(From the May 2015 Issue of PediatricsOnline)
Cerebral edema is a rare but deadly complication of diabetic ketoacidosis (DKA), which is the leading cause of hospitalization, morbidity and mortality for children with diabetes mellitus. Early identification of risk factors and implementation of cerebral-protective measures may be the key to successful outcomes.
A case study in Air Medical Journal by Samantha Gee, MD, an attending physician in Critical Care at Nationwide Children’s Hospital, describes how a 4-year-old boy with type 1 diabetes was successfully treated for DKA and cerebral edema. The child was brought to a community hospital’s emergency department with a one- to two-day history of nausea and vomiting, as well as difficulty breathing and decreased responsiveness. His initial blood work revealed the presence of severe DKA. He was emergently transported via helicopter to Nationwide Children’s, where a brain CT scan confirmed the presence of global cerebral edema.
A child with DKA is at risk for developing cerebral edema with subsequent brain herniation, even if it is the first presentation of DKA in that child. Although the occurrence of cerebral edema is rare — approximately 0.5 to 1 percent of all pediatric DKA cases — an estimated 40 to 90 percent mortality results from DKA-related cerebral edema.
The risk factors for DKA-related cerebral edema include first presentation of DKA, younger age, aggressive fluid resuscitation , administration of sodium bicarbonate or bolus insulin doses with resultant precipitous drops in blood glucose. In this case, no bolus doses of insulin or bicarbonate were given before transport.
Although the complications of cerebral edema are well known, the presence of cerebral edema may be underappreciated in the transport setting, Dr. Gee suggests.
“DKA-related cerebral edema may present clinically as agitation, confusion, combativeness or decreased mentation,” Dr. Gee says. “A patient’s unwillingness to cooperate in the transport setting may, in fact, be an early sign of a change in mental status related to cerebral edema and dehydration.”
Relying on the Cushing triad — hypertension, bradycardia and abnormal breathing — as a signal of increased intracranial pressure is a late finding and signals impending brain herniation, according to Dr. Gee.
“For safe transportation, one must maintain a high index of suspicion and incorporate cerebral-protective measures,” Dr. Gee says. “Simple measures that may be done at the bedside include elevation of the head-of-bed by 30 degrees and maintaining the patient’s head in midline position.”
Fluid management is also critical in cases of suspected cerebral edema, she says. The prevailing theory about the pathophysiology of cerebral edemas is that the brain works to protect itself in response to extreme dehydration by creating intracellular “idiogenic osmoles.” These osmoles contain solutes that enable a favorable osmotic gradient to be created, drawing water from the plasma into the cells. Aggressive fluid resuscitation and/or the administration of hypotonic fluids may put a patient at risk for cerebral swelling due to this osmotic gradient and resultant fluid shifts.
In the recently published case review, the child was admitted to the Nationwide Children’s PICU, and hyperosmolar fluid therapy was initiated to aggressively treat the threat of worsening cerebral edema. His mentation was notably improved 24-hours after PICU admission, and he was back to his baseline mental status by the time he transferred to the regular pediatric floor. He had no appreciated neurologic deficits upon discharge home.
“The patient in this case was maintained on hypotonic intravenous fluids — 1/2 normal saline — which may have contributed to this patient’s clinical course,” Dr. Gee says. “Investigation regarding best practices in fluid management in DKA is currently being studied by the multi-centered PECARN (Pediatric Emergency Care Applied Research Network) with the FLUID study (FLuid therapies Under Investigation in DKA). Until we learn more from this study and others, it remains generally advisable to provide patients isotonic fluids for rehydration.”
Medical management can be lifesaving when initiated at time of presentation and during transport, Dr. Gee says. Although a universal, standardized practice does not currently exist, following the basic ABCs of care and practicing cerebral-protective measures is beneficial for all DKA patients.
Dr. Gee advises practicing cerebral-protective measures for all patients suspected of having cerebral edema: maintaining head-of-bed at 30 degrees with head in midline position, avoidance of hypotonic fluids, avoidance of sodium bicarbonate administration, and avoidance of insulin bolus doses that result in precipitous decreases in serum glucose levels.
“Radiographic confirmation of cerebral edema is not necessary to obtain before starting the acute care management of DKA-related cerebral edema if the clinical suspicion is high and there is a worrisome neurologic exam at presentation,” Dr. Gee says.
Gee SW. The lethargic diabetic: Cerebral edema in pediatric patients in diabetic ketoacidosis. Air Medical Journal. 2015 Mar-Apr, 34(2):109-112.