Cefepime-Induced Seizures: The Overlooked Outpatient Adverse Reaction.

Cefepime is a 4th generation cephalosporin often used for its ability to cover gram-positives, gram negatives, anaerobic bacteria, and, most importantly, pseudomonas. Prior to initiation of cefepime, the medication is dosed based on the renal function to avoid a multitude of its toxicity profiles, including encephalopathy, aphasia, myoclonus, seizures, and nonconvulsive status epilepticus. These risks are increased in the presence of renal impairment. We present a case of a 65-year-old woman who had presented to the emergency department (ED) two weeks after initiation of outpatient IV cefepime therapy with concerns of altered mentation and decreased oral intake. In the ED, the patient was noted to have a creatinine: 5.77 (baseline of 0.76) and urea: 94. During evaluation by the ED provider, the patient was noted to have transient slurring of speech, speech arrest, and tonic-clonic movements on the right. CT of the head, followed by CT angiography of the head and neck, demonstrated no acute intracranial pathology. Spot EEG revealed generalized slowing with unclear left-sided epileptiform discharges. There was a concern for complex partial seizures. Neurology and nephrology were consulted. The patient was given 1 g of levetiracetam, and emergent dialysis was performed. After dialysis, no other epileptiform activity was noted with the improvement of her encephalopathy. The patient returned to her baseline mentation. Here we emphasize the importance of recognizing cefepime's toxicity profile while triaging patients. In the rare event of toxicity, immediate treatment is discontinuing the offending agent and initiation of emergent hemodialysis.

Anomalous origin of the left coronary artery from pulmonary artery misdiagnosed as postpartum cardiomyopathy.

A 30-year-old woman with a history of presumed postpartum cardiomyopathy presented to her primary care physician's office with crescendo angina and shortness of breath. She was found to be in supraventricular tachycardia, managed with the Valsalva maneuver, and was discharged home without any further workup. She again presented with exertional symptoms. Her electrocardiogram revealed abnormal T waves and her stress test was strongly positive. Cardiac catheterization revealed an absent left coronary ostium and a dilated right coronary artery, with large collaterals supplying the left coronary system; coronary computerized tomography revealed the anomalous origin of the left main coronary artery arising from the posterolateral aspect of the pulmonary artery, highly suggestive of the anomalous origin of the left coronary artery from pulmonary artery (ALCAPA) anomaly (Bland-White-Garland anomaly).

Trauma Induced Calcium Pyrophosphate Deposition Disease of the Lumbar Spine.

Inflammatory arthritis, such as pseudogout or otherwise referred to as calcium pyrophosphate (CPP) crystal arthritis or calcium pyrophosphate deposition (CPPD) disease, is characterized by the deposition of crystal formation and deposition in large joints. CPPD is known to affect the elderly population and commonly manifests as inflammation of knees, hips, and shoulders. CPPD disease involving the spine has been infrequently encountered in practice and rarely described in the literature. Here, we describe a case of an 80-year-old female with no known history of inflammatory arthritis who presented with left lower extremity weakness and fall, initially thought to have discitis, later confirming CPPD of the spine through biopsy and ultimately resolution of symptoms with anti-inflammatory agents. Although consisting of different clinical presentations, two other case reports have described CPPD of the spine with similar radiographic findings, to this author's knowledge. With the radiologic similarities, this unique case serves to raise awareness in the medical community and possibly place pseudogout of the spine on the differential list when such cases are encountered. As a result, patients can be initiated on benign anti-inflammatory agents, avoiding invasive testing and unnecessary antibiotic exposure.

Varicella zoster presenting as cranial polyneuropathy.

Cranial polyneuropathy is commonly caused by Lyme disease. We discuss the case of a man who presented with cranial nerve deficits causing dysphagia, dysphonia and facial weakness. This diagnostic dilemma stemmed from a workup that ruled out Lyme and vascular causes leading to an expanded search for infectious explanations, which revealed varicella zoster in the cerebrospinal fluid. On review, this phenomenon is rarely reported, but has been observed with a number of herpes family viruses. In emergency department settings, clinical suspicion should be raised for VZV infection even in the absence of rash in patients that present with multiple cranial nerve palsies.