Publications (17)12.83 Total impact
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Article: 2C or Not 2C: Phenethylamine Designer Drug Review.
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ABSTRACT: New groups of synthetic "designer drugs" have increased in popularity over the past several years. These products mimic the euphoric effects of other well-known illicit drugs but are advertised as "legal" highs and are sold over the internet, at raves and night clubs, and in head shops. The 2C series drugs are ring-substituted phenethylamines that belong to a group of designer agents similar in structure to 3,4-methylenedioxy-N-methylamphetamine (MDMA, Ecstasy). Understanding the pharmacology and toxicology of these agents is essential in order to provide the best medical care for these patients. This review focuses on the pharmacology, pharmacokinetics, clinical effects, and treatment of 2C drug intoxication based on available published literature. Multiple names under which 2C drugs are sold were identified and tabulated. Common features identified in patients intoxicated with 2Cs included hallucinations, agitation, aggression, violence, dysphoria, hypertension, tachycardia, seizures, and hyperthermia. Patients may exhibit sympathomimetic symptoms or symptoms consistent with serotonin toxicity, but an excited delirium presentation seems to be consistent amongst deaths attributed to 2C drugs; at least five deaths have been reported in the literature in patients intoxicated with 2C drugs. 2C drugs are a group of designer intoxicants, many of which are marketed as legal, but may carry risks that consumers are unaware of. These drugs may be characterized by either serotonergic toxicity or a sympathomimetic toxidrome, but a presentation consistent with excited delirium is consistent amongst the reported 2C-related deaths. Treatment of 2C intoxication is primarily supportive, but immediate action is required in the context of excited delirium, hyperthermia, and seizure activity.Journal of medical toxicology: official journal of the American College of Medical Toxicology 03/2013; -
Article: A Life-Threatening Flecainide Overdose Treated with Intravenous Fat Emulsion.
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ABSTRACT: Flecainide is a Vaughan Williams Class Ic antidysrhythmic associated with PR, QRS, and QTc prolongation on the electrocardiogram and development of life-threatening cardiac toxicity in overdose. The cornerstone of treatment is fluid resuscitation and the administration of magnesium and sodium bicarbonate. We report a case of flecainide overdose associated with life-threatening hemodynamic compromise successfully treated with intravenous fat emulsion (IFE) therapy. IFE should be considered as a novel adjunctive therapy in patients with life-threatening toxicity following flecainide overdose. (PACE 2012;00:1-3).Pacing and Clinical Electrophysiology 08/2012; · 1.35 Impact Factor -
Article: Response to "the first published case of a pediatric diphenhydramine overdose whose electrocardiogram shows terminal 40-millisecond frontal plane QRS axis deviation".
Pediatric emergency care 08/2012; 28(8):833. · 0.92 Impact Factor -
Article: Which Xenobiotic(s) Could be Responsible for the Radiologic Findings Below?
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ABSTRACT: BackgroundThe proconvulsive properties of tramadol, bupropion, and nortriptyline have been well documented. Spinal fractures secondary to drug-induced seizures have been rarely reported. Case ReportA 39-year-old female presented with a chief complaint of back pain. She went to bed feeling well in a separate room from her husband. During the previous night, he heard a noise and went into her room, finding her confused and twisted in an awkward position on her bed. Later she complained to him of severe back pain, prompting transport to a hospital. Shortly after arrival in the emergency department, staff witnessed a generalized convulsion. Following a one-hour post-ictal period, she complained of worsened back pain. Lab studies were normal, including a urine tox screen for drugs of abuse. No alcohol was implicated. ECG showed sinus rhythm, HR 113 beats/min, QRS 108 ms, QTc 389 ms. Brain magnetic resonance imaging (MRI) was normal. X-ray and an MRI of the thoracic spine confirmed four contiguous vertebral compression fractures, from T2 through T5. EEG showed diffuse changes consistent with a metabolic or toxicologic process. She denied taking any drugs other than prescribed doses of her medications, which included tramadol, bupropion, and nortriptyline. She had no previous history of seizures, head injury, or CVA. Bupropion and tramadol were discontinued, and seizures did not recur. Case DiscussionThis patient's history, EEG findings, and brain imaging all point to a metabolic or toxic cause. It is likely that her three proconvulsant medications—even at therapeutic doses—synergistically lowered her seizure threshold or even precipitated her seizures. Retrospective studies and case reports portray these drugs as potentially offending agents. ConclusionsSudden onset of back pain during sleep can be an important clue to a seizure complicated by vertebral compression fractures, even in the absence of trauma. Toxicology consultation in seizures of unclear etiology can help discern drugs that offend even in therapeutic doses. KeywordsProconvulsant-Bupropion-Vertebral compression fractureJournal of medical toxicology: official journal of the American College of Medical Toxicology 04/2012; 6(1):72-73. -
Article: Massive atropine eye drop ingestion treated with high-dose physostigmine to avoid intubation.
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ABSTRACT: CASE: A 34-year-old male presented after ingesting 150 mg of atropine. He had altered mental status, sinus tachycardia, dry mucosa, flushed skin, and hyperthermia. Sequential doses of physostigmine, totaling 14 mg, were successful in reversing antimuscarinic toxicity and prevented the need to perform airway control with endotracheal intubation. At completion of treatment, heart rate and mental status had improved, and intubation was never performed. DISCUSSION: Atropine causes anticholinergic toxicity; physostigmine reverses this by inhibiting acetylcholinesterase. Atropine eye drop ingestions are rare. The 14 mg of physostigmine administered is much higher than typical dosing. It is likely the physostigmine prevented intubation. Atropine eye drops can be dangerous, and physostigmine should be considered in treatment.The western journal of emergency medicine 02/2012; 13(1):77-9. -
Article: Wide complex tachycardia in a pediatric diphenhydramine overdose treated with sodium bicarbonate.
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ABSTRACT: Diphenhydramine is an antihistamine commonly implicated in overdose. It has many pharmacologic effects, including sodium channel blockade. Overdoses in toddlers causing QRS prolongation are only rarely reported and never with effective use of sodium bicarbonate. We report a diphenhydramine overdose in a toddler with multiple markers of sodium channel blockade effectively treated with sodium bicarbonate. A 13-month-old infant girl was brought in by the emergency medical service for a witnessed tonic-clonic seizure. Two hours previously, the child had been found with an open bottle of 25-mg diphenhydramine tablets, 24 of which were missing. Midazolam was administered with seizure resolution. Examination revealed 4-mm reactive pupils; nystagmus; warm, dry, flushed skin; and altered mental status. Initial electrocardiograms revealed sinus tachycardia at a rate of 180 beats per minute, a prolonged QRS of 130 milliseconds (from a baseline of 65 milliseconds), and a positive terminal R wave in aVR, which later resolved after sodium bicarbonate treatment. The patient was discharged home the following day with no sequelae. Diphenhydramine toxicity is a common poisoning in children. Toxicity typically presents with signs and symptoms of the anticholinergic toxidrome. Diphenhydramine also has sodium channel-blocking properties, and this can be shown in the form of prolonged QRS and a terminal R wave in aVR. QRS prolongation and aVR abnormalities from diphenhydramine ingestion in a toddler have been reported, but effective use of sodium bicarbonate has not. Electrocardiographic finding consistent with sodium channel blockade should be recognized as a complication of pediatric diphenhydramine overdose, and they seem responsive to hypertonic sodium bicarbonate.Pediatric emergency care 12/2011; 27(12):1175-7. · 0.92 Impact Factor -
Article: Response to Letter to the Editor on Article: Stellpflug SJ, Fritzlar SJ, Cole JB, Engebretsen KM, Holger JS. Cardiotoxic Overdose Treated with Intravenous Fat Emulsion and High-dose Insulin in the Setting of Hypertrophic Cardiomyopathy. J Med Toxicol 2011; 7(2):151-3.
Journal of medical toxicology: official journal of the American College of Medical Toxicology 08/2011; -
Article: High-dose insulin: a consecutive case series in toxin-induced cardiogenic shock.
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ABSTRACT: Cardiovascular medication overdoses can be difficult to treat. Various treatment modalities are currently recommended. To describe patient outcomes and adverse events of high-dose insulin therapy in consecutive overdose patients in cardiogenic shock after implementation of a high-dose insulin protocol (1-10 U/kg/h, while avoiding or tapering off vasopressors). This is an observational consecutive case series of patients identified from a registry. Data were collected by retrospective chart review of patients treated by our toxicology service with this protocol from February 2007 until March 2010. Twelve patients were treated with high-dose insulin. The mean age was 36.5 years (SD 11.7). Seven patients had pre-existing vasopressor therapy, and all were tapered off vasopressors while on insulin. Two patients experienced pulseless electrical activity cardiac arrest prior to high-dose insulin therapy. Intravenous fat emulsion was given to two patients. The mean maximum insulin infusion rate was 8.35 U/kg/h (mean = 8.35, SD 6.34). The mean duration of insulin infusion was 23.5 h (SD 19.7). The mean duration of glucose infusion post-insulin was 25.2 h (SD 17.7). The primary toxins were β-blocker in five, calcium channel blocker in two, combined β-blocker/calcium channel blocker in two, tricyclic antidepressant in one, and polydrug in 2. CLINICAL OUTCOMES: Eleven of 12 patients survived. One patient expired 9 h into insulin therapy from cardiac arrest shortly after the insulin was stopped and a vasopressor re-initiated (protocol deviation). ADVERSE EVENTS: Six patients experienced a total of 19 hypoglycemic events. Hypokalemia (defined as < 3.0 mEq/L) developed in eight patients. ADVERSE SEQUELAE: Necrotic digits occurred in one patient with known clotting disorder after receiving high-dose norepinephrine and INR reversal with fresh frozen plasma prior to insulin therapy. One patient was discharged with mild anoxic injury thought due to pulseless electrical activity arrest prior to insulin therapy. Three of these 12 patients have been previously described in published case reports. High-dose insulin therapy based on a 1-10 U/kg/h dosing guideline and recommending avoidance of vasopressors appears to be effective in the treatment of toxin-induced cardiogenic shock. Hypoglycemia was the most frequent adverse event, followed by hypokalemia. Adverse events did not lead to adverse sequelae.Clinical Toxicology 08/2011; 49(7):653-8. · 2.22 Impact Factor -
Article: What toxicity may result from the xenobiotic responsible for the finding on this plain film? Answer: reduced iron, found in heating pads and instant hand warmers, may result in elevated serum iron concentrations and subsequent iron toxicity.
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ABSTRACT: Disposable heating pads are commonly used products, with reduced iron as their active ingredient. Reduced iron is not expected to cause significant toxicity when ingested orally. We report a case of accidental heating pad ingestion seen on abdominal plain films that resulted in significantly elevated serum iron concentrations.Journal of medical toxicology: official journal of the American College of Medical Toxicology 08/2011; 7(4):327-8. -
Article: Reversal of quetiapine-induced altered mental status with physostigmine: a case series.
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ABSTRACT: Quetiapine overdose is a clinical entity commonly encountered in emergency departments. Quetiapine is a drug with many mechanisms, including antimuscarinic effects. Traditionally, treatment of quetiapine toxicity has been primarily supportive care. Case reports exist documenting improvement in mental status in these patients after administration of physostigmine, a carbamate capable of reversing antimuscarinic toxicity. In this descriptive case series, 3 patients with quetiapine toxicity treated with physostigmine are reported. In each case, the patient had significant altered mental status that was rapidly reversed with administration of physostigmine. In all 3 cases, patient disposition was changed to a lower level of care, requiring less invasive monitoring. In 1 case, intubation was prevented. Because quetiapine toxicity is commonly encountered and the use of physostigmine in this setting is a potentially practice-altering treatment, emergency physicians should be aware of this phenomenon.The American journal of emergency medicine 07/2011; 30(6):950-3. · 1.54 Impact Factor -
Article: Unique configuration of the four-lumen oesophagogastric tamponade tube (Minnesota tube) for the control of massive upper GI bleeding.
Emergency Medicine Journal 06/2011; 28(10):908. · 1.44 Impact Factor -
Article: Transaminitis: the lab test that has inflammation….
Journal of medical toxicology: official journal of the American College of Medical Toxicology 06/2011; 7(3):252-3. -
Article: Cardiotoxic overdose treated with intravenous fat emulsion and high-dose insulin in the setting of hypertrophic cardiomyopathy.
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ABSTRACT: High-dose insulin (HDI) and intravenous fat emulsion (IFE) are used in overdoses, although rarely combined. To our knowledge, IFE therapy has not been reported in overdoses of diltiazem, metoprolol and amiodarone. We report a severe overdose of these drugs treated with HDI and IFE in a patient with hypertrophic cardiomyopathy (HCM). We also discuss the potential clinical implications of the inotropic effects of HDI in the setting of HCM and the use and efficacy of IFE in this overdose.Journal of medical toxicology: official journal of the American College of Medical Toxicology 12/2010; 7(2):151-3. -
Article: Addition of phenylephrine to high-dose insulin in dihydropyridine overdose does not improve outcome.
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ABSTRACT: Vasopressors are commonly used for calcium channel blocker (CCB)-induced cardiogenic shock after calcium and high-dose insulin (HDI). Vasopressor therapy is frequently used in combination with HDI to increase blood pressure and improve outcome. However, no studies have compared the efficacy of HDI to the combination of a vasopressor and HDI in dihydropyridine overdose. We conducted a study to compare the efficacy of HDI to phenylephrine (PE) plus HDI in a porcine model of dihydropyridine toxicity. Cardiogenic shock was induced by administering a nifedipine (NP) infusion of 0.0125 mcg/kg/min until a point of toxicity, defined as a 25% decrease in the baseline product of mean arterial pressure (MAP) × cardiac output (CO). Each arm was resuscitated with 20 mL/kg of saline (NS). The nifedipine infusion continued throughout a 4-h resuscitation protocol. The HDI group was titrated up to 10 units/kg/h of insulin and the HDI/PE group was titrated up to a dose of HDI 10 units/kg/h plus PE 3.6 mcg/kg/min. No baseline differences were found among groups including time to toxicity. Survival was not different between the HDI and HDI/PE arms. When comparing the HDI to the HDI/PE arm no differences were found for cardiac index (CI) (p = 0.06), systemic vascular resistance (p = 0.34), heart rate (HR) (p = 0.95), mean arterial pressure (p = 0.99), pulmonary vascular resistance (PVR) (p = 0.07), or base excess (p = 0.36). In this model of nifedipine-induced cardiogenic shock, the addition of PE to HDI therapy did not improve mortality, cardiac output, blood pressure, systemic vascular resistance (SVR), or base excess.Clinical Toxicology 10/2010; 48(8):806-12. · 2.22 Impact Factor -
Article: "I Shouldn't Have Had Dessert..." A Moonflower Seed Ingestion.
The western journal of emergency medicine 05/2010; 11(2):213. -
Article: Which xenobiotic(s) could be responsible for the radiologic findings below? Answer: any proconvulsant xenobiotic, in this case tramadol, bupropion, and nortriptyline.
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ABSTRACT: The proconvulsive properties of tramadol, bupropion, and nortriptyline have been well documented. Spinal fractures secondary to drug-induced seizures have been rarely reported. A 39-year-old female presented with a chief complaint of back pain. She went to bed feeling well in a separate room from her husband. During the previous night, he heard a noise and went into her room, finding her confused and twisted in an awkward position on her bed. Later she complained to him of severe back pain, prompting transport to a hospital. Shortly after arrival in the emergency department, staff witnessed a generalized convulsion. Following a one-hour post-ictal period, she complained of worsened back pain. Lab studies were normal, including a urine tox screen for drugs of abuse. No alcohol was implicated. ECG showed sinus rhythm, HR 113 beats/min, QRS 108 ms, QTc 389 ms. Brain magnetic resonance imaging (MRI) was normal. X-ray and an MRI of the thoracic spine confirmed four contiguous vertebral compression fractures, from T2 through T5. EEG showed diffuse changes consistent with a metabolic or toxicologic process. She denied taking any drugs other than prescribed doses of her medications, which included tramadol, bupropion, and nortriptyline. She had no previous history of seizures, head injury, or CVA. Bupropion and tramadol were discontinued, and seizures did not recur. CASE DISCUSSION: This patient's history, EEG findings, and brain imaging all point to a metabolic or toxic cause. It is likely that her three proconvulsant medications--even at therapeutic doses--synergistically lowered her seizure threshold or even precipitated her seizures. Retrospective studies and case reports portray these drugs as potentially offending agents. Sudden onset of back pain during sleep can be an important clue to a seizure complicated by vertebral compression fractures, even in the absence of trauma. Toxicology consultation in seizures of unclear etiology can help discern drugs that offend even in therapeutic doses.Journal of medical toxicology: official journal of the American College of Medical Toxicology 03/2010; 6(1):72-3. -
Article: Intentional overdose with cardiac arrest treated with intravenous fat emulsion and high-dose insulin.
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ABSTRACT: Nebivolol, a beta blocker with 3-10 times more beta1 cardioselectivity than metoprolol, has caused hypotension and bradycardia in overdose. We report a nebivolol-induced cardiac arrest in the setting of a polydrug ingestion, successfully resuscitated with intravenous fat emulsion (IFE) and high-dose insulin (HDI). A 48-year-old man was brought to the emergency department after ingesting nebivolol and ethanol, along with possibly diazepam and cocaine. He had a heart rate of 71/min and a blood pressure of 98/61 mmHg. The initial ECG showed sinus rhythm with a QTc of 483 ms and a QRS of 112 ms. Over the subsequent 4 h, he became bradycardic and hypotensive and developed bradyasystolic cardiac arrest. Standard resuscitation including epinephrine had no effect. Spontaneous circulation returned 30 s after a 100 mL bolus of 20% IFE, and the patient then became briefly hypertensive and tachycardic with heart rate and blood pressure measured as high as 123/min and 251/162 mmHg, respectively. His care included IFE infusion along with HDI bolus and infusion with doses as high as 21.8 units/kg/h. With subsequent hypotension, vasopressors were withheld in favor of HDI and supportive care. He was discharged with baseline neurologic function. We hypothesize that after the administration of IFE the epinephrine was able to exert its effect on receptors previously occupied with the nebivolol. This would be congruent with the lipid sink theory of IFE mechanism. We report an overdose involving nebivolol in a polydrug ingestion resulting in cardiac arrest, successfully treated with IFE and a very HDI infusion.Clinical Toxicology 02/2010; 48(3):227-9. · 2.22 Impact Factor
Top co-authors
Top Journals
Institutions
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2010–2012
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Regions Hospital
Saint Paul, MN, USA
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2011
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Miami County Emergency Medical Services
Miami, FL, USA
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2010–2011
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HealthPartners Institute for Education and Research
Bloomington, MN, USA
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