Pediatric Diabetic Ketoacidosis Management in the Era of Standardization

Ildiko H Koves; Catherine Pihoker

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

Complications

Cerebral edema

Cerebral edema generally develops in the first 4–12 h of therapy; however, it can occur prior to therapy initiation and 24 h or more into therapy.^[35,55–58] It is a clinical bedside diagnosis based on diagnostic, major and minor criteria (Box 4).^[3,52] One diagnostic, two major or one or more minor criteria have a sensitivity of 92% and false-positive rate of only 4%.

For high-risk CE patients, mannitol or hypertonic saline needs to be at hand, at the bedside and ready to be used, with a precalculated dose (0.5–1 g/kg mannitol, 5–10 ml/kg 3% 'hypertonic' saline) for the setting of neurological deterioration in overt CE. Doses are administered over more than 30 min may be repeated if there is no response. The intravenous fluid rate must be reduced by 30%.

Other Complications

There are many other potential complications of DKA and its management, as summarized in Table 1. These include electrolyte disturbances, vascular insults, infection, pancreatitis and rhabdomyolysis.

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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

Complications

Cerebral edema

Other Complications

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