Sean M. Bryant

Case Files of the Medical Toxicology Fellowship at the Toxikon Consortium in Chicago: Cocaine-Associated Wide-Complex Dysrhythmias and Cardiac Arrest— Treatment Nuances and Controversies

ConclusionManifestations of cocaine poisoning range widely from mild sympathomimetic overdrive to life-threatening seizures, hyperthermia, and cardiac dysrhythmias. While supportive care, including the judicious use of benzodiazepines and cooling measures, is paramount, the management of cocaine-associated wide-complex dysrhythmias and cardiac arrest regularly includes sodium bicarbonate boluses in order to narrow QRS length. When confronted with refractory dysrhythmias, one must weigh the benefits and risks of further antidysrhythmic therapies. Lidocaine is frequently recommended when sodium bicarbonate fails. While animal studies regularly demonstrate CNS toxicity (seizures) and variable effects on mortality with the use of lidocaine, it has demonstrated effectiveness in suppressing cardiotoxicity associated with cocaine poisoning [22–27]. While experience with using lidocaine may exist, literature support of its use in the patient with cocaineinduced wide-complex dysrhythmias is sparse at best [15,28]. Amiodarone has not been proven to be a viable alternative to sodium bicarbonate or lidocaine, possesses promiscuous pharmacological activity, and cannot be generally recommended for cocaine-associated dysrhythmias in the absence of data supporting its safety and efficacy [1,30].Remembering Paracelsus’s words that all things are poisons certainly includes the current “evidence-based” antidotal therapy utilized to manage poisonings. Picking your poison (i.e., drug) to manage severe cocaine-induced cardiotoxicity may not be as straightforward as some would believe.

Unilateral Blindness Following Acute Methanol Poisoning

A 47-year-old man with history of alcoholism presented to the emergency department with altered mentation and “blurry vision.” He was tachypneic and minimally responsive to external stimuli, requiring endotracheal intubation. Vital signs were temperature 97.8°F, blood pressure 216/139, pulse 140/min, respiratory rate 26/min, and 98% oxygen saturation on room air. The pre-intubation venous pH was 6.79. Notable initial labs were sodium 135 mEq/L, potassium 3.7 mEq/L, chloride 95 mEq/L, total CO2 4 mEq/L, blood urea nitrogen (BUN) 11 mg/dL, creatinine 1.7 mg/dL, anion gap 36, serum osmolality 361 mOsm/kg, ethanol <10 mg/dL. An ethanol infusion, NaHCO3 drip, folic acid 1 mg, thiamine 50 mg, and pyridoxine 50 mg were initiated. The patient was dialyzed for 6 h until resolution of the anion and osmolar gaps. The initial methanol level was 123 mg/dL with a postdialysis level of 17 mg/dL. Ethylene glycol was undetectable. Following extubation, the patient, who had no prior ophthalmologic history and did not wear corrective lenses, was evaluated for persistent visual complaints. On exam, he had 20/20 acuity in the left eye, but only hand motion detection from the right eye. A right afferent pupillary defect and right optic disc pallor were also noted. Due to the unusual deficit, a magnetic resonance imaging (MRI) of the brain and orbits was obtained, revealing bilateral putaminal necrosis and edema at the retrobulbar and intracanalicular portions of only the right optic nerve (Fig. 1). MRI findings and cerebral spinal fluid (CSF) analysis did not provide alternative explanations for the ophthalmologic abnormalities. The patient was discharged on corticosteroids. On follow-up five months later, he had no visual improvement and remained ataxic and dysarthric.

Intramuscular ophthalmic homatropine vs. atropine to prevent lethality in rates with dichlorvos poisoning

IntroductionMost hospitals lack a sufficient supply of atropine to treat, simultaneously, patients poisoned with multiple organophosphorous compound (OC) or nerve agent. The presence of a ubiquitous alternate antidote would prove useful if mass poisoning occurred. Our objective was to evaluate the effect of ophthalmic homatropine (Isopto Homatropine 5%) on survivability in a rat model of significant, acute OC poisoning.MethodsSprague-Dawley rats were randomized to one of five pre-treatment groups (N = 10 per group). Prior to experimentation, animals were pre-treated with intramuscular (IM) injections of either atropine 5 mg/kg, atropine 10 mg/kg, homatropine 10 mg/kg, or homatropine 20 mg/kg. The control group received 0.3 mL normal saline IM. Five minutes later, 25 mg/kg of dichlorvos was subcutaneously administered. Mortality rates were compared using Fisher’s Exact test. Kaplan-Meier survival curves with Logrank analysis was also performed. If alive at 120 minutes, survival was assumed, and the study was terminated.ResultsAll rats pre-treated with normal saline, atropine 5 mg/kg, and homatropine 10 mg/kg died. Survival in the homatropine (20 mg/kg) and atropine (10 mg/kg) groups was 30% and 40% respectively. Times to death ranged between 4 and 12 minutes. Overall comparison of time to death revealed a statistically significant improvement for groups pre-treated with homatropine (20 mg/kg) and atropine (10 mg/kg).ConclusionsPre-treatment with homatropine (20 mg/kg) was comparable with atropine (10 mg/kg) in preventing lethality in this rat model of acute OC poisoning.

Adenosine and Caffeine‐induced Paroxysmal Supraventricular Tachycardia

While we recog-nize their study objectives and included limitations, wefeel that the design of the study faces significant imped-iments, namely, the proper selection of controls and thethreat of validity of results using self-reported data.Caffeine kinetics are nonlinear and the effects of thedrug are dose-dependent.

Communicating Extracranial and Intracranial Abscesses

A 24-year-old man presented to the emergency department complaining of 4–5 days of headache and scalp swelling. He reported similar symptoms intermittently for the past 3 years. Previous treatment with penicillin had resulted in resolution of the swelling and discomfort. Notably, he had a history of a scalp laceration secondary to being hit by a brick on the back of the head 7 years prior. Recurring pain over the mass, dizziness, and blurred vision were also sometimes associated. He was afebrile with normal vital signs. His physical examination revealed no focal neurologic deficits, but was remarkable for a 3 4-cm nontender, nonerythematous fluctuant mass located on the right occiput over the site of the previous trauma. With a working diagnosis of a presumed soft-tissue scalp abscess, standard management consisting of incision and drainage of the lesion was initially pursued. However, this course was deferred in light of the ‘‘waxing and waning’’ nature of the lesion. Because a chronically relapsing subgaleal abscess from remote trauma was considered, the conservative decision was made to obtain an image before any invasive procedure. A computed tomography (CT) scan of the brain (without IV contrast) revealed an extracranial and intracranial ring enhancing mass (Figure 1). Emergent magnetic resonance imaging (MRI) verified a chronic right parieto-occipital epidural abscess with an overlying subgaleal abscess (Figures 2 and 3).

Legal Liability as Poison Center Consultant

To the Editor, We appreciated the article by Curtis and Greenberg: “Legal liability of medical toxicologists serving as poison control center consultants: A review of relevant legal statutes and survey of the experience of Medical Toxicologists” published in September [1]. We conducted a similar review using Westlaw instead of Lexus-Nexus searching state statutes and common law decisions that define poison center indemnification and immunity via search terms (“poison control,” “immunity,” “indemnification”, and “medical director”) [2]. We found similar results of the states that specifically indemnify or limit the liability of poison control center consultants: California, Louisiana, Florida, Texas, Tennessee, Illinois, Arkansas, Florida, and Washington [1, 2]. In addition, we found that several states (North Carolina, Missouri, Connecticut, and Georgia) have common law or statutory “public immunity” doctrines which could hypothetically cover state-created Poison Control Centers (PCCs), but such doctrines do not specifically include PCCs within their scope. We agree with their statement that almost all states have “Good Samaritan” and/or volunteer statutes that potentially exempt volunteers providing emergency consultation through PCCs. These Good Samaritan or sovereign immunity doctrines may protect PCCs to the extent they are state-created, funded, and operated. This area of law, however, remains undefined and no reported cases exist litigating the issue. We also agree with the authors that it is essential that PCC consultants should be aware of specific laws affecting poison control practice in their state, and that other centers can use this information when attempting to initiate legislation in their state.

Hazardous Brick Cleaning

*Department of Emergency Medicine, Rush University Medical Center, Chicago, Illinois, †Department of Emergency Medicine, Loyola niversity Hospital, Chicago, Illinois, ‡Department of Emergency Medicine, Cook County-Stroger Hospital, Chicago, Illinois, and §Illinois Poison Center, Chicago, Illinois Reprint Address: Sean M. Bryant, MD, Department of Emergency Medicine, Cook County-Stroger Hospital, 1900 West Polk, 10 Floor, Chicago, IL 60612