate potassium in intravenous fluids; continuous renal replacement therapy as necessary
Hypophosphatemia	Renal losses	Will normalize with re-establishment of nutritional support Severe hypophosphatemia should be treated
Hypoglycemia	Failure to add glucose to intravenous fluids when serum glucose declines below 300 mg/dl	Addition of 5–12.5% dextrose to intravenous fluids when serum glucose declines below 300 mg/dl
Disseminated intravascular coagulation	Infection, tissue necrosis	Monitor for infection and thrombosis
Central venous thrombosis or stroke^54,65	Prolonged dehydration; DKA represents a hypercoagulable state	Avoid central venous catheterization, if occurs with CVC anticoagulate⁶⁶
Dural sinus, basilar artery thrombosis or stroke^67,68	Prolonged dehydration; DKA represents a hypercoagulable state⁶⁹	If underlying coagulopathy suspected, anticoagulate^70,71
Sepsis	Impaired immunity associated with poorly controlled diabetes mellitus Antecedent for DKA	Antimicrobials
Mucormycosis⁷²	Infection specifically associated with DKA, especially rhinocerebral or pulmonary infections	Infectious disease, otolaryngology consultations Caspofungin, liposomal amphotericin B⁷³
Rhabdomyolysis⁷⁴	Hypophosphatemia, anemia, thrombocytopenia High osmolality on admission, more frequent in the hyperglycemic hyperosmolar state	Preserve good renal blood flow
Pancreatitis^75,76	Associated with abdominal pain, but not always; often associated with elevated BUN	Chemical pancreatitis is common in DKA, but clinical pancreatitis is rare Check amylase, lipase, lipids and calcium levels
Hyperglycemic Hyperosmolar syndrome	Higher risk of thrombosis, rhabdomyolysis, malignant hyperthermia and cerebral edema	Generally requires more careful and individualized fluid therapy, careful sodium, potassium and GCS monitoring Insulin at 0.05–0.1 units/kg/h
Hyperchloremic metabolic acidosis	Large volume resuscitation with normal saline	Use potassium as potassium acetate and potassium phosphate to replace potassium

Box 1. Summary of clinical features at presentation for diabetic ketoacidosis.
Historical features
Polyuria Polydipsia New-onset enuresis Nocturia Weight loss Abdominal pain Fatigue Nausea/vomiting Headache Confusion Candida infection
Clinical signs
Dehydration Kussmaul breathing Ketotic breath Lethargy Vomiting Abdominal tenderness Mental status changes Diaper rash

Box 2. Initial work-up for diabetic ketoacidosis.
Vital signs: blood pressure, heart rate, respiratory rate and temperature Weight GCS score Serum glucose and HbA_1C Blood gas Electrolytes: Na, K, chloride, Ca, Mg and Phos Calculate Na_corrected Osmolality Renal function: BUN, creatinine BOHB or urine ketones If fever history: blood culture, urine analysis (if indicated urine culture) ECG Calculate Na _corrected= measured Na + [(serum glucose as mg/dl−100)/100] × 1.6

BOHB: β-hydroxybutyrate; BUN: Blood urea nitrogen; GCS: Glasgow Coma Scale; HbA_1C: Glycosylated hemoglobin, type A1C.

Box 3. ECG changes during diabetic ketoacidosis.
Hyperkalemia
Prolonged PR interval Shortening of QT Tall, peaked, symmetrical T waves – 'tenting' Evolving sine-wave rhythm
Hypokalemia
Presence of U waves Widening of QT interval Flattened T waves ST segment depression
Hypocalcemia Prolonged QT interval
Other
Prolonged QTc

QTc: Corrected QT.

Box 4. Clinical diagnosis of cerebral edema.
Diagnostic criteria
Abnormal motor or verbal response to pain Decorticate or decerebrate posture Cranial nerve palsy (III, IV and VI) – double vision Abnormal neurogenic respiration
Major criteria
Altered mentation Fluctuating consciousness Sustained HR deceleration Age-inappropriate incontinence
Minor criteria Vomiting Headache Lethargy, not easily roused Diastolic BP >90 mmHg Age <5 years

BP: Blood pressure; HR: Heart rate.
Adapted with permission from [52].

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