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17451

Use of 3% Hypertonic Saline In Pediatric Patients In Diabetic Ketoacidosis with Clinically Evident Cerebral Edema

Friday, October 19, 2012
Room 272-273 (Morial Convention Center)
Sarah M. Szlam1, Michele Walsh1, Andrew Pfeffer2 and Thomas J. Abramo1, (1)Department of Pediatric Emergency Medicine, Monroe Carell Jr. Children's Hospital at Vanderbilt, Nashville, TN, (2)Department of Emergency Medicine, Vanderbilt Medical Center, Nashville, TN

Purpose:

Descriptive retrospective analysis of 3% hypertonic saline (3%HTS) utilization in diabetic ketoacidosis (DKA) patients with clinical evidence of cerebral edema in a PED.

In patients with DKA, cerebral edema is a significant cause of morbidity and mortality. While some patients present with obvious clinical signs, increased recognition of subclinical cerebral edema is prompting more aggressive interventions in pediatric emergency departments (PED). Once suspected, hyperosmolar therapy (mannitol or 3%HTS) is recommended. Currently, the standard therapy is mannitol, which carries significant risks including rebound effects, serum electrolyte imbalance and hypovolemia. While both mannitol and 3%HTS have been shown to be efficacious in reducing intracranial pressure (ICP), limited class I evidence supports mannitol over 3%HTS. In infectious, anoxic, hemorrhagic and metabolic causes of cerebral edema, 3%HTS was more effective and safer than mannitol. Several significant advantages of 3%HTS exist including intravascular volume preservation, especially important in DKA where patients are severely dehydrated. While utilization of 3%HTS in DKA patients with cerebral edema has become more common in intensive care units, studies describing its use in the PED are limited.

Methods:

From 1/2009-2/2012, PED electronic medical records and pharmacy database were queried for DKA patients who received 3% HTS for clinically evident cerebral edema.  Indicators of cerebral edema were based on provider documentation of degree of altered mental status (AMS) and/or headache indicating increased ICP. The patient's initial venous blood gas (VBG), electrolytes, glascow coma scale (GCS), and descriptive mental status were reviewed and compared to the same parameters following 3%HTS administration. All patients were treated with standard DKA management. Study patients received bolus 3%HTS in the PED through a peripheral IV at a dose of 3-5mL/kg. Patient EMRs were reviewed for complications of 3%HTS administration. 

Results:

Thirty patients were identified ages 3-18 years (avg. 11.3, SDą4); 56% female. Twenty patients presented with new onset DKA. Two patients received 3%HTS on two separate DKA visits (total of 32 delivered 3%HTS boluses). Average time to initial 3%HTS bolus was 80 min (range 1-255min). All patients had improved clinical states and GCS after administration of 3%HTS. No negative outcomes, IV infiltrate, significant rises in sodium, or death were observed.

Conclusion:

This small sample size precludes definitive conclusions. In this group 3%HTS improved clinical evidence of cerebral edema as well as commonly trended lab values in DKA. This study demonstrated no expected potential significant outcomes. 3%HTS was found to be efficacious in improving short-term outcomes without significant side effects in this population. A larger diverse validation study utilizing 3%HTS in DKA cerebral edema is warranted.