Faculty Bibliography

Amlodipine is a potent vasodilator with a long half-life and delayed onset of action that is particularly concerning after an overdose. Vasodilation occurs through stimulation of nitric oxide release with increased cyclic guanosine monophosphate (cGMP) production. Methylene blue inhibits guanylate cyclase. This enzyme is responsible for the production of cGMP. Methylene blue also has the ability to scavenge nitric oxide, as well as inhibit nitric oxide synthase. We report the use of methylene blue for refractory shock in a patient with amlodipine toxicity

Experience with toxicity relating to intravenous (IV) paracetamol is discussed in the context of international experience. Issues in management and recent international strategies to minimise hazard are highlighted

Poisoning is a significant public health threat as the second leading cause of injury-related death in the US. Disagreements on cause of death determination may have widespread implications across several realms of public health including policy and prevention efforts, interpretation of the poisoning literature, epidemiologic data analysis, medical-legal case outcomes, and individualized autopsy interpretation. We aimed to test agreement between the cause of death determined by the medical examiner (ME) and a medical toxicologist (MT) adjudication panel (MTAP) in cases of poisoning. This retrospective 7-year study evaluated all deaths attributed to poisoning in one large urban catchment area. Cross-matched data were obtained from Department of Vital Statistics and the Poison Control Center (PCC). Out of >380,000 deaths in the catchment area over the study period, there were 7050 poisonings in the Vital Statistics database and 414 deaths reported to PCC. Cross-matching yielded 321 cases for analysis. The ME and MTAP concurred on cause of death in 66%, which was only fair agreement (kappa 0.25, CI 0.14-0.38). Factors associated with the likelihood of agreement were peri-mortem fire exposures, prehospital cardiac arrest, and timing of drug toxicity (chronic versus acute). In conclusion, agreement for poisoning cause of death between specialties was much lower than expected. We recommend an improved formal process of information sharing and consultation between specialties to assure that all existing information is analyzed thoroughly to enhance cause of death certainty

Contrary to popular opinion, application of extracorporeal therapies for poisonings predates their use for ESRD. Despite this observation, the science of blood purification in toxicology remains desperately stagnant today. In fact, much of our current knowledge is derived from George Schreiner's 1958 review. Original publications are almost exclusively composed of case reports and case series, from which good inference is impossible. Until randomized controlled trials become available, the medical community would be well served by a group mandated to systematically review available literature, extract relevant information, provide recommendations based on current evidence, and propose research initiatives. The EXtracorporeal TReatments In Poisoning workgroup, formed by several international experts in different medical fields and represented by over 20 societies, now has this mission

Background: Myeloneuropathy from chronic exposure to nitrous oxide has been described. Nitrous oxide irreversibly alters B(12) activation, causing signs and symptoms of B(12) deficiency. Objectives: We describe a case of myeloneuropathy secondary to acute use of high-dose nitrous oxide. Case Report: A 24-year-old man presented to the Emergency Department complaining of numbness and tingling of his hands and feet, as well as worsening clumsiness and gait disturbances after escalating use of nitrous oxide in the prior 2 weeks. He was found to have dysmetria, poor proprioception, decreased sensation to vibration and light touch over his extremities, and a mildly positive Romberg sign. Laboratory test values revealed a normal B(12) level but increased methylmalonic acid and homocysteine levels. The patient was admitted to the hospital and started on a course of B(12) injections. He was discharged after 3 days with daily B(12) supplementation. Conclusions: This case demonstrates myeloneuropathic changes secondary to acute high-dose nitrous oxide exposure

BACKGROUND: The differential diagnosis of non-traumatic lower extremity pain and swelling runs the gamut from simple musculoskeletal injury to a possibly life-threatening deep venous thrombosis (DVT). Although evaluation and management are often guided by physical examination and history, a diagnostic study is often required. Institutional factors surrounding diagnostic imaging often lead physicians to empirically treat these patients for DVT with a plan for definitive diagnosis at a later time. OBJECTIVES: We discuss plantaris tendon rupture, the ability of the clinician to differentiate DVT from musculoskeletal injury, and the risks of anticoagulation in the setting of an undifferentiated, painful, swollen lower extremity. CASE REPORT: We report the case of a 57-year-old transgendered woman who presented with left lower extremity pain and swelling and was found to have a rare cause of tennis leg: plantaris tendon rupture. CONCLUSIONS: Frequently, clinical examination and history are insufficient to distinguish DVT from musculoskeletal injury. In these instances, anticoagulation carries a risk of compartment syndrome and hemorrhage with uncertain benefit to the patient. A definitive diagnosis should be sought before initiation of anticoagulation of the swollen, painful lower extremity