Page 37 - Delaware Medical Journal - July-August 2018
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CASE REPORT
Discussion
This case demonstrates the importance of prompt recognition
of euglycemic ketoacidosis, a life-threatening condition. Based
on FDA Adverse Event Reporting System (FAERS) data, which risk of ketoacidosis in type 2 diabetics taking SGLT-2 inhibitors, as compared to Dipeptidyl Peptidase-IV inhibitors.1 There is suspicion that rates in clinical practice may be higher.
Diabetic ketoacidosis may be seen in the setting of blood glucose levels lower than 250 mg/dL, leading to the term “euglycemic DKA.” Predisposing factors to ketoacidosis include insulin dose reduction, acute febrile illness, reduced caloric intake, and alcohol abuse.2 Since SGLT-2 inhibitors reduce excretion of ketone bodies in the urine and enhance fat oxidation, they may cause increased levels of circulating ketone bodies, which, coupled with increased urinary glucose excretion, may lead to euglycemic diabetic ketoacidosis.2,3
It is critical for clinicians to recognize the rare but potentially fatal association between SGLT-2 inhibitors and euglycemic diabetic ketoacidosis.
REFERENCES
1. Blau, J.E., Tella, S.H., Taylor, S.I., and Rother, K.I. Ketoacidosis Associated With SGLT2 Inhibitor Treatment: Analysis of FAERS data. Diabetes Metabolism Research and Reviews 33.8 (2017).
2. JARDIANCE [package insert]. Boehringer Ingelheim Pharmaceuticals, Inc. Ridgefield, CT. July 2016.
3. Pfutzner, A., Klonoff, D., Heinemann, L., Ejskjaer, N., and Pickup, J. Euglycemic ketosis in Patients with Type 2 Diabetes on SGLT2-Inhibitor Therapy — an Emerging Problem and Solutions Offered by Diabetes Technology. Endocrine 56.1 (2017): 212-216.
STUDENT POSTER HONORABLE MENTION
SILENT, But Not Deadly
By Pilin Dhoieam, MS4; Steven Cetel, DO and David Manoff, MD
Introduction
SILENT — Syndrome of Irreversible Lithium Effectuated Neurotoxicity — is a long-term neurological sequelae of acute on chronic, or chronic lithium toxicity. It is important to recognize the development of this syndrome, as it can persist despite treatment.
Case Presentation
A 51-year-old female with longstanding history of bipolar disorder on lithium for 15 years, depression, and hypertension presented to the Christiana Care emergency department with hypoxemic, hypercapnic
the emergency department one week prior to this presentation for
a right-axilla abscess incision and drainage where she was put on a course of trimethoprim-sulfamethoxazole and ibuprofen 800mg. Her
family reports that in the past year, she has had a gradual change in mental status with tremors, ataxia, and a decrease in vision. In the past 24 hours, she developed an acute mental status change where
physical exam, she was lethargic and altered. Tremors were noted in Vital signs revealed she was afebrile and hemodynamically stable. few hours of presentation. Laboratory results showed a BUN 55 mg/ dL and creatinine 3.24mg/dL, where her baseline creatinine is 1.16mg/ dL, and a lithium level of 2.6. Given her elevated lithium level, acute renal injury, and encephalopathy, acute on chronic lithium toxicity most likely precipitated by recent trimethoprim-sulfamethoxazole
and NSAID use was diagnosed and she was admitted to the ICU. Her course was complicated by diabetes insipidus, which led to volume initiated for acute toxicity, as this was the treatment of choice in this case. A diagnosis of SILENT was not made in our patient, due to acute encephalopathy and sedation status post dialysis. However, this was highly suspected due to her history and risk factors. Our patient was complaining of neurological symptoms and the adverse impact it had on her daily life for a year’s duration, which eventually led to this severe neurotoxicity.
Discussion
This case illustrates the importance of detecting neurological symptoms because unfortunately, SILENT can persist despite adequate removal of lithium with hemodialysis. It is a clinical diagnosis that consists of extrapyramidal symptoms, brainstem
and cerebellar dysfunction, and dementia. The risk factors for development include being older than 50 years of age, chronic lithium therapy, impaired renal function, and the development of diabetes insipidus; all of which our patient had.1, 2 With earlier detection
of neurological symptoms, severe persistent neurotoxicity can be prevented.
REFERENCES
1. The Syndrome of Irreversible Lithium-Effectuated Neurotoxicity (SILENT). Pharmacopsychiatry, vol. 22, no. 02, 1989, pp. 81–83., doi:10.1055/s-2007-1014583
2. Lithium/Hydrochlorothiazide. Reactions Weekly, vol. 1556, no. 1, 2015, pp. 178–178., doi:10.1007/s40278-015-2652-9.
RESIDENT AWARDS
RESIDENT ABSTRACT WINNER
Swig and a Miss? Acute intoxication and Diagnosis of Neurosyphilis — Many Forgotten Facts
By Sanjana Bhatia-Patel, DO; David M. Cohen, MD; Kevin K. Patel, MD and Jennifer Goldstein, MD
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