Abstract: PUB010
A Triple Threat? Baclofen Toxicity and Posterior Reversible Encephalopathy Syndrome in the Setting of AKI
Session Information
Category: Trainee Case Report
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Lipnick, Daniella E., Penn State College of Medicine, State College, Pennsylvania, United States
- Roe, Kevin C., Mount Nittany Medical Center, State College, Pennsylvania, United States
Introduction
This is a case of apparent baclofen toxicity and posterior reversible encephalopathy syndrome (PRES). Both conditions are seen in patients with kidney dysfunction but direct association between the two conditions has otherwise been defined. The case highlights areas of special consideration in the evaluation and management of mental status changes in patients with acute kidney injury (AKI). No other reported cases of the combined diagnoses were found on literature review.
Case Description
A 71-year-old female admitted with sepsis due to ESBL E. coli bacteremia and pyelonephritis became unresponsive on her 7th day of hospitalization. There were no abnormal neurologic findings prior to the episode. The patient had been given baclofen 10 mg x 2 doses for back pain within 24 hours of her acute change in mental status. She was non-verbal but opening eyes and withdrawing to pain. The initial presenting signs of infection had been improving with ceftolozane and tazobactam. Serum creatinine was 4.2 mg/dL on admission and had improved to 2.2 mg/dL (baseline 1.5 mg/dL). AKI was attributed to prerenal physiology and sepsis-associated ATN. Mental status changes were attributed to baclofen neurotoxicity. She then developed evidence of partial complex seizures and subsequent imaging revealed findings of PRES. Levetiracetam, antihypertensives, and continued antibiotic therapy were provided. Systolic blood pressure increased to 180 mmHg with a MAP of 115 during the hospitalization. After several days, the patient recovered completely. Creatinine stabilized at 2.0 mg/dL.
Discussion
Medications are a leading cause of acute mental status changes, especially in patients with impaired kidney function. Our case highlights the risks of baclofen toxicity in improving but impaired kidney function. The clinical-radiopathologic diagnosis of PRES may have been missed without imaging. The varying presentations of this condition are a reminder the importance of an expanded differential diagnosis and the need for a better understanding of the pathology. There is no reported association between PRES and baclofen. The role of AKI in the development of PRES is not entirely understood; however, the hypertension-hyperperfusion theory remains a leading consideration in our patient. Management decisions in our patient included forgoing dialysis, blood pressure control, and the use of anti-seizure medications.