S’now Problem: Keep your Cool when Stimulants turn up the Speed

by | Oct 17, 2024 | 0 comments

stimulants

We remain amid an opioid crisis in Canada, with over 8000 deaths (or 22/day) in 2023. The harms of opioid use in society are devastating and cannot be understated – but so too are the harms from stimulant and other substance use. In 2023 there were 3479 apparent stimulant toxicity deaths, which is approximately 10/day. The most common substances were cocaine and methamphetamine. (1)

Health Canada perhaps more accurately now refers to this as the ‘Overdose Crisis’, given the increasingly toxic, contaminated, and unpredictable compositions of all substances in the illegal drug supply.

Objectives

  • Describe a short history of stimulant use worldwide and in Canada
  • Understand and recognize the life-threatening clinical manifestations of stimulant toxicity
  • develop and approach to the emergency treatment of stimulant toxicity, including:
    • Agitation/Psychosis
    • Seizures
    • Hyperthermia
    • Tachycardia and Hypertension
    • Cardiac Arrest
  • Become familar with outpatient treatment options of stimulant use disorder and harm-reduction strategies from the ED.

History

Cocaine

  • 1400s – Coca leaves would be chewed by indigenous South American peoples for their stimulant properties, and to stimulate digestion and suppress appetite.
  • Late 1800s – after the leaves had been taken to Europe and the alkaloid cocaine had been isolated, people began to experiment with cocaine’s various medical properties and publish their findings.
    • 28yo Sigmund Freud published ‘Uber Coca’ in 1884, which was basically a report on his findings when he himself took a lot of cocaine, or when he administered it to his friends and family. In it, he proposes numerous physiological effects and potential therapeutic uses including: 
      1. Stimulant properties
      2. Treatment for dyspepsia and other digestive disorders
      3. Treatment of morphine and alcohol addiction
      4. Treatment for asthma and altitude sickness
      5. An aphrodisiac
      6. At the end includes a few lines on its numbing properties.
    • This last one is where cocaine’s uses really took off, and it was used in various medical procedures such as nerve blocks and ocular surgeries.
  • Recreational cocaine use became more popular in society, including its use in beverages (coca-wine, coca cola) from 1887-1903)
  • Addiction started to be noticed, as well as its association with increased crime. Recreational use was outlawed in 1911 (Canada) and 1914 (US) (2)

stimulants

 

Amphetamines and its derivitives

  • Marketed in France in 1932 as a nasal decongestant, and then narcolepsy and weight loss
  • Supplied to soldiers (on both sides) during WW2 – by the end of the war its use had been restricted to prescription only as violence + withdrawal effects were being noticed
  • 1960s/70s was the start of designer drugs and this has taken off since then (3)

 

stimulants

 

Impact Today

  • Globally in 2024 – cocaine production and consumption is at an all-time high and continues to increase.
  • Stimulants as a general class dominate the ‘novel psychoactive substances’ market, with 35% of all NPS being stimulants
  • In Canada, the last census data on drug use prevalence is from 2019. At that time, approximately 2% of people over the age of 15 reported cocaine use in the last year, 1% reported MDMA, and 0.5% reported methamphetamine
  • Wastewater data trends throughout 2022-2023 have shown consistently increasing cocaine, similar to what is being seen in the rest of the world. Methamphetamine levels on the other hand appear to have stabilized.
  • Canadian healthcare impact in 2023:
    • 3479 [10/d] stimulant-related toxicity deaths
    • 2045 [7/d] stimulant-related poisoning hospitalizations
    • 5426 [15/d] stimulant-related poisoning ED visits

 

Psychopharmacology

Cocaine

  • Raw cocaine is a weak base, that gets converted to a salt to make it a water soluble powder (cocaine hydrochloride)
  • Crack = smokeable and cheaper form of cocaine made by dissolving cocaine in water and adding a strong base
  • Cocaethylene = a new substance formed when a person consumes both cocaine and EtOH. It exerts the same pharmacologic actions as cocaine but with higher potency and a much longer half-life (is also more cardiotoxic)
  • All function by blocking the reuptake of endogenous DA, NE, E, 5HT and increase excitatory amino acid concentration in the brain

 

Amphetamines

  • Phenethylamines = the class that encompasses amphetamines and methamphetamines. Dopamine (DA), norepinephrine (NE) and epinephrine (e) also belong to this class
  • Amphetamines differ from cocaine in that they function both by blocking uptake, and stimulating release of DA, NE, E, (and some cause 5HT release as well)
  • Generally, substitutions at different places in the molecular structure cause different pharmacological and clinical effects

 

stimulants

 

The ‘Unknown White Powder’ – Case Management

1. Agitation

  • Benzodiazapines: RCT and SR level evidence – consensus that this is first line both for control of agitation and management in general (4) 
    • Also hits all other aspects of toxicity including seizures, hyperthermia, tachycardia/HTN 
    • Range of doses in literature:  
      • IV: Diazepam 5-10, 10-20 or midazolam 1-2, 2.5-5 and can repeat within 5 min if needed. Prefer these as they are fast-acting  
      • IM: Midazolam 5-10 or Lorazapam 2-4mg (avoid diazapam as has erratic IM absorption) 
  • Antipsychotics:  
    • Multiple concerns with antipsychotics including: rigidity/dystonia and hyperthermia, cardiac dysrhythmias/prolonged QTc, decrease the seizure threshold, and can be hepatotoxic to an already compromised liver (3)  
    • Systematic review on the topic in 2019 that included 73 papers, the only 1 RCT above, 426 pts, and concluded: “There is neither a clear benefit of antipsychotics over benzos nor a definitive signal of harm noted. We encourage clinicians to adapt treatment based on specific circumstances and characteristics of their individual patients.” (5) 
    • In summary: not entirely contraindicated, but no clear evidence of safety.  
  • Dexmedetomidine: 
    • No RCTs or high level evidence, but some promising case reports (6) 
  • Ketamine: Recommended by the ASAM/AAAP guidelines if refractory to benzos/antipsychotics, not based on much evidence (7). Theoretically it could be useful.  

2. Seizures

  • Etiology: Global increase of excitatory neurotransmitters, causing mostly generalized tonic clonic seizures  
    • Consider hyponatremia as a possible etiology in cases of MDMA 
      • MDMA = more serotonergic. Serotonin is involved in ADH release – hence causing hyponatremia (3)
      • Profound serotonin syndrome is another diagnostic consideration, especially with polypharmacy. 
    • Consider head trauma or spontaneous ICH as etiology 
  • Management: (1) Benzos, (2) Barbituates, (3) Propofol  
    • If seizures are ongoing after adequate doses of benzodiazepines, you should likely a) consult a toxicologist for next steps, and b) consider other etiologies, as seizures from stimulant toxicity are actually generally short-lived and benzo-responsive. 

3. Hyperthermia/Cooling

  • Significance:  
    • “Elevated temperature represents the most critical abnormal vital sign” (3), uncontrolled hyperthermia is independently associated with morbidity and mortality (8) 
      • Hyperthermia can lead to rhabdomyolysis and renal failure, liver failure, DIC, hyperkalemia, and multi-organ failure  
      • 2/3 of cases where body temp was >41.5% are fatal (MDMA specific) (9) 
      • Hyperthermia of >38.9 for >30 minutes increases morbidity and mortality (3) 
      • Patients with a temperature of >41 for >20 min are likely to go into DIC  
      • Several studies even showing that stimulant toxicity is more prevalent and more lethal when the ambient temp outside is elevated (10,11) 

 

stimulants

 

  1. Increased psychomotor agitation, muscle contraction, activity = increased heat production  
  2. Vasoconstriction limits dermal blood flow and impairs heat dissipation  
  3. Increased circulating levels of D, NE, 5HT in the hypothalamic thermoregulatory centre activates HPA axis = thermogenesis and toxicity dependent on circulating thyroid and adrenal hormones (8) 
  4. Environmental, setting that these substances are more often used (Dance parties/raves, outdoor festivals)  

 

Management of Hyperthermia

  • Core temp monitoring with rectal, esophageal or bladder probe  
  • Tylenol has not been shown to be effective as it functions by decreasing the hypothalamic set point, which is not the mechanism of hyperthermia  
  • Control temp FAST (time-dependent effects as above)  
    • Generally want to lower to <38.9 within 20-30 min  
  • 2 main components of management:  
    1. Sympatholysis, control agitation  
      • AVOID physical restraints where possible as they can increase isometric muscle contraction and hyperthermia. There is evidence that they cause harm (12) 
      • Benzos decrease psychomotor agitation and decrease sympathomimetic outflow, decreasing vasoconstriction (13) 
      • Barbiturates, NM blockade, and intubation to facilitate cooling (probably in consultation with ICU/toxicologist)  
    2. External cooling
      • Ice water immersion generally works 2x as fast as evaporative cooling (3)  
      • Stop cooling at 38 degrees C (8)

 

4. Hypertension/Tachycardia

  • Benzos: First line as above, HIGH doses, will be enough in most cases 
    • Functions by decreasing sympathetic outflow 
    • Universally agreed upon including by our local experts   
  • Phentolamine is recommended in tox literature:  
    • An RCT from 1989. This RCT involved 45 patients who were randomized to receive intracoronary (i.e. in the cath lab) phentolamine vs. placebo after intranasal cocaine administration. Their results showed that phentolamine was effective in reducing vasoconstriction and hypertension/MAP, but could also cause mild tachycardia in some cases. Since this time there have been no further RCTs or high quality studies on the use of phentolamine, intracoronary or otherwise. 
    • There are 2 more case reports published in 1992 and 2006, which showed that phentolamine was again effective and safe in treating cocaine-induced hypertension. Both were specifically in the setting of chest pain/myocardial ischemia as opposed to just hypertension that is refractory to benzodiazepines. (14,15) 
    • 1mg q3-5min, can repeat. One case report used a cumulative dose of 2mg, the other of 3mg (16)  
  • Nitrates and CCBs have similar levels of evidence (17) 
    • Non-dihydropyridine CCBs are less likely to have reflex tachycardia and are preferred (dilt, verapamil)  
      • Can be used to control SVTs as well  
    • Nitroprusside and nitroglycerine can be used 
    • BOTH classes can be helpful to treat hypertension, but may cause a reflex tachycardia
  • Beta Blockers
    • “Unopposed alpha phenomenon” originated from case report (1985, Ramoska) and a prospective trial of 30 pts in 1990 who were given intracoronary propranolol (selective BB)  
      • In 1985, Ramoska and Sacchetti reported the first case of unopposed α-stimulation in an agitated, cocaine-toxic patient. After receiving propranolol, the patient’s blood pressure increased from 170/118 to 180/140 mm Hg, but heart rate decreased from 112 to 104 beats per minute (bpm). Despite this increase in blood pressure, no adverse event or outcome occurred. The patient’s agitation resolved, and he left against medical advice. (18) 
      • In 1990, Lange and associates published the first prospective human investigation of propranolol (selective BBer) after cocaine administration. 10 pts received intracoronary propranolol after cocaine  – and vasoconstriction was consistently noted. There was 1 event of complete occlusion and STE that was reversed with nitro. This study is typically cited as having 1 adverse event – although vasoconstriction was noted in general in the intervention group who received propranolol (19) 
    • Three years later, this same research group performed a similar study with the mixed β1-/β2-/α1-blocker labetalol. Nine participants were administered cocaine, which increased their mean arterial pressure and decreased the coronary arterial area. Unlike their previous study of propranolol, labetalol decreased MAP but had no significant effect on coronary arterial area. There were no adverse events. (20) 
    • In 1991, Sand and colleagues published a cohort of 7 patients with cocaine toxicity treated with esmolol, a short-acting selective β1-blocker.  Esmolol reliably decreased heart rate but had an inconsistent effect on blood pressure. There was 1 treatment failure with esmolol for control of hypertension. There were 3 adverse events: Hypotension, a rise in blood pressure, which was treated with labetalol, and nausea and vomiting (21) 
    • In 2007, Fareed et al published a case report of a patient with cocaine-induced ACS who received IV metoprolol (specific b1), and subsequently developed chest pain, hypotension, and died (22) 
    • In 2009, Gomez et al reported on a patient with cocaine-induced ACS who got propranolol (specific b1), and had worsening of his chest pain and ST changes. He was treated with PCI and was fine. (23) 
    • ALL of these authors then came together and in 2017 published a review of the existing evidence over the last 30 years.  

They sought to investigate the dogma that: “B blocker use has been cited as an absolute contraindication, despite limited and inconsistent clinical evidence.” They also explore alternative explanations of the proposed “unopposed alpha stimulation” phenomenon, and list 16 different physiological mechanisms that cocaine alone could have caused the deleterious events other than beta blocker administration. Their review included a total of 2124 subjects who received beta blockers, and 7 adverse events as previously outlined, with causal association unclear. There were NO ‘unopposed alpha’ events reported for the use of combined a/b blockers: such as labetalol and carvedilol. 

  • Now, they don’t specifically say the number of patients of the 2124 who received labetalol/carvedilol – I looked over their table of all included studies, and quite a few of the larger ones are specified as simply including ‘unspecified beta blockers’, or have a list of like 3+ different ones that are used. I was able to count specifically 84 patients who received labetalol/carvedilol (24)
     
  • Of note there have been some more recent studies on the management of chronic cardiac disease, namely heart failure in the setting of cocaine use, that have actually showed neutral to positive results, although these were not regarding the treatment of patients with acute cocaine toxicity.    

 

Expert opinion of toxicologist Dr. Lisa Thurgur:

I take my CMPA hat and I tell myself: “Why would I use a beta blocker?” When if something did go wrong, and you ended up with a hypertensive crisis, someone is going to go back and look at your chart, and the question is always going to be ‘what would a reasonable physician in your position have done’, and right now, whether you believe the evidence or not, most peer experts would question the fact that you used a beta-blocker.

 

Bottom Lines on Beta-Blockers:

  • No single agent consistently and effectively mitigates tachycardia, HTN, coronary vasoconstriction, chest pain, and agitation 
  • Options include Benzos – which are the safest first line although may not be 100% effective. Other options include: nitrates, CCBs, phentolamine, and depending on the resource – BBs  
  • To be clear, currently, the use of BBs is recommended against by our local toxicologists as well as the vast majority of toxicology resources 
  • Adverse events have been reported with the use of selective B1 blockers 
  • No adverse events with labetalol/carvedilol 
  • Overall, events appear to be quite rare. If labetalol were given in the context of an undifferentiated hypertensive crisis, it’s probably low risk. In an undifferentiated patient having a hypertensive crisis, I would not advise withholding labetalol (a medication us and our nurses are very familiar with) just because cocaine remains on the differential. 
  • I would certainly advise against delaying care to seek collateral or a negative urine drug screen.  
  • Keep in mind caution surrounding beta blockers really applies to the acutely toxic patient. Beta blockers should not be contraindicated simply in patients with a history of cocaine use disorder or in those who last used 1-2 days prior. 

 

 

5. Brief note on cardiac arrest and intubation

The 2023 AHA guidelines provided a specific update in cocaine and sympathomimetic poisoning.

  • Cocaine induces tachycardia via B-adrenergic agonism, and HTN by peripheral a-adrenergic agonism via catecholamine reuptake inhibition  
  • Phenethylamines similar, but also increase release of catecholamines  
  • Generally you are not going to be able to tell what exactly was used  
    1. Cocaine is more cardiotoxic/arrhythmogenic for many reasons:  
    2. Na+ channel blockade, best described as a Class 1C antiarrhythmic. Slows conductance during phase 0 of the AP, causing QRS prolongation and a wide complex tachycardia  

 

stimulants

 

  • Moderate strength recommendations, limited evidence:  
    • Bicarb: 1-2mEq/kg followed by infusion, target pH <7.55 (25)
      • Functions as specific antidote via: 
        • Impairs Na+ channel blocker’s ability to bind to the Na+ channel  
        • Increases the number of open channels, directly reversing blockade  
        • Increases availability of Na+ to pass through the channel  
    • Lido: 1-1.5mg/kg 
      • May seem counterintuitive, but AHA also recommends for class 1A and other 1C sodium channel blocker overdose as well  
  • Intubation: succinylcholine is contraindicated due to the high risk of rhabdomyolysis and hyperkalemia. As well, the same plasma cholinesterase metabolizes cocaine as succinylcholine, so simultaneous use will prolong toxicity (3)

 

 

6. Decontamination after stabilization

  • You can use activated charcoal, but ingestions are rarely oral (except MDMA)
  • Theoretically if someone took MDMA or ate cocaine in the waiting room, could be beneficial to administer AC (26) (3)

 

7. Workup

  • BG to r/o hypoglycemia  
  • Tox panel incl. ASA, APAP, EtOH  
  • CBC + BMP, bHCG 
  • Trop + CK + ECG 
  • Consider adding fibrinogen as high risk for DIC  
  • VBG: Expect metabolic acidosis – lactic (27,28) 
  • NO studies on the specific management of stimulant induced acidosis  
    • Lactate from seizures and ++ muscle contraction/vigorous exercise picture  
    • Lactate from accelerated glycolysis/beta agonism (incr, glycolysis à incr. pyruvate à incr. lactate)  
    • Lactate from hypoperfusion/ischemia  
  • Other toxic hot + crazy workup: TSH, blood cultures etc.  
  • Urine drug screens not indicated, discussed elsewhere they lack sensitivity and specificity.

 

 

Disposition/Outpatient

Unfortunately, even in the outpatient addiction medicine world there aren’t many strong recommendations for patients with stimulant use disorder, and evidence is even more scant from the ED. There are no FDA approved treatments for stimulant use disorder. I want to discuss 3 things I think we can do from the ED, even based on limited evidence, to reduce harm in these patients.  

 

1. Overdose prevention 

 

2. To encourage safer consumption 

  • It is recommended that patients use safer consumption services (SCS) for both overdose prevention and safer consumption practices as they can get supplies there. SCS have been shown to:  
    • Reduce drug-related M+M 
    • Reduce infections and risky injection behaviours  
    • Increase SUD treatment initiation 

 

stimulants

As a reminder there are 4 sites in Ottawa. Sommerset likely will close in March 2025 ☹

 

  • In addition to directing our patients to these sites, we can advise them to:  
    • Not use alone  
    • Use one substance at a time  
    • And consume a test dose to gauge substance strength and effects – they can always use more later  

 

3. Referrals/direction to community supports  

  • Royal RAAM clinic and Sandyhill RAM clinic only do ETOH/opioids  
  • RecoveryCare locations do see a fair number of patients with stimulant use and their information is already included on our discharge addictions resources handout, and patients can walk in or call ahead to self-refer.
  • HIV/hepatitis/STI screening actually get done during a patient’s intake appointment at Recovery Care. And they can treat STIs and uncomplicated hep C themselves  
  • Patients who are unhoused can be advised to seek care from Ottawa inner City Health at local shelters. They have a dedicated psychiatrist and mental health team and prescribe regulated stimulants. They also can help with other social determinants of healthcare.  

 

Summary

  1. Benzos and cooling have the best evidence for acute treatment
  2. Our toolbox contains: benzos, nitrates, CCBs, phentolamine
  3. We should remember to use Bicarb and Lido in these WCT/arrests
  4. While treatments for stimulant use disorder are currently limited, some Harm reduction that we can implement from the ED includes:
    1. Overdose prevention with naloxone kits
    2. Encouraging safe consumption practices referrals/guidance on where to seek care

 

 

References

1. Ottawa PHA of. Federal, provincial, and territorial Special Advisory Committee on the Epidemic of Opioid Overdoses. Opioid- and Stimulant-related Harms in Canada. [Internet]. 2024 [cited 2024 Aug 31]. Available from: https://health-infobase.canada.ca/substance-related-harms/opioids-stimulants/

2. Redman M. Cocaine: What is the Crack? A Brief History of the Use of Cocaine as an Anesthetic. Anesth Pain Med. 2011;1(2):95–7.

3. Nelson L, Howland MA, Smith S, Goldfrank L, Hoffman R, Lewin N. Goldfrank’s Toxicologic Emergencies 11th edition. 11th ed. McGraw Hill Education; 2019.

4. Wodarz N, Krampe-Scheidler A, Christ M, Fleischmann H, Looser W, Schoett K, et al. Evidence-Based Guidelines for the Pharmacological Management of Acute Methamphetamine-Related Disorders and Toxicity. Pharmacopsychiatry. 2017 May;50(3):87–95.

5. Connors NJ, Alsakha A, Larocque A, Hoffman RS, Landry T, Gosselin S. Antipsychotics for the treatment of sympathomimetic toxicity: A systematic review. Am J Emerg Med. 2019 Oct;37(10):1880–90.

6. Lam RPK, Yip WL, Wan CK, Tsui MSH. Dexmedetomidine use in the ED for control of methamphetamine-induced agitation. Am J Emerg Med. 2017 Apr;35(4):665.e1-665.e4.

7. The ASAM/AAAP Clinical Practice Guideline on the Management of Stimulant Use Disorder. Journal of Addiction Medicine. 2024 Jun;18(1S):1.

8. Eyer F, Zilker T. Bench-to-bedside review: mechanisms and management of hyperthermia due to toxicity. Critical care (London, England) [Internet]. 2007 [cited 2024 Aug 31];11(6). Available from: https://pubmed.ncbi.nlm.nih.gov/18096088/

9. Gowing LR, Henry-Edwards SM, Irvine RJ, Ali RL. The health effects of ecstasy: a literature review. Drug and Alcohol Review. 2002;21(1):53–63.

10. Auger N, Bilodeau-Bertrand M, Labesse ME, Kosatsky T. Association of elevated ambient temperature with death from cocaine overdose. Drug Alcohol Depend. 2017 Sep 1;178:101–5.

11. Marzuk PM, Tardiff K, Leon AC, Hirsch CS, Portera L, Iqbal MI, et al. Ambient temperature and mortality from unintentional cocaine overdose. JAMA. 1998 Jun 10;279(22):1795–800.

12. Lavonas EJ, Akpunonu PD, Arens AM, Babu KM, Cao D, Hoffman RS, et al. 2023 American Heart Association Focused Update on the Management of Patients With Cardiac Arrest or Life-Threatening Toxicity Due to Poisoning: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2023 Oct 17;148(16):e149–84.

13. Marco CA, Gupta K, Lubov J, Jamison A, Murray BP. Hyperthermia associated with methamphetamine and cocaine use. The American Journal of Emergency Medicine. 2021 Apr 1;42:20–2.

14. Chan GM, Sharma R, Price D, Hoffman RS, Nelson LS. Phentolamine therapy for cocaine-association acute coronary syndrome (CAACS). J Med Toxicol. 2006 Sep;2(3):108–11.

15. Use of Phentolamine for Cocaine-Induced Myocardial Ischemia. New England Journal of Medicine. 1992 Jul 30;327(5):361–361.

16. Schep LJ, Slaughter RJ, Beasley DMG. The clinical toxicology of metamfetamine. Clinical Toxicology. 2010 Aug 1;48(7):675–94.

17. Richards JR, Garber D, Laurin EG, Albertson TE, Derlet RW, Amsterdam EA, et al. Treatment of cocaine cardiovascular toxicity: a systematic review. Clin Toxicol (Phila). 2016 Jun;54(5):345–64.

18. Ramoska E, Sacchetti AD. Propranolol-induced hypertension in treatment of cocaine intoxication. Annals of Emergency Medicine. 1985 Nov 1;14(11):1112–3.

19. Lange R, Cigarroa R, Flores E, McBride W, Kim A, Wells P, et al. Potentiation of Cocaine-Induced Coronary Vasoconstriction by Beta-Adrenergic Blockade. Annals of Internal Medicine. 1990 Jun 15;112(12):889–968.

20. Influence of labetalol on cocaine-induced coronary vasoconstriction in humans – PubMed [Internet]. [cited 2024 Oct 11]. Available from: https://pubmed-ncbi-nlm-nih-gov.proxy.bib.uottawa.ca/8506886/

21. Experience with esmolol for the treatment of cocaine-associated cardiovascular complications – PubMed [Internet]. [cited 2024 Oct 11]. Available from: https://pubmed.ncbi.nlm.nih.gov/1671639/

22. Fareed FN, Chan G, Hoffman RS. Death temporally related to the use of a Beta adrenergic receptor antagonist in cocaine associated myocardial infarction. J Med Toxicol. 2007 Dec;3(4):169–72.

23. Izquierdo Gómez MM, Domínguez-Rodríguez A, Gálvez Rodríguez M, Marrero Rodríguez F. Reflections on beta-adrenergic receptor blockers and cocaine use. A case in point. Rev Esp Cardiol. 2009 Apr;62(4):455–6.

24. Richards JR, Hollander JE, Ramoska EA, Fareed FN, Sand IC, Izquierdo Gómez MM, et al. β-Blockers, Cocaine, and the Unopposed α-Stimulation Phenomenon. J Cardiovasc Pharmacol Ther. 2017 May;22(3):239–49.

25. Hoffman RS. Treatment of patients with cocaine-induced arrhythmias: bringing the bench to the bedside. British Journal of Clinical Pharmacology. 2010;69(5):448–57.

26. Tomaszewski C, McKinney P, Phillips S, Brent J, Kulig K. Prevention of toxicity from oral cocaine by activated charcoal in mice. Ann Emerg Med. 1993 Dec;22(12):1804–6.

27. Alshayeb H, Showkat A, Wall BM. Lactic acidosis in restrained cocaine intoxicated patients. Tenn Med. 2010;103(10):37–9.

28. Drake TR, Henry T, Marx J, Gabow PA. Severe acid-base abnormalities associated with cocaine abuse. J Emerg Med. 1990;8(3):331–4.

 

Author

  • Dr. Seliga is a resident physician in Emergency Medicine at the University of Ottawa. She has special interests in Inner City Health and Addiction Medicine.

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