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A Case of Diabetic Ketoacidosis Precipitating Cerebral Edema and Herniation Requiring Hemicraniotomy FREE TO VIEW

Clinton Colaco, MD; Brendon Colaco, MD; Mohan Rudrappa, MD; Penchala Mittadodla, MD; Rajani Jagana, MD; Nikhil K. Meena, MD
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University of Arkansas for Medical Sciences and the John McClellan Veterans Affairs Medical Center, Little Rock, AR

Chest. 2014;146(4_MeetingAbstracts):250A. doi:10.1378/chest.1992532
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SESSION TITLE: Critical Care Case Report Posters I

SESSION TYPE: Affiliate Case Report Poster

PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM

INTRODUCTION: Dibetic Ketoaciosis (DKA) and hyperglycemia worsen cerebral edema and neurological function. On the other hand, cerebral edema can also precipitate DKA. We present an unusual case of a young man who was found to have a sellar tumor and went into DKA, which worsened his neurological condition causing cerebral herniation. Further, cerebral edema made the management of DKA more challenging.

CASE PRESENTATION: A 32 year old male with developmental delay and Type 1 diabetes was found to have a sellar lesion on Computerized tomography scan of the brain during evaluation for intractable headache. On admission, patient went into DKA. His DKA was difficult to manage and he required up to 50 units of insulin (greater than 1U/kg) per hour. Consequently, patient developed cerebral edema and raised intra-cranial pressure (ICP). Neurosugery placed an external ventricular drain (EVD) which led to minimal improvement in the ICP and ketoacidosis. Worsening ketoacidosis and cerebral edema led to progressive neurological decline with the manifestation of Cushing’s triad indicating impending herniation. Patient was intubated for airway protection and taken to the operating room for a hemi-craniotomy. Following the decompressive surgery, patient’s DKA resolved rapidly.

DISCUSSION: Hyperglycemia is associated with, and can worsen cerebral edema. Our patient with DKA required upto 50 units of insulin an hour to manage his hyperglycemia. In fact, he received 1200 units of insulin that day. While cerebral edema was caused by hyperglycemia, resultant raised ICP was an added insult which exacerbated his DKA. After hemi craniotomy, the DKA resolved rapidly and patient’s sugars were then well controlled with a combination of long acting and subcutaneous insulin amounting to a total of 65 units a day.

CONCLUSIONS: Relief of cerebral edema by hemicraniotomy was essential for the resolution of a very difficult to treat case of DKA. Typically, rapid correction of DKA is considered to contribute to the development of cerebral edema. Our case demonstrates that ketoacidosis and malignant cerebral edema may interact leading to a vicious cycle, which can be broken if both these conditions are aggressively treated.

Reference #1: Glaser N et al. (2014). Brain cell swelling during hypocapnia increases with hyperglycemia or ketosis. Pediatric diabetes. doi: 10.1111/pedi.12114

Reference #2: Glaser N et al. (2012). Effects of hyperglycemia and effects of ketosis on cerebral perfusion, cerebral water distribution, and cerebral metabolism. Diabetes, 61(7), 1831-1837

DISCLOSURE: The following authors have nothing to disclose: Clinton Colaco, Brendon Colaco, Mohan Rudrappa, Penchala Mittadodla, Rajani Jagana, Nikhil K. Meena

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