Clin Toxicol Research Articles

SHOCK FROM NADOLOL OVERDOSE: THE FIRST REPORTED CASE OF SUCCESSFULLY TREATED WITH CONTINUOUS RENAL REPLACEMENT THERAPY (CRRT)

SHOCK FROM NADOLOL OVERDOSE: THE FIRST REPORTED CASE OF SUCCESSFULLY TREATED WITH CONTINUOUS RENAL REPLACEMENT THERAPY (CRRT)

POISON IN OUR POCKETS: MANAGEMENT OF LIFE-THREATENING ISOPROPANOL INTOXICATION

TOPIC: Critical Care TYPE: Fellow Case Reports INTRODUCTION: Isopropanol is a readily available substance, which can cause disastrous consequences if ingested even in a relatively small amount. High degree of suspicion is required for identification. This issue has become more concerning in light of the increasing exposure to household disinfectants and cases of toxicity in the context of the Covid-19 pandemic. CASE PRESENTATION: A 70 year-old African American woman presented after being found difficult to arouse by her son. Her last known well was 1 hour prior to presentation. She was profoundly lethargic on arrival, hypotensive and having profuse hematemesis. She was intubated for airway protection. Her hypotension did not respond to intravenous fluid and required vasopressors to maintain a mean arterial pressure of 65 mmHg. She was found to have ketonuria and severely elevated osmolar gap with no acidosis. Her mental status continued to deteriorate and she became dependent on mechanical ventilation. After further probing, her son noted he had found an empty bottle of rubbing alcohol in her room. No evidence of co-ingestion of other toxic substances were found on laboratory evaluation. She was observed for 8 hours with no discernible improvement in her mental status or hemodynamics. Hemodialysis was initiated for isopropanol clearance. Within 1 hour the patient became alert and hemodynamically stable. She was extubated without incident and mental status returned to baseline. DISCUSSION: Isopropanol is one of the most ubiquitous toxic substances, especially in the midst of the Covid-19 pandemic. Unlike ethylene glycol and methanol, isopropanol is more toxic than its metabolites. It reaches peak serum levels within minutes of ingestion. The minimum documented lethal dose is estimated at 100 ml. Isopropanol intoxication presents non-specifically, usually manifesting as central nervous system impairment and gastrointestinal upset. Most ingestion only result in mild symptoms. Massive ingestion may result in hemorrhagic gastritis or circulatory collapse. Hypotension is associated with a near 50% mortality rate. Identification of isopropanol poisoning is challenging due to its non-specific symptoms and subtle laboratory abnormalities. An increased osmolal gap and positive ketonemia are frequently the only abnormalities observed. In life threatening cases hemodialysis has been utilized with some success as a rescue therapy. CONCLUSIONS: Isopropanol intoxication requires a high degree of clinical suspicion is required for early identification and intervention in life threatening cases. In doing so significant morbidity and mortality may be prevented. No antidotes or neutralizing agents are currently available. Further study is needed to determine which patients would benefit most from hemodialysis with isopropanol intoxication. REFERENCE #1: Abramson S, Singh AK. Treatment of the alcohol intoxications: ethylene glycol, methanol and isopropanol. Curr Opin Nephrol Hypertens. 2000 Nov;9(6):695-701. doi: 10.1097/00041552-200011000-00017. PMID: 11128434. REFERENCE #2: Slaughter RJ, Mason RW, Beasley DM, Vale JA, Schep LJ. Isopropanol poisoning. Clin Toxicol (Phila). 2014 Jun;52(5):470-8. doi: 10.3109/15563650.2014.914527. Epub 2014 May 9. PMID: 24815348. REFERENCE #3: King LH Jr, Bradley KP, Shires DL Jr. Hemodialysis for isopropyl alcohol poisoning. JAMA. 1970 Mar 16;211(11):1855. PMID: 5467117. DISCLOSURES: No relevant relationships by Philip Almalouf, source=Web Response No relevant relationships by Alexander Angelidis, source=Web Response No relevant relationships by Robert Petrossian, source=Web Response No relevant relationships by Farheen Surtie, source=Web Response

AGITATED, ALTERED, AND ELONGATED: THE RISKS OF DIPHENHYDRAMINE OVERDOSE

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Overdose has become a leading cause of injury-related death in the United States. Rapid recognition of a toxidrome is vital in determining management. CASE PRESENTATION: A young, unknown female was brought to the ED after being found agitated and combative. Evaluation was notable for tachycardia, mydriasis and diaphoresis. She received intramuscular diphenhydramine (DPH), haloperidol and lorazepam for agitation.She developed a wide QRS complex with polymorphic ventricular tachycardia (VT) concerning for Torsades de pointes, terminated by precordial thump. She was intubated for airway protection. Magnesium and sodium bicarbonate (NaHCO) pushes were administered for sustained monomorphic VT with return to sinus tachycardia. Electrocardiogram was significant for prolonged QTc of 607ms and QRS >150ms. Initial toxicology was negative for acetaminophen, salicylate and ethanol.NaHCO infusion with goal pH 7.5 to maintain a narrow QRS was started. She had persistently prolonged QT interval. Overdrive transcutaneous pacing was unsuccessful, so isoproterenol (IPN) infusion was started. NaHCO and IPN infusions were discontinued at 48 hours with no further arrhythmias. Extended toxicology screen was positive for DPH. On extubation, she endorsed consumption of >1.25g DPH. DISCUSSION: Classic anticholinergic symptoms of tachycardia, mydriasis and delirium are also the toxidrome for DPH overdose. Severe toxicity is observed after ingestion of >1.0g (1). Cardiac toxicity is exhibited as widening of QRS and QTc intervals (1-3). Similar to TCA overdose, QRS widening is manifested from blockade of the fast-closing myocardial sodium channels (2-3). Treatment for QRS widening with NaHCO is anecdotally recommended (2-3). In this case, bolus and infusion of NaHCO successfully shortened the patient's QRS duration. One case report suggested using lipid emulsion therapy(3); however, DPH intoxication was not suspected initially thereby limiting its use. Since presenting symptoms of DPH and anticholinergic toxicity overlap, physostigmine must be avoided due to QRS prolonging effects (2). This case reminds of cautious administration of the "B52" cocktail for agitated patients. The use of intravenous DPH, haloperidol and lorazepam can be used to calm acutely agitated or aggressive patients; yet, it should be avoided with unknown ingestions.Further, QT prolongation and polymorphic VT can result from DPH's ability to weakly block the delayed rectifier potassium channels (2). Traditionally resolving this includes overdrive pacing and magnesium supplementation, which were administered in this case. However, failed overdrive transcutaneous pacing led to IPN infusion to induce tachycardia-associated QTc shortening. CONCLUSIONS: High suspicion and familiarity with toxidromes can lead to early diagnosis and intervention for critically ill patients presenting with agitated altered mental status. REFERENCE #1: Radovanovic D, Meier PJ, Guirguis M, Lorent JP, Kupferschmidt H. Dose-dependent toxicity of diphenhydramine overdose. Hum Exp Toxicol. 2000 Sep;19(9):489-95. doi: 10.1191/096032700671040438 REFERENCE #2: Jang DH, Manini AF, Trueger NS, et al. Status epilepticus and wide-complex tachycardia secondary to diphenhydramine overdose. Clin Toxicol (Phila). 2010;48(9):945-948. doi:10.3109/15563650.2010.527850 REFERENCE #3: Abdi A, Rose E, Levine M. Diphenhydramine overdose with intraventricular conduction delay treated with hypertonic sodium bicarbonate and i.v. lipid emulsion. West J Emerg Med. 2014;15(7):855-858. doi:10.5811/westjem.2014.8.23407 DISCLOSURES: No relevant relationships by Joy Ayyoub, source=Web Response No relevant relationships by Lauren Catalano, source=Web Response No relevant relationships by Sydney Emerson, source=Web Response No relevant relationships by Shahrzad Zonoozi, source=Web Response

LIFE-SAVER INSULIN: "THE MORE THE BETTER"

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Calcium channel blockers (CCB) are cardiovascular drugs that act on L-type calcium channels. Toxic exposures related to CCB is estimated to be 4.16% of all prescription overdoses. Toxicity leads to peripheral vasodilation, conduction blockade, and reduction in myocardial contractility. Additionally, high doses of CCBs inhibit the release of endogenous insulin and induce a state of hypoinsulinemia. In this state, myocardial cells are unable to uptake glucose for metabolic activity, which can be detrimental in the setting of shock. Treatment of CCB overdose revolves around administration of fluids, calcium, vasopressors, and ionotropic agents. Furthermore, cases involving cardiogenic shock should consider prompt addition of hyperinsulinemic-euglycemic therapy (HIET). The mechanisms by which HIET treats CCB overdose is theorized to be due to improved glucose uptake by myocardial cells, a concentration dependent ionotropic effect and systemic vasodilation. CASE PRESENTATION: A 41-year-old male with hypertension and major depressive disorder presented in shock after he intentionally ingested 600mg amlodipine in combination with alcohol. Despite aggressive initial measures with intravenous fluids, glucagon, calcium gluconate and high-dose vasopressor therapy ((nor-)epinephrine, vasopressin and angiotensin II), his condition worsened. He was intubated and started on HIET (bolus of intravenous insulin 1unit/kg followed by an infusion which was steadily increased to 8units/kg/hr). A continuous infusion of D25W was administered to maintain euglycemia and plasmapheresis was started to aid in the removal of amlodipine.The patient's course was further complicated by acute renal failure which led to overt volume overload. Continuous renal replacement therapy (CRRT) and eventually intermittent hemodialysis were started. Ultimately, he was gradually weaned off vasopressor support over 7 days while on HIET. DISCUSSION: The presented case highlights the importance of HIET in treating refractory cardiogenic shock caused by CCB overdose. Concomitant renal failure can be additive to the patient's clinical picture due to high quantities of intravenous volume needed with HIET. To our knowledge this is the first case to successfully utilize prolonged HIET with CRRT for CCB overdose. This case demonstrates that there may be promise in the utility of prolonged HIET for cases of complex CCB overdose with refractory shock. Due to lack of large sample sizes and randomized controlled studies, consideration for prolonged therapy or its role in renal failure should be given on a case-by-case scenario. CONCLUSIONS: Prolonged HIET is a promising treatment for cases of complex CCB overdose with refractory shock. REFERENCE #1: Gummin DD, Mowry JB, Spyker DA, Brooks DE, Fraser MO, Banner W. 2016 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 34th Annual Report. Clin Toxicol (Phila) 2017;55:1072–252 REFERENCE #2: Graudins A, Lee HM, Druda D. Calcium channel antagonist and beta-blocker overdose: antidotes and adjunct therapies. BrJ Clin Pharmacol 2016;81:453–61 DISCLOSURES: No relevant relationships by Shijo Benjamin, source=Web Response No relevant relationships by Md Islam, source=Web Response No relevant relationships by Maulin Patel, source=Web Response No relevant relationships by Mirja Wirtz, source=Web Response

EXTRACORPOREAL MEMBRANE OXYGENATION MODALITY DETERMINED BY POINT-OF-CARE ULTRASOUND IN A PATIENT WITH AMLODIPINE OVERDOSE: A CASE REPORT

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: The use of calcium channel blockers (CCB) as first-line antihypertensive therapy has correlated with increased incidences of CCB overdose. Massive CCB overdose proves difficult to manage as patients are prone to refractory distributive shock and noncardiogenic pulmonary edema. Extracorporeal membrane oxygenation (ECMO) has been a successful rescue therapy in CCB overdose. Veno-arterial (VA) ECMO has been the traditional modality used as it provides both cardiac and pulmonary support. However, recent case reports have described successful use of veno-venous (VV) ECMO for CCB overdose when cardiac function is preserved. We present a case of amlodipine overdose where VV ECMO was used instead of VA ECMO. This decision was guided by a point of care ultrasound (POCUS) exam that demonstrated a hyperdynamic left ventricle (LV) and normal right ventricle (RV) function immediately prior to cannulation. The patient subsequently improved, was decannulated, and survived to hospital discharge. CASE PRESENTATION: A 52-year-old male intentionally overdosed with amlodipine (750mg total). Emergency medical services were notified and transported the patient to the nearest critical access hospital. The patient became hypoxic, developed multipressor shock and met criteria for severe acute respiratory distress syndrome. On hospital day two the patient remained hypoxic despite an FiO2 of 1.0, deep sedation, neuromuscular blockade (NMB) and prone positioning. His shock was refractory despite infusions of norepinephrine, epinephrine, vasopressin and phenylephrine in addition to stress dose steroids and methylene blue. Our ECMO team was consulted for intervention. Prior to cannulation, cardiac POCUS revealed a hyperdynamic LV and preserved RV function. This guided our decision to implement VV instead of VA ECMO. The patient was cannulated then transported to our tertiary care institution. On ECMO day 2, the patient came off epinephrine and phenylephrine and NMB was discontinued. On ECMO day 4, the patient remained on norepinephrine alone and followed simple commands during a sedation holiday. On ECMO day 7 the patient no longer required vasopressors and was decannulated. The patient underwent tracheostomy placement, was placed on a long-term ventilator wean and discharged on hospital day 21. DISCUSSION: CCB overdose leading to refractory shock presents a difficult challenge for clinicians. There is promising data regarding the use of VA ECMO and, recently, VV ECMO as a rescue treatment in addition to supportive critical care in these cases. Selection of the appropriate ECMO modality prior to cannulation is paramount to optimize cardiopulmonary support. CONCLUSIONS: We assert that this case demonstrates the potential for utilizing POCUS as a tool to help decide what ECMO modality to use in patients with CCB overdose. Further study into POCUS as a means of determining ECMO modality is warranted. REFERENCE #1: Fadhlillah F, Patil S. Pharmacological and mechanical management of calcium channel blocker toxicity. BMJ Case Rep. 2018;2018:bcr2018225324. Published 2018 Aug 27. doi:10.1136/bcr-2018-225324 REFERENCE #2: Haughey R, Vernick W, Gutsche J, Laudanski K. Use of veno-venous extracorporeal membrane oxygenation to treat severe combined calcium channel blocker and angiotensin converting enzyme inhibitor overdose. Perfusion. 2019 Mar;34(2):167-169. doi: 10.1177/0267659118798181. Epub 2018 Sep 3. PMID: 30175658. REFERENCE #3: Lindeman E, Ålebring J, Johansson A, Ahlner J, Kugelberg FC, Nordmark Grass J. The unknown known: non-cardiogenic pulmonary edema in amlodipine poisoning, a cohort study. Clin Toxicol (Phila). 2020 Nov;58(11):1042-1049. doi: 10.1080/15563650.2020.1725034. Epub 2020 Mar 2. PMID: 32114860. DISCLOSURES: No relevant relationships by Jonathon Davis, source=Web Response No relevant relationships by Jon Greenberg, source=Web Response No relevant relationships by Logan Rosenberg, source=Web Response

TOLUENE-INDUCED ACUTE LUNG INJURY: CASE REPORT

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Toluene is an aromatic hydrocarbon widely used as a solvent in industrial and commercial products including paints, adhesives, ink, and rubber. It is occasionally used as an inhalant drug for its intoxicating properties. While mostly known for producing neurologic effects, here we report a case of toluene induced acute lung injury. CASE PRESENTATION: A 61-year-old female with a medical history of alcohol abuse, depression, congestive heart failure with preserved ejection fraction presented with one week of weakness and shortness of breath. She had been seen twice in the week prior having tested negative for SARS-COV2. In the emergency department, O2 saturation was 70% with respiratory distress on room air requiring high flow nasal cannula support. Labs were notable for a potassium of 2.7 mmol/L, acute kidney injury, elevated transaminases, lactate of 2.8 mmol/L and leukocyte count of 9800/nL. CT showed diffuse bilateral ground glass opacities involving the lung parenchyma concerning for atypical including viral pneumonia. Upon admission to the ICU she developed worsening hypoxia and respiratory failure requiring intubation.A discussion with the patient's husband revealed she had a history of glue sniffing. She had recently been decreasing her alcohol intake and substituting this with an increased frequency of sniffing both permanent markers and modeling glue. This raised suspicion for chemical pneumonitis secondary to toluene induced acute lung injury. DISCUSSION: Toluene is a highly lipophilic molecule readily inhaled via the lungs and distributed widely throughout the body producing side effects like ethanol intoxication via interfering mainly with GABA receptors. Neurologic manifestations range from euphoria and hallucinations to cognitive dysfunction and ataxia with chronic use. It specifically causes renal tubular acidosis typically manifesting as a normal anion gap hyperchloremic acidosis with hypokalemia. It can also cause hepatic injury and cardiac automaticity and conduction abnormalities.Acute lung injury secondary to toluene has been described but less frequently reported. Toxicity can result in Reactive Airway Dysfunction Syndrome (RADS) from acute or chronic exposure to various chemical irritants. All hydrocarbons, including toluene, can cause chemical pneumonitis by direct contact with the pulmonary parenchyma and destroying alveolar and capillary membranes resulting in vascular permeability and edema. Symptoms may include cough, wheezing, respiratory distress, and hypoxia. Bilateral interstitial infiltrates may be delayed for several hours after the development of pneumonitis. There is no specific antidote for toluene toxicity. CONCLUSIONS: Treatment for toluene and many chemical induced pneumonitides consists of supportive care, supplemental oxygen, bronchodilators, inhaled and systemic glucocorticoids and may require intubation and admission to an ICU in severe cases. REFERENCE #1: Camara-Lemarroy CR, Rodríguez-Gutiérrez R, Monreal-Robles R, González-González JG. Acute toluene intoxication--clinical presentation, management and prognosis: a prospective observational study. BMC Emerg Med. 2015;15:19. Published 2015 Aug 18. doi:10.1186/s12873-015-0039-0 REFERENCE #2: Alberts WM, do Pico GA. Reactive airways dysfunction syndrome. Chest. 1996;109(6):1618-1626. doi:10.1378/chest.109.6.1618 REFERENCE #3: Tormoehlen LM, Tekulve KJ, Nañagas KA. Hydrocarbon toxicity: A review. Clin Toxicol (Phila). 2014;52(5):479-489. doi:10.3109/15563650.2014.923904 DISCLOSURES: No relevant relationships by Ryan Lee, source=Web Response No relevant relationships by Dominic Valentino, source=Web Response

MIRACLE DRUG UNDER FIRE: HYDROXYCHLOROQUINE OVERDOSE TOXICOKINETICS EXPLORED

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Hydroxychloroquine (HCQ) is a medication used in the treatment of malaria, lupus and rheumatoid arthritis. The drug gained popularity during the early stage of the Coronavirus Disease 2019 (COVID-19) pandemic as an emergency use therapy. It has since been shown in numerous studies that HCQ can actually cause more harm than good. However, its media attention has led to an increase in overdose cases, which can be fatal due to cardiac complications. We present a case of a patient with access to HCQ for COVID-19 prophylaxis who overdosed in a suicide attempt with a favorable outcome. CASE PRESENTATION: A 38-year old Asian American female with no significant history was found 4-6 hours after ingesting approximately 27 grams of oral HCQ. She was admitted to the intensive care for shock and severe hypokalemia (1.7 mmol/L). The pills were obtained from an overseas third party vendor for COVID-19 prophylaxis. Vitals on arrival were BP 60/30 mmHg, HR 66 bpm, temperature 94.9 fahrenheit. Based on previous case reports and studies on chloroquine, the patient was started on an epinephrine and versed drip, including 2 doses of 60mg diazepam. A single dose of activated charcoal was administered. Initial electrocardiogram revealed conduction abnormalities with QT interval of 549ms (629ms with Bazett's correction). The patient received 240 meq of potassium in a span of 25 hour and began to develop hyperkalemia of up to 6.4 mmol/L. After 48 hours, the patient's blood pressure and potassium levels normalized. On hospital day 4, she was successfully extubated with a favorable remaining hospital course. DISCUSSION: The most life threatening sequelae seen in HCQ overdoses are cardiac arrhythmias due to electrolyte imbalances, mainly potassium. Hyperkalemia after initial severe hypokalemia has been observed in numerous case reports of HCQ overdose and thought to be intracellular shifts rather than relative depletion. Thus, caution should be taken in the correction of initial hypokalemia. A review of previous cases shows an inverse relationship between potassium and HCQ levels, as with our case. Reported toxicity half-life ranges between 11.6 and 31 hours. Our case had an approximate peak concentration of 27 µg/ml after 4-6 hours after ingestion with an estimated observed half-life of 27 hours based on recorded concentrations over 45 hours, assuming 1st order elimination. Our patient's hypokalemia began to reverse during the 2nd half-life period which is also consistent with other reported cases. CONCLUSIONS: We believe that during the 2nd half-life, when more than 50% of the drug is eliminated, is the period when correction of hypokalemia should be taken with more caution. While these are only observations based on a few case reports, they can provide more insight on how to better manage electrolyte imbalances which can avoid fatal arrhythmias and circulatory arrest. REFERENCE #1: de Olano, J., Howland, M. A., Su, M. K., Hoffman, R. S., & Biary, R. (2019). Toxicokinetics of hydroxychloroquine following a massive overdose. The American journal of emergency medicine, 37(12), 2264-e5. REFERENCE #2: Jordan, P., Brookes, J. G., Nikolic, G., Le Couteur, D. G., & Le Couteur, D. (1999). Hydroxychloroquine overdose: toxicokinetics and management. Journal of Toxicology: Clinical Toxicology, 37(7), 861-864. REFERENCE #3: Palatnick, W., Meatherall, R., Sitar, D., & Tenenbein, M. (1997). Hydroxychloroquine kinetics after overdose. J Toxicol Clin Toxicol, 35, 496.Miller, D., & Fiechtner, J. (1989). Hydroxychloroquine overdosage. The Journal of rheumatology, 16(1), 142-143. DISCLOSURES: No relevant relationships by Fatima Anjum, source=Web Response No relevant relationships by James Kang, source=Web Response No relevant relationships by Hyfaa Mashaal, source=Web Response No relevant relationships by James Pellegrini, source=Web Response

N-Acetylcysteine Interference With Creatinine Measurement: An In Vitro Analysis

N-Acetylcysteine Interference With Creatinine Measurement: An In Vitro Analysis

Acetaminophen and the Developing Lung: Could There Be Lifelong Consequences?

Acetaminophen and the Developing Lung: Could There Be Lifelong Consequences?

Why Does the Food and Drug Administration Need to Ban Kratom?

Kratom (Mitragyna speciosa) is an herb with no current indication for medical use with potentially addictive properties, yet it is being used in the management of pain, depression, and anxiety. The agent’s pharmacology lends itself for concern regarding recreational misuse (Drugs of Abuse, 2017). Kratom’s increasing popularity for use in the USA is reflected by National Poison Data System data that in 2011 there were 13 cases reported to poison control centers while in 2017 there were 682 calls in response to kratom exposure (Kratom exposure in the US linked to serious medical outcomes, 2019; Post et al. in Clin Toxicol. 57:847–54, 2019). Subjects most commonly use kratom for the self-treatment of pain, mood swings, and opioid-related withdrawal symptoms (Grundmann in Drug Alcohol Depend. 176:63–70, 2017). Known serious adverse events include hallucinations, delusions, reduced respiratory drive, and death (Kratom: unsafe and ineffective, 2019). Additional anecdotally reported side effects include hypothyroidism, seizure, hepatotoxicity, coma, and injury to the posterior white matter of the brain (Anwar et al. in MMWR Morb Mortal Wkly Rep. 65:748–9, 2016; Nelsen et al. in J Med Toxicol. 6:424–6, 2010; Sheleg and Collins in J Addict Med. 5:300–1, 2011; Castillo et al. in Proc (Baylor Univ Med Cent). 30:355–7, 2017). At this time, kratom remains without regulations on a federal level. The substance’s opioid-like pharmacology, ease of use, and lack of demonstrated safety or efficacy justify the need for continued extensive research (Brooks, 2019).

SPICE GOT US IN A PICKLE: A CASE OF SYNTHETIC MARIJUANA-INDUCED CARDIOMYOPATHY AND RHABDOMYOLYSIS

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Spice is a commonly used name for synthetic cannabinoids (SCs) which are chemical analogs of naturally occurring cannabinoids. They are increasingly used for their hallucinogenic effects, low cost and ease of availability. They are not detected in routine urine assays and their detection requires specialized urine drug screens making them an attractive option for young adults. There are case reports of cardiomyopathies associated with their overdose. We discuss the case of a young male who presents with rhabdomyolysis and cardiomyopathy after an intentional overdose of Spice. CASE PRESENTATION: A 21-year-old male with a past medical history of major depressive disorder and substance abuse (heroin, marijuana, spice) was brought in by emergency medical services after being found unresponsive. His vital signs were BP 78/46 mmHg, HR 97 beats per minute, RR 20 times a minute, temperature 100F, saturating 93% on room air. On physical exam, his pupils were pinpoint and he had a Glasgow Coma Scale of 8 (eye 2, verbal 2, motor 4) with decerebrate posturing. Labs showed pH of 6.94, bicarbonate of 12, Urine Drug Screen was positive for opiates and cannabinoids, lactate of 16.4, Creatinine of 2.3, a creatinine kinase of >22,000 and a troponin of 3.35. An EKG on admission showed sinus rhythm with short PR interval and J point elevation most noticeable in lead 1. Bedside ultrasound showed bi-ventricular failure with severe global hypokinesis. He was intubated and started on Dobutamine and Norepinephrine drips. On day 3, pressors were weaned off, he was extubated and Echo showed improved Left Ventricular function off pressors. His acute kidney injury resolved with hemodynamic support and Creatinine of 0.8 on discharge. He admitted to sniffing Heroin and smoking Spice prior to admission and he was discharged home. It was suspected he had spice induced cardiomyopathy and AKI. The patient had no history of coronary artery disease or alcohol use, no evidence of valvular abnormality and no signs of sepsis and the cardiomyopathy was attributed to Spice. He did not have prolonged hypotension, nephrotoxic medication use and his kidney injury was attributed to rhabdomyolysis. DISCUSSION: There are case reports of ST-elevation myocardial infarctions triggered by SC use; most of these have been young patients with normal-appearing coronary arteries on angiography. SCs bind to CBR1 receptors with a higher affinity than natural cannabinoids leading to direct negative inotropic effect on cardiomyocytes. While most case reports of SC-induced nephropathy involve acute tubular necrosis, our patient presented with rhabdomyolysis-induced nephropathy. CONCLUSIONS: SCs are far more dangerous than their natural counterparts and as they require special assays for detection, health care providers should be cognizant of their use and effects. Reference #1: Ting JYS. Reversible cardiomyopathy associated with acute inhaled marijuana use in a young adult. Clin Toxicol (Phila) 2007;45:432–4. https://doi.org/10.1080/15563650601073587. Reference #2: Bhanushali GK, Jain G, Fatima H, Leisch LJ. Thornley-Brown D. AKI associated with synthetic cannabinoids: A case series. Clin J Am Soc Nephrol. 2013;8:5236. https://doi.org/10.2215/CJN.05690612 DISCLOSURES: No relevant relationships by Iman Khan, source=Web Response

PC-FACS

PC-FACS

UNUSUAL CASE OF INTERSTITIAL LUNG DISEASE

SESSION TITLE: Diffuse Lung Disease 1 SESSION TYPE: Fellow Case Reports PRESENTED ON: 10/07/2018 03:30 pm - 04:30 pm INTRODUCTION: Interstitial Lung Disease can be associated with a broad range of diseases, exposures, drugs, and can be idiopathic. Silicosis has been understood as a cause of pulmonary disease for centuries. Silicosis inhalation is seen by occupational exposure such as sandblasting, mining, and masonry. Injected silicone is a liquid form of silicone and is commonly used in plastic and reconstructive surgery. We present a case of silicone injection that caused pulmonary fibrosis. CASE PRESENTATION: A middle aged Transgender female underwent breast implants and silicone thigh, gluteal, and hip injections. The injections were done in by unlicensed non-physician practitioners located in a home. Two weeks after the procedures the patient developed a severe skin reaction causing infection and skin breakdown. Several weeks after recovery the breast implants opened and caused skin necrosis and infection in the breasts. A bilateral mastectomy had to be completed. After recovery the skin became thickened and fibrotic. Two years later the patient developed worsening shortness of breath, dyspnea on exertion, and hypoxia. She presented to the emergency room where a chest xray showed bilateral upper lobe infiltrates. A CT chest showed severe fibrotic changes in middle and upper lung zones. Associated groundglass opacities, mild bronchiectasis, and interlobular connective-tissue thickening in bilateral lower lobes was also present. Pulmonary function tests noted severe restrictive lung disease with severely low oxygen exchange. Pathology of surgical biopsy showed extensive multinucleated foreign body giant cells. Many of the giant cells included non-polarizable microdroplets which were suggestive of silicone droplets. DISCUSSION: Acute lung injury from venous or arterial injection is most understood complication in literature. Chronic injury causing progressive massive fibrosis is rare. When silicone is mixed with soft tissue a fibroblastic response is generated. With history, clinical findings, imaging, and pathology our suspicion of silicone injection induced lung fibrosis was confirmed. CONCLUSIONS: Silicone is considered as inert agent, physicians especially pulmonologists need to be aware of its complications which may range from local tissues necrosis to progressive massive fibrosis1. Risk of complications increases with illicit injections or if performed by unskilled practitioners. Most of the pulmonary complications due to silicon implants, described in literature are acute like acute pneumonitis or diffuse alveolar damage and only few case reports are available for chronic pulmonary pathology like Granulomatous pneumonitis and progressive massive fibrosis2, 3.Recognition of acute and chronic complications is important as treatment of chronic complications is limited. Reference #1: Narins RS, Beer K. Liquid injectable silicone: a review of its history, immunology, technical considerations, complications, and potential. Plast Reconstr Surg. 2006;118(3 suppl):77S–84S. Reference #2: Chastre J, Basset F, Viau F, et al. Acute pneumonitis after subcutaneous injections of silicone in transsexual men. N Engl J Med. 1983;308(13):764–767. Reference #3: Clark RF, Cantrell FL, Pacal A, et al. Subcutaneous silicone injection leading to multi-system organ failure. Clin Toxicol (Phila). 2008;46(9):834–837. DISCLOSURES: No relevant relationships by Dipen Kadaria, source=Web Response No relevant relationships by Adnan Khan, source=Web Response No relevant relationships by Anthony Mattox, source=Web Response No relevant relationships by April McDonald, source=Web Response

SHOE SHINING: HAZARDOUS TO THE HEALTH

SESSION TITLE: Occupational and Environmental Lung Diseases SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Hydrocarbons are ubiquitous in society and are found in many common household products, including gasoline, cleaning agents, mineral oil, and industrial solvents. In 2016, the American Association of Poison Control Centers reported 29,796 cases of hydrocarbon exposure, with approximately 20 deaths attributed to this exposure. There are three main types of hydrocarbon exposure: children with unintentional ingestion of household hydrocarbons, workers with dermal or inhalational occupational exposures, and adolescents and young adults with intentional inhalational abuse. CASE PRESENTATION: Our patient is a 40-year-old male sailor who presented to the emergency department with productive cough and dyspnea. Approximately two hours prior to arrival, the patient was waterproofing his boots in an enclosed space. On initial evaluation, his heart rate was in the 100s, respiratory rate in the 30s, and oxygen saturation in the 70s%. His exam was notable for diffusely diminished breath sounds. He was placed on 10 liters via nonrebreather. The Poison Control Center was contacted, and the inhaled toxin was identified as a petroleum-based hydrocarbon. A chest x-ray showed diffuse bilateral hazy opacities. He was admitted to the intensive care unit and placed on high-flow nasal cannula with flow and FiO2 titrated to maintain oxygen saturation greater than 92%. A high resolution CT scan of the chest showed diffuse bilateral upper and central lobe predominant groundglass opacities with subpleural sparing consistent with diffuse alveolar damage. Treatment with high dose steroids and bronchodilators was initiated, and over the next 48 hours the patient had significant improvement. He was discharged on a tapering dose of prednisone and supplemental oxygen at 4 liters per minute for exertion. After discharge, his spirometry showed a mild restrictive pattern with a mild reduction in DLCO; he no longer required supplemental oxygen. Follow up chest imaging is currently pending. DISCUSSION: The mechanisms by which hydrocarbons cause pulmonary toxicity are dose-dependent, and include alveolar and interstitial edema, desquamation of pneumocytes, and disruption of surfactant. Hypoxia results from a combination of ventilation-perfusion mismatch, shunt formation, and bronchospasm. Initial imaging may be normal, with delay of radiographic changes for several hours after the development of pneumonitis. Radiographic findings typically demonstrate bilateral interstitial infiltrates, though may also reveal pneumatocele, pneumothorax, pleural effusions, and lung necrosis; additionally, intra-alveolar oils can coalesce into nodules surrounded by fibrosis called parafinomas. While symptoms usually resolve within a few days, radiographic abnormalities may last months. Most cases of hydrocarbon lung toxicity resolve with supportive care of oxygen and ventilatory support, but there have been case reports of benefit from corticosteroids, whole or segmental lung lavage, and intratracheal surfactant in severe cases, though there is no firm evidence for these treatments. CONCLUSIONS: Hydrocarbons are found in several household products, making exposure to these items not uncommon. While the acute effects of hydrocarbon toxicity are well recognized, the long-term effects of acute and chronic exposure require further research. Reference #1: Connellan SJ. Lung diseases associated with hydrocarbon exposure. Resp Med 2017; 126:46-51. Reference #2: Gummin DD, Mowry JB, Spyker DA, Brooks DE, Fraser MO, Banner W. 2016 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 34th Annual Report, Clin Toxicol 2017;55:(10)1072-1254. Reference #3: Tormoehlen LM, Tekulve KJ, Nanagas KA. Hydrocarbon toxicity: A review. Clin Toxicol 2014; 52:479-489. DISCLOSURES: No relevant relationships by Jeannette Collins, source=Web Response No relevant relationships by Angeline Lazarus, source=Web Response

HIGH DOSE INSULIN AND VA ECMO FOR POISON-INDUCED CARDIOGENIC SHOCK

SESSION TITLE: Critical Care 2 SESSION TYPE: Med Student/Res Case Report PRESENTED ON: 10/09/2018 05:00 PM - 06:00 PM INTRODUCTION: High dose insulin therapy (HDI) is an emerging and increasingly well described intervention for poison-induced cardiogenic shock (PICS). PICS due to beta-blocker or calcium channel blocker overdose is both frequent and life-threatening [1]. When traditional therapies such as fluid resuscitation, cardiac pacing, atropine, calcium, glucagon, vasopressors and inotropes fail to provide hemodynamic stability, HDI can be effective [2-7]. While the current literature is limited to case series and animal models [2-7], we present a case of successful HDI in a patient with beta-blocker toxicity. CASE PRESENTATION: We report a 36-year-old female who presented in cardiogenic shock secondary to polypharmacy overdose, including significant amounts of propranolol. She suffered cardiopulmonary arrest shortly after arrival to the hospital. Despite aggressive resuscitation, she required emergent venoarterial extracorporeal membrane oxygenation (VA ECMO) support to achieve hemodynamic stability. HDI was subsequently initiated by assessing hemodynamic responsiveness to progressively increased bolus doses, starting with 1 unit per kilogram. HDI was continued with an insulin infusion at 15 units/kilogram/hour. She demonstrated an excellent response, and was successfully transitioned off VA ECMO support and all vasoactive medications. The following day, the insulin drip was carefully weaned to avoid large potassium shifts. The patient was eventually discharged to home, neurologically intact with normal biventricular function by echocardiogram. DISCUSSION: This patient demonstrated a rapid and robust response to HDI in the setting of profound cardiogenic shock. Despite requiring escalation of care to VA ECMO, HDI allowed for rapid discontinuation of this salvage therapy. Several mechanisms of action have been postulated for HDI, including a direct positive inotropic effect and multiple favorable metabolic properties [3,5,8-12]. HDI also induces vasodilation, which improves both microcirculation and systemic perfusion [5,11]. While evidence for specific dosing regimens remains limited, the doses used in this case are consistent with previously described values including bolus doses of 1 unit per kilogram and infusions of 10 units/kilogram/hour or more [13-15]. CONCLUSIONS: In patients with PICS due to either calcium channel blockers or beta-blockers, HDI can be a definitive and life-saving treatment. While large clinical trials are lacking, sufficient evidence exists to consider this therapy in patients with PICS refractory to traditional treatment [16]. Note: All sixteen references available in uploaded document Reference #1: DeWitt CR, et al. Pharmacology, pathophysiology and management of calcium channel blocker and beta blocker toxicity. Toxicol Rev 2004, 23:223-38 Reference #2: Yuan TH, Kerns WP, Tomaszewski CA, Ford MD, Kline JA. Insulin-glucose as adjunctive therapy of severe calcium channel antagonist poisoning. J Toxicol Clin Toxicol 1999, 37:463-74 Reference #3: Megarbane B, et al. The role of insulin and glucose (hyperinsulinemia/euglycemia) therapy in acute calcium channel antagonist and beta-blocker poisoning. Toxicol Rev 2004, 23:215-22 DISCLOSURES: No relevant relationships by Benjamin Abrams, source=Web Response No relevant relationships by David Douin, source=Web Response No relevant relationships by Scott Wolf, source=Web Response

The safety of high-dose insulin euglycemia therapy in toxin-induced cardiac toxicity: Page CB, Ryan NM, Ibister GK. Clin Toxicol. 2018; 56(6):389-396

The safety of high-dose insulin euglycemia therapy in toxin-induced cardiac toxicity: Page CB, Ryan NM, Ibister GK. Clin Toxicol. 2018; 56(6):389-396

Quick Consult

marijuana, cannabinoid hyperemesis syndrome: marijuana, cannabinoid hyperemesis syndromeFigureFigureFigureA 28-year-old man presented to the ED with diffuse abdominal pain, nausea, and more than 15 episodes of non-bilious, non-bloody emesis over the previous 48 hours. His pain was worst in the morning, but improved after a hot shower. Of note, the patient had used products similar to this on a daily basis. (Photo.) This was his fourth visit to the ED for abdominal pain over the past year. Previous visits have included an extensive workup, including unremarkable abdominal CTs, labs, and upper endoscopy. What is the most appropriate diagnosis, and what are the treatment options? Find the diagnosis and case discussion on p. 16. Diagnosis: Cannabinoid Hyperemesis Syndrome Cannabinoid hyperemesis syndrome (CHS) is characterized by cyclic episodes of moderate to severe diffuse abdominal pain, nausea, and emesis in patients endorsing frequent marijuana use. Many patients present repeatedly, and undergo multiple rounds of costly, nondiagnostic tests. The diagnosis of CHS is becoming increasingly common, and is likely due to an increase in the THC content of marijuana, the prevalence of marijuana use, and the availability of commercial marijuana. Shifts in laws and stigma about marijuana use may also be influencing the frequency with which patients report marijuana use to physicians. CHS can be separated into three phases: prodromal, hyperemetic, and recovery. The prodromal phase may last months to years, and involves low-level abdominal discomfort from frequent marijuana use. The hyperemetic phase typically lasts up to 48 hours, and involves intense episodes of non-bilious, non-bloody emesis, sometimes more than five times per hour. Episodes occur cyclically at an interval of weeks to months, and asymptomatic periods may or may not involve marijuana use. (Curr Drug Abuse Rev 2011;4[4]:241.) The pathophysiology of CHS is still an active area of investigation, but may involve CB1 receptors in the gastrointestinal tract and central nervous system. (Pharmaceuticals [Basel] 2010;3[7]:2163.) Initial use of marijuana may provide a therapeutic effect to the patient with decreased nausea and abdominal pain, while chronic use eventually tips the scale toward nausea, pain, and emesis. The recovery phase, which almost invariably coincides with marijuana cessation, is characterized chiefly by a lack of hyperemetic episodes. Confidently diagnosing CHS can be challenging. Excluding the diagnosis of cyclic vomiting syndrome is difficult because both conditions involve cyclic episodes of abdominal pain, nausea, and emesis. Some studies indicated that the only way to discriminate between the syndromes is whether marijuana cessation causes remission. (Ger Med Sci 2017;15:Doc06.) CHS is also more often associated with frequent marijuana use and symptomatic relief via hot showers. (Curr Drug Abuse Rev 2011;4[4]:241.) Up to 92 percent of patients diagnosed with CHS endorse symptomatic relief when taking hot showers. (J Med Toxicol 2017;13[1]:71.) It is important in the ED to exclude acute diagnoses such as pancreatitis, bowel obstruction, or cholecystitis while not repeating prior negative workups. Chronic diagnoses, such as irritable bowel syndrome, Crohn's, or celiac should be investigated by the primary care physician. Treatment in the ED consists primarily of IV fluids and antiemetic medications. Haloperidol (5-10 mg IV) may be beneficial because of the dopamine antagonism and interactions between CB1 and dopamine pathways. (Am J Ther 2017;24[1]:e64.) Recent research suggests that capsaicin creams applied in the ED can also provide quick symptomatic relief. A suggested mechanism of action involves TRPV1 receptors in nociceptive pathways. (Clin Toxicol [Phila] 2017;55[8]:908.) No long-term pharmacologic interventions have been shown to reduce the intensity or frequency of episodes, and cessation of marijuana use is the only intervention that has consistently demonstrated efficacy. (J Med Toxicol 2017;13[1]:71.) Broaching the topic of marijuana as a causative agent while the patient is in the ED is challenging. Many patients resist the idea that marijuana use may be causing their symptoms. Discussion of CHS should be reserved for the end of the visit when symptoms have significantly resolved. It is useful to engage the patient in a conversation on the paradoxical causative role of marijuana. Admitting that cannabis can provide nausea relief in many situations and elaborating on CHS may help reduce resistance to the diagnosis. Engaging patients in the idea that marijuana, like many other medications and remedies, may have side effects is also useful. These conversations help reduce return visits, which are common for CHS patients. This patient received treatment in the ED with IV normal saline and haloperidol with significant improvement. After engaging him in a thoughtful discussion about his cannabis use, he acknowledged that cannabis may have side effects in some patients and agreed to a trial of cannabis cessation to see if his symptoms would resolve.

The Use of High Dose Insulin Therapy in a Case of Diltiazem (Calcium Channel Blocker) Poisoning

SESSION TITLE: Critical Care 1 SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: In cases of calcium-channel blocker (CCB) poisoning patients develop bradycardia, hypotension, hyperglycemia, metabolic acidosis and cardiogenic shock. Often conventional therapy fails and leads to mortality. We report a case of CCB poisoning and use of High-dose insulin (HDI) therapy with marked improvement. CASE PRESENTATION: This is a 47-year-old male with a history of CAD, hypertension presented to the emergency department (ED) with complaints of chest pain. In ED, the patient became combative with the staff and had to be chemically restrained with Haldol and Ativan. He was admitted to medical ICU for bradycardia and hypotension. As a suicide attempt, he had overdosed on Diltiazem (CCB). He was intubated to protect his airway. He was persistently hypotensive with bradycardia and junctional rhythm on ECG and received IV atropine, glucagon, and calcium with no improvement. Subsequently required four vasopressors. He was initially placed in transcutaneous pacing and later temporary pacemaker was placed for symptomatic bradycardia. He was started on High Dose Insulin (HDI) therapy for calcium channel blocker overdose. He continued to have hyperglycemia (blood glucose 500-600 mg/dl) which is a known complication of CCB poisoning, insulin infusion was continued. He was found to have metabolic acidosis (CCB poisoning) for which he was started initially on Bicarbonate infusion and later continuous renal replacement therapy (CRRT). He was transferred to a tertiary center, due to acute respiratory distress syndrome (ARDS), where aggressive diuresis and ARDS protocol were used. The patient was extubated and after supportive therapy and Psychiatry clearance was discharged home. DISCUSSION: The proposed mechanism for HDI in CCB poisoning and cardiogenic shock: 1. increased inotropy, 2. increased intracellular glucose transport, and 3. vascular dilatation. HDI is not a vasopressor. To the contrary, insulin is a vasodilator of the systemic, coronary, and pulmonary vasculature. Insulin enhances microvascular perfusion at the capillary and pre-capillary concentration to achieve perfused capillary density similar to that of exercising muscle. Decreasing vascular resistance by these mechanisms (independent of inotropy) results in enhanced cardiac output.[1] Initial recommended dose of insulin, a bolus of 1 U/kg followed by 0.5-1 U/kg/h continuous infusion. The infusion rate increased by 2 U/kg/h every 10 min to a maximum of 10 U/kg/h if no increase in cardiac output or clinical improvement is seen. The most common side effects of HDI is hypokalemia and hypoglycemia, close monitoring is required. CONCLUSIONS: The current case illustrates how there could be a delay in therapy for drug poisoning and failure of conventional therapy, in severe cases. We should be aware of the alternative treatments. In this case, prompt action and aggressive intervention saved this patient’s life. Reference #1: Engebretsen, K.M., et al., Clin Toxicol (Phila), 2011. 49(4): p. 277-83. DISCLOSURE: The following authors have nothing to disclose: Rana Wajahat, Wajahat Lodhi, Narendrakumar Alappan No Product/Research Disclosure Information

A Peculiar Case of Phosphine Toxicity

SESSION TITLE: Occupational and Environmental Lung Diseases SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: Phosphine gas is a colorless, flammable and highly toxic gas. Despite aggressive measures, phosphine gas toxicity has a very high mortality rate due to cardiopulmonary failure. We present an unusual case of aluminum phosphide toxicity who was the sole survivor in her family. CASE PRESENTATION: A 45-year-old woman with no medical problems presented to emergency room (ER) with acute onset of nausea, vomiting, diarrhea and dyspnea. Four children also presented with similar symptoms. Family was discharged with diagnosis of acute gastroenteritis. Because of worsening respiratory distress, family again presented to ER. Diagnosis of phosphine toxicity (PT) was made based on history. Husband sprayed Aluminum Phosphide (AP) rodenticide underneath the trailer about 2 weeks ago. Then he attempted to wash out the substance with water, which resulted in creation of phosphine gas. All four children passed away in the ER from severe cardiogenic shock and acute hypoxic respiratory failure from pulmonary edema. She was intubated due to worsening multi-organ failure. Bedside ultrasound showed significantly reduced ejection fraction. Patient was started on vasopressors and inotropes. Patient was taken to cath lab for emergent Impella ventricular support device. Arrangements were made to transfer patient to a tertiary care center for extracorporeal membrane oxygenation (ECMO). Patient was supported with ECMO until patient stabilized. She was discharged home in stable condition without any organ injury. She was the sole survivor of the family due to aggressive management of cardiorespiratory failure. DISCUSSION: Metallic phosphides (zinc and aluminum phosphide) are used worldwide as rodenticides and pesticides. They are banned in US so toxicity is rare here. Acute respiratory failure can occur due to pulmonary edema. Mortality often occurs from severe cardiac toxicity which leads to cardiac arrhythmias or refractory shock and cardiac failure. The cornerstone of treatment is supportive measures, which include oxygen and possible intubation for respiratory support; IVF, vasopressors for hypotension and shock. However, aggressive treatment by emergent Impella and ECMO support was necessary. CONCLUSIONS: PT is a fairly rare occurrence but remains to be a public health threat. Its high mortality rate and when the gas dissipates into the air can affect a large population. Supportive measures are the mainstay of treatment. More research needs to be conducted in order to expand knowledge of the treatment. It is strongly recommended to transfer these patients to ECMO supporting centers as they deteriorate rapidly and are unresponsive to ACLS protocol when the cardiovascular system collapses. Reference #1: Gupta S, Ahlawat SK. Aluminum phosphide poisoning--a review. J Toxicol Clin Toxicol 1995; 33:19. DISCLOSURE: The following authors have nothing to disclose: Totini Chatterjee, Omar Salh, Thien Vo, Manish Patel No Product/Research Disclosure Information

Medically Clear

Medically Clear