Case Presentation: A 76-year-old male with past medical history of prostate cancer, hypertension, diabetes, chronic kidney disease, and COPD presented after an episode of dizziness leading to a near fall. The day prior to admission, he had multiple episodes of vomiting and poor oral intake. He also noted intermittent “shaking movements” involving his arms and torso that began earlier that day. On arrival, the patient was afebrile, blood pressure was 111/61 pulse was 64, and patient was saturating 98% on room air. Upon evaluation, the patient was noted to have significant asterixis at rest. Labs were relevant for a BUN of 33, Creatinine to 2.2 (baseline 1.4). Serum bicarb was 25. A workup for asterixis was initiated. Ammonia level was normal at 38 µmol/L. A venous blood gas (VBG) showed a pH of 7.25 and pCO₂ of 60 mmHg, compared to a prior VBG (one year earlier) with a pH of 7.42 and pCO₂ of 39 mmHg. There were no clinical or laboratory signs of cirrhosis or liver dysfunction. Despite the VBG showing CO₂ retention, the patient had no history of obesity, a clear lung exam, and a normal serum bicarbonate level-which argued against a chronic cause of hypercapnia. Upon further history, the patient reported taking 1800 mg of gabapentin the day prior to help with his chronic back pain. The asterixis was suspected to be secondary to gabapentin toxicity in the setting of acute kidney injury (AKI). Gabapentin was discontinued, with spontaneous resolution of asterixis over the subsequent days.
Discussion: We surmise that in our patient, several episodes of vomiting led to AKI, which in turn reduced clearance of gabapentin, resulting in its accumulation and subsequent neurotoxicity manifesting as asterixis. The temporal association with high-dose gabapentin use, lack of alternative explanations such as hepatic encephalopathy, and spontaneous resolution after drug cessation all support this mechanism. Gabapentin is a commonly prescribed medication for various types of neuropathic pain. Gabapentin toxicity is a well-established phenomenon with high-risk populations including the elderly, those with underlying kidney disease1, and those with COPD (2). Gabapentin can lead to respiratory depression and even COPD exacerbations, particularly with concurrent use of other sedating medications (3). Gabapentin toxicity can manifest with symptoms such as dizziness, ataxia, somnolence, or asterixis (4). Asterixis is a known toxic side effect of gabapentin through modulation of GABAergic pathways and possible CO₂ retention, ultimately disrupting motor control and causing negative myoclonus
Conclusions: Although gabapentin is frequently prescribed, physicians should exercise caution when using it in elderly patients, those with COPD, and those with chronic kidney disease. These populations are particularly vulnerable to gabapentin accumulation and toxicity. Patients should be counseled to temporarily hold the medication in the setting of profound vomiting, poor oral intake, or other situations that may precipitate AKI.