Catherine Ngo

Effects of Hyperglycemia and Effects of Ketosis on Cerebral Perfusion, Cerebral Water Distribution, and Cerebral Metabolism

Diabetic ketoacidosis (DKA) may cause brain injuries in children. The mechanisms responsible are difficult to elucidate because DKA involves multiple metabolic derangements. We aimed to determine the independent effects of hyperglycemia and ketosis on cerebral metabolism, blood flow, and water distribution. We used magnetic resonance spectroscopy to measure ratios of cerebral metabolites (ATP to inorganic phosphate [Pi], phosphocreatine [PCr] to Pi, N-acetyl aspartate [NAA] to creatine [Cr], and lactate to Cr) and diffusion-weighted imaging and perfusion-weighted imaging to assess cerebral water distribution (apparent diffusion coefficient [ADC] values) and cerebral blood flow (CBF) in three groups of juvenile rats (hyperglycemic, ketotic, and normal control). ATP-to-Pi ratio was reduced in both hyperglycemic and ketotic rats in comparison with controls. PCr-to-Pi ratio was reduced in the ketotic group, and there was a trend toward reduction in the hyperglycemic group. No significant differences were observed in NAA-to-Cr or lactate-to-Cr ratio. Cortical ADC was reduced in both groups (indicating brain cell swelling). Cortical CBF was also reduced in both groups. We conclude that both hyperglycemia and ketosis independently cause reductions in cerebral high-energy phosphates, CBF, and cortical ADC values. These effects may play a role in the pathophysiology of DKA-related brain injury.

The management of an unusual case of pan-enteritis developing after colectomy for refractory Ulcerative ColitisP-131.

ease maintained on immunosuppressants who developed severe varicella blepharitis. CASE DESCRIPTION: A 22-year old female with ileal Crohn’s disease and a few episodes of VZV blepharitis during childhood was admitted for a severe zoster outbreak while on prednisone (60mg PO daily) for IBD. She was diagnosed with Crohn’s disease two years prior, started on prednisone and Entocort. Six months prior to admission, she self-discontinued Entocort due to improved symptoms. Two weeks prior to VZV outbreak, she was admitted for Crohn’s flare with bloody diarrhea and pain. She was found to have pancolitis on colonoscopy, with biopsies significant for chronic, active disease. After a course of IV Solumedrol, she improved and was discharged on oral prednisone. One week after admission, she returned with a new outbreak of varicella, presenting with pain and vesicles over the right distribution of cranial nerve five. Physical exam showed a cluster of vesicles on the right upper eyelid with associated inflammation and erythema. Ophthalmology was consulted and suggested treatment with Acyclovir 400mg PO five times daily for ten days followed by Acyclovir 800mg PO twice daily for prophylaxis while on immunosuppressive therapy. Her outbreak cleared after approximately six days of treatment with oral acyclovir. She was later transitioned from prednisone to an anti-TNF agent while continuing oral acyclovir for prophylaxis. DISCUSSION: This case highlights the issue of reactivated VZV in an IBD patient on immunosuppressants. While some studies demonstrate improved treatment for VZV outbreak with prednisone, others have found that steroids have no impact on disease in the healthy population. The IBD patient population has increased risk of infection, and has been found to have not only increased incidence of VZV infection but also disease severity while on immunosuppressants such as steroids. There are no clear guidelines for treatment in this case; this patient improved with the high dose antiviral therapy while continuing immunosuppressants. There are also no guidelines for VZV vaccination in this patient population. While the Zostavax has been well studied to reduce the general population’s risk of developing active VZV infection, and is much used in some immunosuppressed populations, there are no studies evaluating the vaccine in IBD patients. Previous vaccination may have prevented a severe outbreak in this patient. Further study is warranted in this high risk population.