Pediatric Diabetic Ketoacidosis Management in the Era of Standardization

Ildiko H Koves; Catherine Pihoker

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

Insulin

During DKA

As DKA is a result of an absolute or relative insulin-deficient state, the cornerstone of DKA therapy is insulin. Insulin is essential to normalize blood glucose levels and to suppress further lipolysis and ketogenesis. The delivery of insulin should be in the form of a continuous infusion using regular- or short-acting insulin at 0.05–0.1 units/kg/h. Recent pediatric studies found comparable effectiveness and safety^[48] and a more gradual reduction in the effective plasma osmolality over the first 12 h^[49] with 0.05 units/kg/h insulin infusion rate. Younger and newly diagnosed patients are likely to be more insulin sensitive, requiring lower dosing. As with initial fluid resuscitation, the blood glucose levels generally drop quite rapidly; it is recommended to commence the insulin infusion at 1–2 h following fluid resuscitation. Insulin boluses are not recommended to be used at the start of therapy, as they may increase the risk of CE.^[33,34]

It is not recommended to stop an already initiated insulin infusion, but rather to introduce dextrose infusion with a 'two-bag system' if the blood glucose fall is more than 100 mg/dl/h (5.6 mmol/l/h) or the blood glucose level is less than 300 mg/dl (<17 mmol/l). Details of the two-bag system are given in the following section. In severe hypokalemia not responding to maximal doses of potassium supplementation, a decrease in insulin infusion may be considered.

After Resolution of DKA

Transition to subcutaneous insulin is recommended when ketoacidosis resolves, and generally coincides with the introduction of oral fluids and tolerating an oral diet. Therefore, it is ideal to transition patients around mealtimes. In certain circumstances, transition to only basal insulin is recommended when resolution of acidosis occurs at night, when the patient is likely to remain asleep and not eat. To prevent rebound hyperglycemia, the first subcutaneous insulin injection should be given at least 30 min before stopping the insulin infusion. The dose and type of subcutaneous insulin used is dependent on local preferences and the insulin types available. The authors recommend a basal–bolus insulin regimen with glargine or detemir as basal insulin and aspart or lispro as short-acting insulin.

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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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Pediatric Diabetic Ketoacidosis Management in the Era of Standardization

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During DKA

After Resolution of DKA

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