The Tox Cave
The Tox Cave will dissect interesting ED cases from the perspective of a toxicologist, focusing on applying up-to-date management of the poisoned patient.
The name Tox Cave was coined by a former toxicology fellow to describe our small office space, likening it to the Bat Cave. The Tox Cave is where Drexel toxicology fellows and attendings have gathered to discuss the nuances of toxicology over the years.
Monday, November 02, 2015
A 21-year-old woman presented with a sore throat, low-grade fever, body aches, swollen glands, and generalized malaise for three days. The patient said her symptoms had worsened over the past day. She denied any difficulty breathing but endorsed pain and difficulty swallowing.
Her initial vital signs were blood pressure 132/84 mm Hg, heart rate 113 bpm, respiratory rate 22 bpm, temperature 100.4°F, and pulse oximetry 100% on room air. She was diagnosed with a peritonsillar abscess, and the EP applied a topical anesthetic to the area prior to draining it. During the procedure, the patient’s pulse oximetry dropped to 85%, heart rate increased to 124, and respiratory rate increased to 28. The patient appeared cyanotic, and was diagnosed with methemoglobinemia from benzocaine spray
Thursday, October 01, 2015
John Nakamura Remy
A 30-year-old woman presented with altered mental status. Her boyfriend reported that she took a handful of unknown pills about two hours before. Initial vital signs include a temperature of 38°C, heart rate of 130 beats/min, respiratory rate of 18 breaths/min, blood pressure of 112/83 mm Hg, and pulse oximetry of 97% on room air.
Her physical exam is significant for pupils 6 mm bilaterally and reactive to light, dry mucous membranes and skin, and decreased bowel sounds. She was alert but confused. Her initial ECG showed a sinus tachycardia with a rate of 133 and a QRS of 89 and QTc of 443.
The differential diagnosis in this patient includes:
n Anticholinergic (antihistamines, TCA, phenothiazines)
n Sympathomimetic agents (amphetamines, caffeine, cocaine, PCP)
n Salicylate toxicity
n Sedative/hypnotic withdrawal
A single therapeutic adult dose of diphenhydramine ranges from 25 to 100 mg every six hours. Manifestations of toxicity may occur after ingestion of three to five times the daily dose. The fatal oral dose is estimated to be between 20 to 40 mg/kg.
Radovanovic et al. analyzed the dose-dependent toxicities associated with diphenhydramine in a retrospective analysis of 232 diphenhydramine intoxications followed by a prospective analysis of 50 patients. It demonstrated that a critical ingestion limit of 1,000 mg was necessary to produce severe symptoms (delirium/psychosis, seizures and coma), but cardiac abnormalities developed at doses of 400 mg and 500 mg. (Hum Exp Toxicol 2000;19:489.)
Sedation is a common adverse effect of diphenhydramine that may be observed in therapeutic and overdose settings. CNS stimulation may be more common in children and young adults than the CNS sedation observed in older adults. Patients may also present with symptoms of the anticholinergic toxidrome as a result of central and peripheral antimuscarinic activity: mydriasis, flushed and dry skin, fever/hyperthermia, tachycardia, delirium, hypoactive bowel sounds, and urinary retention. Seizures and status epilepticus may occur in more severe manifestations of anticholinergic activity. Rhabdomyolysis has also been reported, which may be caused by a primary drug-induced rhabdomyolysis or a secondary rhabdomyolysis resulting from compression of muscle compartments while unresponsive or muscular hyperactivity (psychomotor agitation or seizures). Compartment syndrome requiring fasciotomies has also been reported.
Cardiac manifestations of diphenhydramine toxicity consist mainly of tachycardia associated with hypertension or hypotension. Higher concentrations have been shown to cause a prolonged QT interval. A prolonged QT interval is thought to be the result of modulation of IKr and HERG1 potassium channels. Massive ingestions have been reported to inhibit fast sodium channels producing a prolonged QRS on the ECG, and associated myocardial depression with refractory hypotension. Cases of torsades de pointes, bundle branch blocks, and AV dissociation have also been reported. Delayed or prolonged toxicity from this drug, as well as co-ingestants, may also occur because this anticholinergic medication has the potential to delay gut motility. Diphenhydramine cross-reacts in some of the standard urine drug immunoassays to produce a false positive result for antidepressants (TCA) and phencyclidine (PCP).
The workup of a patient with suspected diphenhydramine toxicity should include an ECG, a serum acetaminophen level (diphenhydramine is often found in combination products), and creatine kinase.
Patients should be placed on a continuous cardiac monitor. Antidotal therapy with physostigmine may be used in patients with severe delirium or tachycardia. One retrospective study compared the efficacy of physostigmine and benzodiazepines for treating anticholinergic poisoning. (Ann Emerg Med 2000;35:374.) They found physostigmine controlled agitation and reversed delirium in 96 percent and 87 percent of patients, respectively, compared with benzodiazepines, which controlled agitation in 24 percent of patients and was ineffective for delirium. Caution is advised for patients with a history of seizure or intraventricular conduction delay, however. Sodium bicarbonate (1-2 mEq IV) may be used for QRS-interval prolongation and myocardial depression. Lipid emulsion therapy has been used in cases of severe toxicity because diphenhydramine is lipid-soluble.
Our patient became progressively agitated with worsening delirium, and her repeat ECG demonstrated a sinus tachycardia. The patient was noted to be picking at things in the air in front of her. She was administered 1 mg of physostigmine IV over five minutes, and her vitals stabilized and her delirium cleared within 10 minutes. She reported that she had gotten into a fight with her boyfriend, and had ingested a handful of diphenhydramine. The patient was admitted for further observation.
1. Vearrier D, Curtis JA. Case Files of the Medical Toxicology Fellowship at Drexel University. J Med Toxicol 7.3 2011;7(3):213.
2. Abdi A, Rose E, Levine M. "Diphenhydramine Overdose with Intraventricular Conduction Delay Treated with Hypertonic Sodium Bicarbonate and IV Lipid Emulsion. West J Emerg Med 2014;15(7):855.
3. Thakur AC, Aslam AK, et al. QT interval prolongation in diphenhydramine toxicity. Int J Cardiol 2005;98(2):341.
Tuesday, September 01, 2015
The parents of a 16-month-old boy who presented to the ED were concerned that he was too sleepy. His initial point-of-care glucose was noted to be 42 mg/dL, and he was somnolent but arousable, and was given orange juice.
Twenty minutes later, the child’s symptoms had completely resolved. Toxicology was consulted for evaluation of a possible toxic ingestion, and a medication inventory was recommended.
Differential Diagnosis of Hypoglycemia in Children
n Ethanol intoxication
n Beta blocker intoxication
n Salicylate toxicity
n Insulin injection
n Endocrine disorder (hypopituitarism, Addison’s disease, myxedema)
n Hepatic or metabolic disease
n Unripe ackee fruit
Two hours later, the patient became lethargic again, and a repeat blood glucose was 55 mg/dL. Again, he was arousable, and treated with orange juice and 5 ml/kg of 10% dextrose in water.
Further history revealed that the father is prescribed metoprolol, glipizide, lisinopril, and atorvastatin. The mother does not take any medications, and the only over-the-counter medications in the house are acetaminophen and ibuprofen.
Because of the rebound hypoglycemia after glucose administration and the lack of other findings, we were concerned that the child had ingested glipizide, a sulfonylurea.
What is a Sulfonylurea?
Sulfonylureas are used for treating type 2 diabetes mellitus. They were accidently discovered in World War II when sulfonamides, which were used to treat typhoid fever, were found to cause hypoglycemia. Second-generation sulfonylureas — glyburide, glipizide, glimepiride, and gliclazide — were created in the 1970s, and are the medications in use today.
Sulfonylureas exert their effects on pancreatic beta cells by inhibiting potassium efflux from the cell, leading to depolarization and increased calcium influx into the cell. The increase in intracellular calcium causes insulin secretion via exocytosis.
The second-generation sulfonylureas are rapidly absorbed, and peak serum concentrations are reached in two to four hours. They are primarily metabolized by the liver and excreted by the kidney. Their duration of action is 12-24 hours, and they can be markedly increased in overdose or in those patients with renal failure.
Antidote for Sulfonylurea Poisoning
Octreotide is a long-acting synthetic analog of somatostatin, an endogenous hormone, which suppresses insulin release from beta cells. It binds to the somatostatin receptors and inhibits calcium influx into the cell, leading to hyperpolarization of the cell and decreased insulin secretion from pancreas. Octreotide also inhibits the secretion of glucagon, growth hormone, and gastrin.
Octreotide can be administered subcutaneously (SC) or intravenously (IV). Octreotide has a bioavailability of 100% with peak serum concentrations achieved in 15-30 minutes. The elimination half-life is 88-100 minutes. The dose of octreotide is 1 mcg/kg SC or IV every six hours in children and 50 mcg every six hours in adults. Administration of octreotide should be discontinued when serum glucose levels have stabilized and the glucose infusion can be tapered off. Serum glucose concentrations should be monitored every hour during treatment, and patients should be observed for rebound hypoglycemia for at least 24 hours after the last dose of octreotide.
Should the hypoglycemia be treated with glucagon? Glucagon raises the blood glucose by glycogenolysis, and this makes it efficacy-dependent on the hepatic glycogen stores that can be depleted in patients with prolonged hypoglycemia. Glucagon is short-acting and its effects peak within 30 minutes. The half-life of glucagon is 20 minutes, so a single dose of glucagon would be minimally effective in sulfonylurea-induced hypoglycemia with a potential to cause rebound hypoglycemia.
Managing Sulfonylurea Ingestion
Asymptomatic patients who present with sulfonylurea ingestion should have a point-of-care glucose completed, must be continuously monitored for any hypoglycemic sequelae, and must receive a basic metabolic panel to evaluate renal function.
Hypoglycemic patients should receive a dose of IV dextrose, and should be fed if they are awake and alert. As noted, octreotide decreases endogenous insulin release. The glucose will cause a release of endogenous insulin in patients who receive glucose for hypoglycemia, causing them to become hypoglycemic again. Patients therefore should be treated with octreotide (according to the recommendations above) in addition to glucose.
After octreotide is given, the patient should be admitted to a monitored hospital setting where he can get hourly point-of-care glucose measurements until his glucose levels stabilize for four to six consecutive measurements. After this, patients should be monitored for signs of hypoglycemia (tachycardia, diaphoresis, lethargy) hourly with serum glucose levels measured every two to four hours. Exogenous dextrose should be limited as much as possible, and if the patient was started on a glucose drip, this should be decreased and stopped if he maintains his glucose levels. The patient should be allowed to eat and drink normally.
Patients who are asymptomatic after an unintentional ingestion of a sulfonylurea may be monitored in the emergency department for eight hours, and then be discharged and monitored at home by family if they do not develop hypoglycemia and have normal renal function. Children who are asymptomatic must be monitored through an overnight sleep cycle because they are at risk of developing significant hypoglycemia during this fasting period.
All intentional ingestions of a sulfonylurea should be admitted to the hospital.
The child we saw in our ED was administered 1 mcg/kg octreotide and admitted to the ICU. His blood glucose was monitored every hour for the first four hours and remained stable. He was also monitored hourly for signs of hypoglycemia (diaphoresis, tachycardia, lethargy). He was slowly weaned off the glucose infusion, required no further octreotide, and was discharged 24 hours after the initial administration of octreotide.
1. Calello DP, Kelly A, Osterhoudt KC. "Case files of the medical toxicology fellowship training program at the Children’s Hospital of Philadelphia: A pediatric exploratory sulfonylurea ingestion. J Med Toxicol 2006;2(1):19.
2. Glatstein M, Scolnik G, Benter Y. Octreotide for the treatment of sulfonylurea poisoning. Clin Toxicol 2012;50(9):795.
3. Nelson L, Lewin N, et al, eds. Goldfrank's Toxicologic Emergencies. 9th edition. New York: McGraw Hill, 2011.
Monday, August 03, 2015
A 37-year-old woman is brought into the emergency department by EMS after being found down next to a bottle of an unknown substance. (See photo.) Her family said she was initially tearful and repeatedly mumbling, “I’m sorry,” and became progressively less responsive.
She was obtunded and intubated for airway protection upon arrival to the ED. Her initial vital signs were a temperature of 98.8°F, heart rate 110 bpm, blood pressure 187/118 mm Hg, respiratory rate 22 bpm, and pulse oximetry 98% on ventilator. Initial ABG reveals a pH 6.89, pCO2 16, pO2 174, and bicarbonate 3.1. Pertinent lab results include a metabolic panel with an anion gap of 24, creatinine 1.23, ammonia of 103, and a positive urine drug screen for THC.
What is the differential diagnosis for a patient with a large anion gap? For this patient, we considered the possible etiologies included in the mnemonic MUDPILES.
M Methanol, metformin
D DKA, AKA, or any ketoacidosis
P Paracetamol, paraldehyde
I Iron, isoniazid
E Ethylene glycol, ethanol
Acetaminophen, salicylate, and ethanol levels were negative. Initial lactate is 5.6 mmol/L, and serum osmolality is 354. Her metabolic panel is below:
What is this patient’s osmolal gap? Osmolal gap= serum osmolality - calculated osmolality [(2 x serum Na) + (serum glucose/18) + (serum BUN/2.8) + (serum ethanol/4.6)]. In this case: Calculated osmolality = (2x135) + (200/18) + (14/2.8) + (0/4.6) = 286
Osmolal gap = 354 - 286 = 68
What products contain methanol or ethylene glycol?
n De-icing solutions
n Windshield washer fluid
n Engine coolant antifreeze
n Paint removers
n Shoe dyes
n Solid cooking fuel used in camping
n Embalming fluid
n Contaminant in moonshine or fermented beverages
Methanol and ethylene glycol themselves are relatively nontoxic and primarily cause CNS sedation. Toxicity stems from their metabolism to toxic metabolites.
The toxic metabolite of methanol formic acid causes retinal and optic nerve injury, and may lead to permanent blindness. Ischemic or hemorrhagic injury to the basal ganglia have also been described.
The toxic metabolites of ethylene glycol lead to acute renal injury and ultimately to renal failure by tubule damage and by the formation of calcium oxalate crystals, which lead to tubule obstruction. Systemic hypocalcemia may also occur as the oxalic acid metabolite precipitates with calcium.
The parent compounds initially cause an elevation of the osmolal gap after ingestion. As they are metabolized to their toxic acid metabolites, the osmolal gap decreases and the anion gap increases, causing a profound anion gap metabolic acidosis.
Treatment should begin immediately based on history, clinical exam, elevated osmolal gap, or a metabolic of unknown cause. Confirmatory testing done by measuring serum ethylene glycol or methanol levels should not delay treatment because these tests are generally sent to outside laboratories and may take some time to provide results. Consultation with a medical toxicologist or poison control center is recommended because these patients are a potentially serious medical emergency.
Initial treatment of a toxic alcohol ingestion requires the use of an inhibitor of alcohol dehydrogenase. Prior to the discovery of fomepizole in 1963, ethanol had been used to block the metabolism of methanol and ethylene glycol to their toxic metabolites. Alcohol dehydrogenase preferentially metabolizes ethanol, and therefore would not be available to metabolize methanol or ethylene glycol.
In fact, a patient who has ingested ethanol and a toxic alcohol has unknowingly protected himself from metabolizing the toxic alcohol to a toxic metabolite while his ethanol level remains greater than 100 mg/dL. Fomepizole has now replaced ethanol as the antidote of choice for toxic alcohol ingestion in the United States, and it has no contraindications and no known adverse effects. A 15 mg/kg IV loading dose of fomepizole should be administered followed by 10 mg/kg doses every 12 hours if a toxic alcohol ingestion is suspected. Repeated doses of fomepizole induce cytochrome P450 metabolism, so clinical guidelines recommend increasing fomepizole dosing to 15 mg/kg every 12 hours after 48 hours. No dose adjustments are needed for patients with renal or hepatic disease. Treatment should continue until methanol or ethylene glycol levels are less than 20 mg/dL.
Hemodialysis should be considered in those patients with end-organ toxicity or severe acidosis. The severe acidosis indicates that a majority of the toxic alcohol has already been metabolized, in which case the efficacy of fomepizole is minimal. Clinical guidelines also recommend initiating hemodialysis with a methanol level higher than 50 mg/dL because toxic levels of methanol, along with inhibition of metabolism from fomepizole, will lead to a prolonged half-life. It is important to remember that hemodialysis will not only remove the toxic alcohols and their metabolites but will remove the antidote as well, making it necessary to increase fomepizole dosing to 10 mg/kg every four hours during hemodialysis.
A recent challenge to the treatment of toxic alcohol poisoning is the current national shortage of fomepizole. Hospitals have begun to develop or revisit protocols for the therapeutic use of ethanol for toxic alcohol poisoning. This nationwide shortage makes it important to know how to dose and treat with both antidotes.
Dosing may be challenging because of variability in metabolism between patients, so frequent monitoring is required. Most pharmacies have a 10% ethanol solution available. Administration via a central venous catheter is preferred because of the risk of phlebitis, but a large vein may also be considered for administration of IV ethanol.
IV ethanol dosing (initial blood ethanol concentration=0):
n Loading dose:
n 8 mL/kg ethanol 10% intravenous solution
n Give over 20 to 60 min as tolerated.
n Loading dose may be omitted if serum ethanol level is higher than 100.
n If serum ethanol level is detected, decrease loading dose proportionally.
n Maintenance dose (non-drinkers)
n 1 mL/kg/hr ethanol 10% solution
n Maintenance dose (drinkers)
n 2 mL/kg/hr ethanol 10% solution
n Maintenance dose during hemodialysis
n 2 to 3.5 mL/kg/hr ethanol 10% solution
n Obtain serum ethanol levels after the loading dose and frequently during maintenance therapy.
n Target blood ethanol concentration: 100–150 mg/dL
n Monitor every two hours until goal is achieved or after a change in the infusion rate.
n Once stable, monitor every four to six hours.
n Blood glucose
n Every two hours and immediately if any signs/symptoms of hypoglycemia
n Metabolic panel & acid-base status
n Every six hours
n Acute drop in serum bicarbonate or increase in anion gap should prompt immediate evaluation of blood gas and ethanol concentration.
n Observe for adverse effects
n Inebriation or sedation
n Local phlebitis
n Acute flushing, palpitations, postural hypotension in those with atypical aldehyde dehydrogenase enzyme
n Use of interacting drugs that may cause disulfiram-type reactions (metronidazole, furazolidone, procarbazine, chlorpropamide, some cephalosporins, and Coprinus mushrooms)
n Pregnancy category C. Administration should be done in consultation with toxicologist/obstetrician.
Consider adjunctive therapies in treating toxic alcohol patients, such as bicarbonate for significant acidosis in methanol poisoning or ethylene glycol toxicity. Bicarbonate functions by shifting methanol’s toxic metabolite formic acid to the less toxic dissociated form, formate, which has a lower affinity for target sites for toxicity.
The administration of cofactors is thought to have a theoretical advantage for producing nontoxic metabolites, but has not been proven in clinical studies. Folinic acid and folic acid (50 mg IV every four to six hours) enhance the metabolism of methanol’s toxic metabolite formate because it is metabolized to water and carbon dioxide. As cofactors, pyridoxine (50 mg IV every six hours) and thiamine (100 mg IV every six hours) enhance the metabolism of ethylene glycol to nontoxic metabolites, limiting accumulation of the metabolite responsible for renal toxicity and metabolic acidosis.
Our patient was treated with intravenous ethanol (because of the fomepizole shortage), sodium bicarbonate infusion, pyridoxine, thiamine, and folic acid. Nephrology was consulted, and hemodialysis was initiated within six hours of ED presentation. The patient had a prolonged hospital course and returned to baseline by hospital day 8. Although the patient’s initial ethylene glycol level at presentation returned at only 45 mg/dL, the significant metabolic acidosis and acute kidney injury on presentation suggest a significant amount of ethylene glycol had been metabolized by the time she presented.
1. Kearney TE. Chapter 187. Ethanol. In: Olson KR. ed. Poisoning & Drug Overdose, 6th edition. New York, NY: McGraw-Hill; 2012.
2. Brent J. Fomepizole for ethylene glycol and methanol poisoning. New Engl J Med 2009;360(21):2216.
3. Headline: Matt Groening via Homer Simpson, The Simpsons, Episode 171; March 16, 1997.
Wednesday, July 01, 2015
A 22-year-old man with no past medical history presented to the emergency department with altered mental status. He was brought in by police who reported using a TASER on him three times after he became violent with them. His friends report he smoked K2. His initial vital signs included a temperature of 99.9°F, a heart rate of 137 bpm, blood pressure of 151/76 mm Hg, a respiratory rate of 22 bpm, and pulse oximetry of 98% on room air. The patient was agitated and combative, and was placed in four-point restraints.
K2 is a synthetic cannabinoid. Other commonly used synthetic cannabinoids include spice, moon rocks, comatose candy, and black mamba. Typically, the synthetic cannabinoid chemicals are sprayed onto a plant material and sold in packets marketed as incense or aromatherapy. Most come with a warning label of “not for human consumption” to hide its intended use and avoid regulatory control. Synthetic cannabinoids were first reported in 2008. Local and federal agencies have been enacting ordinances and placing many of the identified synthetic cannabinoids into Schedule 1 status to control sale and distribution and manage the potential public health threat. Synthetic cannabinoids, however, may still be available via the Internet and in gas stations and head shops.
The recent resurgence of designer drug abuse with unusual presentations and high degree of severity with intoxication has put this drug at the forefront of the public consciousness again. The New York Times reported the recent rise in New York ED visits from spice: more than 1,000 cases had been reported to regional poison control centers in April, which is more than double the cases reported from January to March 2015. (April 24, 2015; http://nyti.ms/1FIvoaN.) Most of these were not confirmed with testing but rather by self-reports.
NPR likewise wrote about the recent surge in K2 usage throughout the country. (April 27, 2015; http://n.pr/1KtCTn9.) Patients who habitually used K2, called K heads, had been having adverse and severe reactions to this new batch of K2. Hospitals sent samples of these drugs for testing and detected XLR-11, a synthetic cannabinoid known to cause renal damage. Other samples sent have been found to contain synthetic cannabinoids and synthetic cathinones (bath salts). Some samples contained a chemical that had never been seen by the lab before.
Our patients report expectations of a “mellow high,” but instead these patients have been presenting with psychotic or sympathomimetic symptoms. Recent news reports have shown that some of the new K2 makes patients act like they are on PCP. Common findings are nausea, vomiting, abdominal pain, anxiety, agitation, delirium, coma, psychosis, hallucinations, myoclonus, hyperthermia, and tachycardia.
Of concern, recent reports describe symptoms that are not typically expected after the use of synthetic cannabinoids, including CNS depression, bradycardia, hypotension, and seizures.
Testing should be considered for patients presenting after reported or suspected use of a synthetic cannabinoid. Such tests include:
- A thorough evaluation for signs of end-organ injury
- Basic Metabolic Panel: Renal injury has been known to occur with several types of synthetic cannabinoids.
- Renal biopsies have shown acute tubular necrosis and interstitial nephritis.
- CK: Rhabdomyolysis has commonly been reported.
- EKG and cardiac enzymes: Synthetic cannabinoids have been shown to cause myocardial infarction. Coronary artery vasospasm is one proposed mechanism.
- Head CT: Embolic stroke has been described in the literature.
- Synthetic cannabinoids are not detected by the standard urine drug screen. They bind the cannabinoid receptor as does natural marijuana, but these compounds are synthetic and have a different chemical structure.
- Specific blood or urine testing for synthetic cannabinoids or their metabolites are of limited utility in acute managing these patients, but may be considered a confirmatory test when collecting epidemiological data to assist in characterizing epidemics of use.
- Additionally, consider testing for alternative drugs based on similar presentations and recent reports of abuse in the community: bath salts and stimulant designer drugs.
- Do a work-up for additional/alternative diagnoses (i.e., trauma).
Generally, the most common problem with these patients is controlling their agitation. These patients should be aggressively sedated because prolonged agitation and physical restraints can lead to hyperthermia, rhabdomyolysis, and worsening acidosis. One algorithm we propose:
§ *Initial use of benzodiazepines: Ativan 2 mg IV q 2-4 minutes until sedation or a total of 20 mg, or Valium 10 mg IV wait 10 minutes. If not sedated, then increase by 10 mg every 10 minutes for a cumulative total of 100 mg of Valium.
§ If the patient has psychotic symptoms, you may consider 5 mg IV Haldol x 2 or 10 mg IV Geodon or 10 mg IV Zyprexa.
§ If the patient continues to be agitated following either a total of Ativan 20 mg or Valium 100 mg, then you may consider ketamine IV (100 mg for an adult) or 5 mg /kg IM.
§ If the patient continues to be agitated, he should be paralyzed and intubated as the final step for sedation.
* This is only one algorithm we use, and there are many others that may be just as effective. No trials have compared one sedation algorithm with the next. Patients may be affected differently by medications, so always have airway equipment available in case of oversedation.
Once the agitation is controlled, good symptomatic and supportive care should be instituted. There is no specific antidote for synthetic cannabinoid toxicity, and patients should be closely monitored for hyperthermia.
To control agitation, our patient received a total of Ativan 14 mg IV, ketamine 120 mg IV, and then required intubation with rocuronium and was started on a Versed infusion. The patient was admitted to the ICU. His creatine kinase maxed at 16,000. The patient returned to baseline mental status, and was extubated the next day.