Opioid addiction is a major public health problem. Through a commitment to individualized treatment plans meant to help patients meet personal goals, behavioral therapy can encourage abstinence and help prevent relapses that can have debilitating consequences. This case describes a 31-year-old male with heroin relapse who presented with flaccid quadriparesis as well as loss of sensation below the T2-3 spinal level, loss of rectal tone, and urinary retention. A urine drug screen (UDS) was positive for opiates and amphetamines. Autoimmune serologies were negative. Cerebrospinal fluid (CSF) analysis was negative for any acute ongoing infectious process. Magnetic resonance imaging (MRIs) of the cervical and thoracic spine showed increased intramedullary signals with spinal cord expansion from C2-T2, indicating acute transverse myelitis. Upon completion of the aforementioned work-up, idiopathic transverse myelopathy (TM) was diagnosed, and the patient was started on intravenous (IV) methylprednisolone; he also received five sessions of plasmapheresis. By process of elimination, suspicion remained of a diagnosis of opioid-induced myelopathy. The patient showed mild improvement in his original sensory deficits and flaccid quadriplegia.

Many drugs are known to potentially cause liver injury; however, only a few reports investigate the association between levofloxacin and acute liver failure (ALF).  The case describes a 65-year-old man who was admitted with primary diagnoses of cerebrovascular accident (CVA) and acute coronary syndrome (ACS) who developed an upper respiratory tract infection for which he was started on levofloxacin. Following its administration, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) increased more than 100-fold above the upper limit of normal. Over the next 24 hours, AST peaked at 9334 U/L, ALT at 4525 U/L, prothrombin time to 24.6 seconds, international normalized ratio (INR) to 2.22, and serum ammonia to 157 µmol/L. The patient developed signs and symptoms of decompensated liver disease, namely hepatic encephalopathy (HE). Levofloxacin was discontinued immediately, and evidence-based treatment per society guidelines from The American Association for the Study of Liver Diseases consisting of IV n-acetylcysteine as well as lactulose and rifaximin was initiated. Such medical management resulted in clinical resolution of his ALF, but he had a poor overall prognosis and eventually succumbed to critical illness.

Amantadine, which is known for its antiviral activity, is presently used as therapy for Parkinson's disease. Adverse effects, such as cardiac arrhythmias, have been described in patients after ingestion of amantadine. Here, we present a patient who suffered a cardiac arrest following ingestion of a low dose of amantadine. A 71-year-old man was admitted to the emergency department for a witnessed cardiac arrest. He had developed an upper respiratory tract infection the preceding week and was prescribed 100 mg of amantadine. Within half an hour of taking the first dose, the patient collapsed. He was found to be in asystole by emergency medical services, and advanced cardiac life support protocols were initiated, including cardiopulmonary resuscitation and intubation for airway protection. However, he sustained multiple recurrences of cardiac arrest, and despite all resuscitation efforts, the patient expired.