Pediatric Baclofen Overdose


A 16 year-old male presented to the emergency department after intentional overdose of 200 mg of baclofen. The patient was found in his bedroom by family members approximately 10 hours after ingestion with reported twitching, vomiting, unresponsiveness, and possible seizure activity. On arrival to the emergency department, the patient was awake, alert, and oriented; tearful, but otherwise asymptomatic.


Physical Exam

Vital signs included blood pressure 150/76, heart rate 112, temperature 99.2 F (37.3 C), respiratory rate 26, SpO2 97%. Physical exam showed frequent bilateral upper greater than lower extremity myoclonic jerks. The patient’s neurologic exam and physical exam were otherwise unremarkable.



The patient’s toxicological workup was pertinent for undetectable salicylate, acetaminophen, and ethanol levels. His urine drug screen was negative. EKG showed sinus tachycardia with normal QRS and QTc intervals. A head CT previously completed at an outside hospital was normal. The rest of his laboratory evaluation including CBC, electrolyte levels, and hepatic function tests, was unremarkable.



Baclofen is a centrally-acting skeletal muscle relaxant which functions as a GABA-B receptor agonist, believed to inhibit synaptic transmission of signals to the muscle from the spinal cord. Baclofen is typically prescribed for symptoms related to severe muscle spasm, such as in spinal cord injury or chronic neurologic disease (e.g. multiple sclerosis.) The medication can be administered either orally, or via an intrathecal pump.

Baclofen is absorbed rapidly from the GI tract in a dose-dependent manner, with peak serum levels occurring after ~1 hour (with a range of 0.5-4 hours). However, this has been found to be highly variable in pediatric patients. Its volume of distribution is also highly variable among pediatric patients, with nearly 50% interindividual variability. The reason for this variability is not clearly understood.

Baclofen is primarily excreted renally, with a serum half-life of 4.5 hours in pediatric patients, and a CSF half-life of 1.5 hours in intrathecal administration.

Baclofen overdose typically manifests with neurologic symptoms and dysautonomia. Symptoms are variable and may include: CNS depression/coma, hypotonia, hyporeflexia, seizure, respiratory depression, tachycardia, bradycardia, hypertension, hypotension, and arrhythmia. In adults, ingestions of >200 mg appear to correlate with an increased risk of respiratory failure, mechanical ventilation requirement, and ICU admission time.

 In an unfortunate case series, a group of teenagers overdosed on 60-600 mg of baclofen for recreational purposes. Patients displayed symptoms of overdose in 1-2 hours. 9 of 14 were intubated. Of 8 that were followed longitudinally: 7 were comatose, 6 were hypothermic, 5 were bradycardic, 4 were hypertensive, 8 were hyporeflexic, 3 had PVCs, and 2 had tonic-clonic seizures. The mean time of intubation was 40 hours. All patients recovered.



Treatment of baclofen overdose is primarily supportive with IV fluids, hemodynamic and respiratory support, and antiepileptics as needed. Activated charcoal may also be considered. There are case reports of physostigmine being effective in low/moderate overdoses; however, its use is controversial. Finally, hemodialysis does shorten clearance time and resolution of toxicity in patients with normal and impaired renal function.



Patients should be monitored until symptoms resolve. Depending on the dose ingested, the length of time since ingestion, clinical status, and laboratory analysis, they may be monitored either on the floor with telemetry or in the ICU.



The patient was treated with a 1 liter normal saline bolus and 1 mg of lorazepam IV; his hemodynamics normalized, his myoclonic twitching resolved, and he remained stable without seizure or complication throughout emergency department stay. He was admitted to the pediatric ICU for overnight monitoring, where he remained asymptomatic and had normal vital signs. The patient was then transferred to inpatient psychiatry for mental health treatment.



Baclofen overdoses typically present with a combination of altered mental status and or seizure, hypotonia, and dysautonomia. Treatment is primarily supportive and most patients recover with IV fluids, hemodynamic and respiratory support, and antiepileptics as-needed (usually benzodiazepines.) Activated charcoal should be considered. Patients should be admitted either to medical floor with telemetry or ICU depending on clinical status; they should remain admitted until symptoms resolve (typically several days, depending on ingested dose).

Faculty Reviewer: Dr. Jane Preotle 










Acetaminophen, Acetylcysteine, and Anaphylaxis With a Twist


A 15 year-old male, with a past medical history of intermittent asthma, presents with a chief complaint of diffuse abdominal pain, nausea, and two episodes of non-bloody, non-bilious emesis. His symptoms began five hours prior to arrival, and are not accompanied by diarrhea, constipation, genitourinary, urologic, or musculoskeletal symptoms. He provides limited history and appears tearful. On direct questioning, he endorses that he attempted suicide the night prior by taking a “handful of ibuprofen.” He does not know the exact number of pills, but estimates somewhere between 50 and 100, and does not know the dose strength. His mother, a clinical pharmacist, believes they were 200 mg tablets, and that there were no other pills in the house. The patient endorses feelings of depression in the prior month, and blames himself for his father having fallen off a roof (without injury) two years prior. He attends high school and is up-to-date on his vaccinations. He is a non-smoker, does not use alcohol, and endorses occasional marijuana use.  His only medication is an albuterol inhaler as needed.

Physical Exam

Initial vital signs: BP 122/82, HR 68 BPM, Temp 98.6 F, RR 20, and SpO2 100% on room air. Physical exam is notable for RUQ and LUQ tenderness without peritoneal signs. There are no scars or superficial cuts. He is tearful, but alert and oriented to person, place, and time.

Results and Management

The patient was placed on a cardiorespiratory monitor. Workup consisted of an EKG plus typical toxicologic labs, and consultation from poison control.

His EKG showed normal intervals and aVR morphology. Labs were notable for an acetaminophen level of 27 ug/mL and a slight elevation in transaminases, with AST 56 IU/L, and ALT 62 IU/L. On further questioning, the patient confessed that multiple types of pills were taken. Ingestion occurred at 2:00 AM, 14 hours prior to arrival. Given the poor history and elevated acetaminophen level, treatment based on the Rumack-Matthew nomogram (Figure 1) was felt to be beneficial.

Figure 1: Rumack-Matthew nomogram for acetaminophen ingestion.

Figure 1: Rumack-Matthew nomogram for acetaminophen ingestion.

The patient’s mother was concerned about his history of asthma, and her knowledge that NAC can cause bronchospasm; however, the benefits of treatment were felt to outweigh the risks. He was started on a standard 21-hour protocol, with a loading dose followed by two tapering doses.

Approximately one hour after the initial loading dose, the patient began to experience wheezing, a diffuse urticarial rash over the face, neck, shoulders, and thorax, and oral angioedema. He also became tachycardic. Given concern for a severe allergic reaction, bronchospasm, and possibly anaphylaxis, the infusion of NAC was held and he was treated with nebulized albuterol, IV diphenhydramine, IM epinephrine, IV normal saline, and IV corticosteroids. He was monitored in the emergency department for three hours, although his reaction resolved within 30 minutes.

Disposition and Resolution

The decision to restart NAC was considered, weighing the risk of possible anaphylaxis against the benefit of NAC to minimize potential hepatic insult. Given the low acetaminophen level, a repeat drug level and hepatic function panel were sent to inform this decision. These repeat labs came back with an undetectable acetaminophen level (now at 15 hours post-ingestion) and unchanged transaminase levels. NAC was not restarted on the basis of presumed completion of metabolism. The patient was admitted to the pediatric intensive care unit for monitoring, serial drug levels, and hepatic function panels. No further treatment was required during hospitalization. He was transferred to the psychiatry service on hospital day three for inpatient management of suicidal ideation and major depressive disorder. He did well with therapy and was discharged.

Case Discussion

This case illustrates elements of toxicity from two common over-the-counter medications, complicated by an adverse reaction to a life-saving treatment. Acetaminophen toxicity is a common emergency department phenomenon, and while ibuprofen is generally well-tolerated, it can cause toxicity at high doses.

Acetaminophen is metabolized by the liver via two pathways. First, conjugation to sulfate or glucuronide, which generates non-toxic metabolites, and second, via the CYP450 system, which generates a toxic free-radical metabolite, N-acetyl-P-benzoquinone (NAPQI).  NAPQI is neutralized by glutathione (Figure 2).

Figure 2: Acetaminophen metabolism.

Figure 2: Acetaminophen metabolism.


When acetaminophen is consumed in toxic doses, the pathways leading to nontoxic metabolites are overwhelmed and the accumulation of NAPQI depletes glutathione. In turn, the liver is unable to eliminate free oxygen radicals via glutathione, resulting in oxidative damage and mild, moderate, or fulminant liver failure if glutathione is not regenerated.

Patients are typically asymptomatic until 24-48 hours after an acute ingestion. Single doses over 150-200 mg/kg in healthy children pose significant risk of hepatotoxicity. Symptoms initially are nonspecific, with nausea, vomiting, and malaise, and can progress over a course of days to weeks to liver failure, recovery, or death. Treatment depends on the level of ingestion, the time from ingestion, and the presence of hepatic damage, but generally consists of gastric decontamination within the first hour after ingestion, oral or intravenous NAC, and supportive care. [1]

Ibuprofen, a non-steroidal anti-inflammatory drug, acts on cyclooxygenase enzymes to prevent conversion of arachidonic acid to prostaglandins and thromboxane, disrupting the gastric mucosal barrier and renal blood flow. At toxic doses, it can cause nausea, abdominal pain, gastritis, and renal failure. In severe presentations, acidosis and electrolyte disturbances are seen. The therapeutic window of ibuprofen is broad; toxicity typically does not occur until doses reach the 200-400 mg/kg range. Even in such cases, it is often mild and self-resolving with supportive care. The patient in this case likely consumed less than 100-200 mg/kg, which is unlikely to cause significant symptoms. His nausea, vomiting, malaise, and abdominal pain were likely secondary to gastric irritation from both ingestions in the early phase. [2]

NAC can be given orally or intravenously to manage acetaminophen overdose. Considerations for route depend on the severity of presentation and patient tolerance to PO medications. The duration of treatment varies by route. With IV, which was chosen for our patient due to poor PO tolerance and limited clarity around the time and quantity of ingestion, a loading dose (150 mg/kg administered over one hour) is then followed by tapered IV infusions over the next twenty hours (50 mg/kg administered over four hours, and 100 mg/kg administered over sixteen hours).

Unfortunately, NAC administration can be complicated by anaphylactoid reactions. These reactions are commonly limited to cutaneous symptoms of flushing and pruritus, with bronchospasm, angioedema, and shock occurring in <2% of patients. [3] Yarema and colleagues found in 2018 that 75.4% of anaphylactoid reactions to NAC fall within the cutaneous category. Of the total reactions observed, 95.4% of them occurred within the first five hours of treatment, which correlates with the delivery of high concentrations of drug. Female gender was associated with a more severe reaction, while higher serum acetaminophen concentrations were associated with less severe reactions. [4]

Pakravan et al further researched the mechanism of this reaction in 2008. They found that levels of serum histamine correlated with reaction severity, but that regardless of severity, there was no increase in serum tryptase or inflammatory cytokines. This suggests a non-mast-cell source of histamine and thus, a non-IgE-mediated reaction. This distinguishes the reaction from true anaphylaxis, however, the final common histaminergic pathways are similar, making clinical differentiation nearly impossible and arguments for different treatments in the initial stage largely academic. [5]

The pathophysiology of anaphylaxis and anaphylactoid reactions stems from the effect of histamine on vascular and bronchial smooth muscle leading to cutaneous vasodilation and third-spacing (hives, rash, pruritis), bronchospasm (wheezing), and reduced systemic vascular resistance (tachycardia, hypotension). Reversing this pathophysiology and providing supportive care is accomplished through intramuscular epinephrine (increases systemic vascular resistance and decreases bronchoconstriction), intravenous H1/H2 blockers (decreases vasodilation and third-spacing), nebulized beta-agonists (relieves bronchospasm), intravenous glucocorticoids (anti-inflammatory), and intravenous fluids (intravascular resuscitation, increases cardiac output). [7]

Yamamoto et al researched the frequency of occurrence as related to the treatment timeline, finding that the reaction will most commonly occur during the initial loading dose (61%), that a smaller fraction will occur over the next four hours (37%), and that the least frequent fraction occurs during the terminal taper (2%). [6]

Regardless, this anaphylactoid reaction prompts considerations about appropriate treatment and, if stopped, how and whether or not to restart the drug. The reaction itself, even when severe, typically does not necessitate cessation of therapy. A common approach to managing the reaction includes temporarily holding the infusion, initiating the normal anaphylactic countermeasures, then restarting the infusion at half of the previous rate after symptom control. Generally, the ongoing infusion is well-tolerated once histaminergic blockade is in place. This off-target effect has no effect on the critical reaction of regenerating hepatic glutathione stores. NAC is very effective at preventing fulminant hepatic failure, even in severe cases of overdose, and restarting treatment should be a high priority.

In this case, the patient’s parents refused to restart the medication given his severe reaction. He had not been previously exposed to NAC, which suggests that his reaction was likely anaphylactoid as opposed to anaphylaxis. His acetaminophen level at 14 hours had scored onto the lowest acceptable treatment line on the Rumack-Matthew nomogram and his liver function was only notable for a minimal-mild elevation in transaminases. Given the lower concern for severe toxicity, and repeat labs demonstrating an undetectable acetaminophen level with no appreciable change in hepatic function, the parents and treatment team were comfortable without restarting it in this case.

Lastly, an additional complication of NAC relates to coagulopathy. Sandilands et al reported elevations in INR in association with NAC treatment; however, an initial rise in INR, assuming it stabilizes, is not indicative of progressive liver failure. Elevations typically stabilize around an INR of 1.3, which is not concerning for increased risk of bleeding. [8]

In summary, treatment with NAC may be complicated by histamine-mediated anaphylactoid reactions, which are commonly limited to cutaneous reactions easily treated with histamine antagonists. Severe reactions may necessitate adjunct treatment from inhaled or intravenous beta-agonists, intramuscular beta-agonists, intravenous glucocorticoids, and fluids. True anaphylaxis requires previous sensitization. Unless extenuating circumstances or clinical context exist, NAC should be restarted after treating the reaction. Elevations in INR are common and do not imply liver failure unless they continue to rise.


Faculty Reviewer: Dr. Jane Preotle


  1. Farrell SE, Miller MA. Acetaminophen Toxicity. Wolters Klewer, eMedicine. Updated 22 Jan 2018. Accessed 24 Sep 2018.

  2. Wiegand TJ, Schlamovitz GZ. Nonsteroidal Anti-inflammatory Drug Toxicity. Wolters Klewer, eMedicine. Updated 20 Dec 2017. Accessed 16 Sep 2018.

  3. Blackford MG, Felter T, Gothard MD, Reed MD. Assessment of the clinical use of IV and oral NAC in the treatment of acute acetaminophen poisoning in children: a retrospective review. Clin Ther.  2011; 33(9):1322-30 (ISSN: 1879-114X)

  4. Yarema M, Chopra P, Sivilotti MLA, et. Al. Anaphylactoid Reactions to Intravenous N-Acetylcysteine during Treatment for Acetaminophen Poisoning. J Med Toxicol. 2018 Jun;14(2):120-127. Doi: 10.1007/s13181-018-0653-9.

  5. Pakravan N, Waring WS, Sharma S et. Al. Risk Factors and Mechanisms of Anaphylactoid Reactions to Acetylcysteine in Acetaminophen Overdose. J Clin Tox 2008 Jun;46:697-702.

  6. Yamamoto T, Spencer T, Dargan PL, Wood DM. Incidence and management of N-acetylcysteine-related anaphylactoid reactions during the management of acute paracetamol overdose. Eur J Emerg Med. 2014 Feb;21(1):57-60. doi: 10.1097/MEJ.0b013e328364eb22.

  7. Bailey B, McGuigan MA. Management of Anaphylactoid reactions to IV N-acetylcysteine. Ann Emerg Med. 1998 Jun;31(6):710-5.

  8. Sandilands EA, Bateman DN. Adverse reactions associated with acetylcysteine. Clin Toxicol (Phila). 2009 Feb;47(2):81-8.

Tough on Stains... and on Bodies

The Case

Figure 1: :Laundry Detergent Pod  By  Soulbust  - Own work, CC BY-SA 4.0,

Figure 1: :Laundry Detergent Pod

By Soulbust - Own work, CC BY-SA 4.0,

A previously healthy 12-month-old male was brought to the Emergency Department by his parents 20 minutes after ingesting a laundry detergent pod. The patient’s mother reported finding the child with pieces of the lining of an ALL Mighty Pacs detergent pod in his mouth. She removed the pieces and noted the packet was empty of liquid. At that point, the child started gagging and vomiting “almost immediately.” En route to the ED the patient had 2-3 more episodes of clear emesis. On arrival, he continued to have non-bloody, non-bilious emesis and dry heaves. Vitals were within normal limits with oxygen saturations in the mid 90s. On exam, the child was noted to have a hoarse voice and was mildly somnolent but easily arousable. He was drooling and crying in pain with swallowing, but his oropharynx was otherwise clear. Stridor was noted as well as suprasternal, substernal and supraclavicular retractions. The child was given Zofran, a 20cc/kg fluid bolus and decadron. ENT was consulted for increasing stridor and upper airway symptoms. The patient underwent nasopharyngeal scope at beside and was found to have mild vocal cord edema. He was taken emergently to the OR for definitive airway and bronchoscope. GI was also consulted for endoscopy. 


In the OR the child was intubated and underwent formal bronchoscopy and endoscopy. Significant findings included:

  1. Watery edema of the supraglottic structures
  2. Mild mucosal changes in the proximal esophagus
  3. Somewhat nodular proximal esophagus with patchy edema and mild sloughing of the mucosa (Fig 1. a, b, c)
  4. Mild patchy sloughing and nodularity distally
  5. One small erosion in the stomach
  6. Normal duodenum
  7. Congenital laryngomalacia and elliptical cricoid consistent with congenital subglottic stenosis

Detergent Pods

Laundry detergent “pods” or “packets” are small, often colorful, dissolvable packs containing concentrated laundry detergent. These laundry capsules have been in Europe since 2001, but were introduced to United States markets in 2010. [1] Laundry pods have been identified as a threat to pediatric patients who are often attracted to the candy-like appearance of the pods. The most common route of toxicity is via ingestion in patients younger than 5 years of age.[2] Recently, however, teenagers have become a significant percentage of the patient population via the “Tide Pod Challenge,” a viral, social-media campaign that dares teens to eat the pods. Detergent pods are often packaged in soft linings that consist of a water-soluble polyvinyl alcohol membrane that easily dissolves when exposed to saliva or moist skin.[3] The liquid mixture inside is usually composed of an anionic and a nonionic detergent as well as a cationic surfactant. All contain irritants and some brands also contain alkaline substances.[4] The alkaline nature of detergent pods can cause inflammation and mucosal destruction in the oropharynx, larynx and esophagus.[5]

Ingestion of detergent pods is associated with more severe symptoms than traditional laundry detergent.[6] One explanation for this is the concentrated nature of the detergent pack and the ingredients, which may include propylene glycol and ethoxylated alcohols.[7] Propylene glycol is found in great proportion in detergent packets than in typical detergent formulations.[8] It is not clear exactly how detergent pods cause injury, but there are several explanations.[9] When ingested, propylene glycol is metabolized by the liver to form lactate, acetate and pyruvate. The increased lactate results in a metabolic acidosis. The drug is excreted in the urine, but at higher doses of propylene glycol the renal tubules ability to secrete the drug is impaired. In children, propylene glycol remains in the blood longer than in adults, which results in more toxic effects, such as renal failure and CNS depression. Another important ingredient in laundry pods is ethoxylated alcohols, which can cause sedative effects. Lethargy is a unique feature of pod ingestion that is not seen with less concentrated detergent formulations.[10]

Ingredient Proposed Effect Clinical Manifestation
Alkalinity Inflammation and damage to oral, laryngeal and esophageal mucosa Hoarse Voice, Dysphagia, Drooling, Stridor, Respiratory Distress
Multiple Noxious response Nausea, vomiting, diarrhea
Propylene glycol Conversion to lactic acid and impaired renal clearance CNS Depression, Metabolic acidosis, Renal insufficiency
Phosphates Caustic Rash, Burns


In the case of any suspected ingestion local poison control should be contacted for advice. Management efforts should initially focus on stabilizing airway, breathing and circulation. If eyes are involved, copious irrigation should begin as soon as possible, as delayed irrigation may be associated with increased morbidity, including burns.[11] Any contaminated clothing should be removed. Activated charcoal, whole bowel irrigation, or gastric lavage is not indicated in the treatment of alkaline ingestions such as detergents.[12] Charcoal and whole bowel irrigation has not been shown to have an effect. Gastric lavage is contraindicated due to risk of perforation and aspiration.[13]

The most important aspects of management are supportive care and symptom control. It is necessary to monitor for respiratory failure and depressed mental status, which may lead to the need for mechanical ventilation. Steroids have been used to mitigate airway edema, but studies have not confirmed their utility.[14] Zofran and other anti-emetics are useful for nausea and vomiting. Fluids should be administered for metabolic derangements or losses secondary to emesis. Endoscopy is important for injury staging and can help to risk stratify patients, however, many complications are delayed. Esophageal stricture is a rare, but possible, long-term sequela.[15]

Case Conclusion

The patient was admitted to the pediatric ICU for further care and management. On hospital day 1 frothy secretions were noted to be draining from his endotracheal tube. He was treated with Lasix for pulmonary edema and had improvement. Decadron was continued for a total of 4 doses of 0.5mg/kg. Feeds were given via NG tube. On hospital day 2 the child underwent repeat endoscopy to monitor for possible progression of mucosal damage. On hospital day 3 he was successfully extubated. Prior to discharge the patient was tolerating a regular pediatric diet with instructions to avoid acidic foods and juices. On hospital day 4 the child was discharged with ENT and GI follow-up. He was instructed to take omeprazole daily for 4-6 weeks

Faculty Reviewer: Dr. Jane Preotle


[1] Celentano A, Sesana F, Settimi L, Milanesi G, Assisi F, Bissoli M, Borghini R, Della Puppa T, Dimasi V. Accidental exposures to liquid detergent capsules. SKIN. 2012 May 25;5:0-9.

[2] Stromberg PE, Burt MH, Rose SR, Cumpston KL, Emswiler MP, Wills BK. Airway compromise in children exposed to single-use laundry detergent pods: a poison center observational case series. The American journal of emergency medicine. 2015 Mar 1;33(3):349-51.

[3] Bonney AG, Mazor S, Goldman RD. Laundry detergent capsules and pediatric poisoning. Canadian family physician. 2013 Dec 1;59(12):1295-6.

[4] Fraser L, Wynne D, Clement WA, Davidson M, Kubba H. Liquid detergent capsule ingestion in children: an increasing trend. Archives of disease in childhood. 2012 Aug 1:archdischild-2012.

[5] Zargar SA, Kochhar R, Nagi B, Mehta S, Mehta SK. Ingestion of strong corrosive alkalis: spectrum of injury to upper gastrointestinal tract and natural history. American Journal of Gastroenterology. 1992 Mar 1;87(3).

[6] Valdez AL, Casavant MJ, Spiller HA, Chounthirath T, Xiang H, Smith GA. Pediatric exposure to laundry detergent pods. Pediatrics. 2014 Nov 10:peds-2014.

[7] Beuhler MC, Gala PK, Wolfe HA, Meaney PA, Henretig FM. Laundry detergent “pod” ingestions: a case series and discussion of recent literature. Pediatric emergency care. 2013 Jun 1;29(6):743-7.

[8] Shah LW. Ingestion of Laundry Detergent Packets in Children. Critical care nurse. 2016 Aug 1;36(4):70-5.

[9] Huntington S, Heppner J, Vohra R, Mallios R, Geller RJ. Serious adverse effects from single-use detergent sacs: Report from a US statewide poison control system. Clinical toxicology. 2014 Mar 1;52(3):220-5.

[10] Shah LW. Ingestion of Laundry Detergent Packets in Children. Critical care nurse. 2016 Aug 1;36(4):70-5.

[11] Haring RS, Sheffield ID, Frattaroli S. Detergent Pod–Related Eye Injuries Among Preschool-Aged Children. JAMA ophthalmology. 2017 Mar 1;135(3):283-4.

[12] Riordan M, Rylance G, Berry K. Poisoning in children 4: household products, plants, and mushrooms. Archives of disease in childhood. 2002 Nov 1;87(5):403-6.

[13] McGregor T, Parkar M, Rao S. Evaluation and management of common childhood poisonings. American family physician. 2009 Mar 1;79(5).

[14] Anderson KD, Rouse TM, Randolph JG. A controlled trial of corticosteroids in children with corrosive injury of the esophagus. New England Journal of Medicine. 1990 Sep 6;323(10):637-40.

[15] Smith E, Liebelt E, Nogueira J. Laundry detergent pod ingestions: is there a need for endoscopy?. Journal of medical toxicology. 2014 Sep 1;10(3):286-91.