Tox Takedown: Tachy with a Good Night’s Rest – Dr Ajani

History and Physical:

It is nearing 10:45pm on New Year’s Eve as you work your swing shift and are dreading being in the ‘hot seat’ for the next resuscitation that might be tweeted in the next 15 minutes. A patient is on his way in with altered mental status, with a last known well of approximately 4 hours prior to arrival. A family member accompanies the patient to the ER who mentions that the patient always gets depressed during the holiday seasons.

H&P pertinent details:

Further history, review of medical record and physical exam findings reveal the patient has a history of hypertension, diabetes, polysubstance abuse and overdose in the past. You determine the patient has 4mm pupils which are reactive and he is not bradypneic. Patient does not have any needle tracks on his arm. Family member did bring his medications to the hospital, which include:

  • Norvasc 10mg po qd,
  • Lopressor 25mg po bid,
  • Lantus 18 units qhs,
  • Lispro 7 units tidac,
  • Seroquel 75mg po qd,
  • Cogentin 1mg po bid, and
  • Aspirin 81mg po qd.

Physical exam reveals:
VS 37.5, 120, 132/89, 18, 95% 2L NC
General: confused, depressed LOC
Neuro: pupils 4mm and reactive, localizes to pain, opens eyes to pain, and mumbles incomprehensible words. Currently controlling secretions.
Skin: no obvious signs of IVDA, non-diaphoretic

The EKG is obtained:



Differential Diagnosis:

As you decide to cancel your post-work night-cap with your man squeeze, you consider the pharmacologic differential diagnosis for this patient. Let’s consider the adverse drug events for this patient’s medication list:

  • beta blocker: bradycardia, hypotension, altered mental status (from tissue hypoperfusion), bronchospasm, hypoglycemia (relative to stress level), vasoconstricted (cool to touch)
  • calcium channel blocker: bradycardia, hypotension, altered mental status (from tissue hypoperfusion), diaphoresis/warm to touch (vasodilation), ileus
  • anticholinergic: hot/bilnd/red/dry/mad, tachycardia. (Classic pimping question: how do you differentiate
  • sympathomimetic overdose vs anticholinergic overdose? From the skin exam! Sweat glands need acetylcholine to work)
  • alpha blocker: hypotension, reflex tachycardia, erection, small pupils (sometimes)

The next thing of course is to measure a glucose level. Can hypoglycemia present this way? Of course it can! Often, patients who are hypoglycemic have a surge of sympathetic activity and can be tachycardic, diaphoretic, and obtunded. However, the nurse in the resuscitation bay tells you that the fingerstick glucose measurement is 70.

You look at a sleepy patient that is breathing and tachycardia and the pupils are small. You look up at your attending and say “I don’t know WTF is going on!” but then you remember THIS tox takedown. This is classic sleepy-tachy. You look at the med list for any potential culprits (all the anti’s antihistamine, anticholinergica, antidepressant, antipsyhotic) and find the likely suspect: QUETIAPINE.

EKG findings of isolated atypical antipsychotic overdose:
Prolonged QT = 6g of quetiapine
Prolonged QTc => risk of Torsades de Pointes, though unlikely if patient gets proper supportive care
Torsades risk increases with bradycardia (due to relative prolongation of QTc)


Antipsychotic medications are largely classified as:
Typical (1st generation). Table 1.

Table 1

  • high or low potency based on binding to D2 receptor
  • good for positive symptoms, not good for negative symptoms
  • can have cross-reactivity with M1 cholinergic receptor (olanzapine/quetiapine/colazpine)
  • peripheral tissue effects (block alpha-1 receptor leading to hypotension
  • block K channel in heart leading to prolonged QT).

Table 2

Atypical (2nd generation)

  • Often affect multiple neurotransmitter subtypes


First, the obvious. Focus on ABC’s. The fingerstick glucose was 70, and you’re unsure if this is a relatively low value for the patient, so you offer him an amp of D50 without any change. He is a gentleman, so he accepts. You also consider naloxone.

To effectively treat anti-psychotic overdose, you must first understand how antipsychotics work. As many antipsychotic medications have cross-reactivity with multiple neurotransmitter subtypes, often the clinical picture is not a clear one. Blockade of histamine receptors and acetylcholine receptors centrally often causes patients to present with a decreased level of mentation (sleepy) and elevated heart rate (tachy). As with anticholinergic overdoses, the patient may also have low-grade hyperthermia (not necessarily ‘fever’) due to ineffective mechanisms of heat dissipation. The etiology of the tachycardia is often multifactorial, from elevated temperature, reflex sympathetic response from hypotension, and anticholinergic effect.

Treatment highlights:

  • IV fluids
  • Temperature control
  • Replete electrolytes
  • Ride out the tachycardia (bradycardia increases QTc relatively, increased risk of Torsades)
  • AC (single-dose activated charcoal) – single dose AC can usually be effective, even if given after one hour of ingestion (delayed gut motility from anti-cholinergic effect)
  • Torsades – treat per ACLS (Mg, overdrive pacing)
  • Physostigmine (reversal of anticholinergic effect) – the ONLY acetyl-cholinerase that crosses blood-brain barrier – for treatment of refractory altered mental status/hyperthermia – Not to be used in patients with prolonged QRS, any heart block, arrhythmia


  1. Juurlink DN. Chapter 69. Antipsychotics. In: Nelson LS, Lewin NA, Howland M, Hoffman RS, Goldfrank LR, Flomenbaum NE. eds. Goldfrank’s Toxicologic Emergencies, 9e . New York, NY: McGraw-Hill; 2011.
  2. Burns E. Life in the fast lane: ECG Library – Quetiapine Toxicity. Accessed September 9, 2015.
  3. Gelenberg A et al. Medscape. Maintaining Metabolic and Cardiovascular Health in Patients with Schizophrenia: Perspectives and Long-term Care. Accessed September 9, 2015.
  4. Casey DE et al. The Pharmacology of Weight Gain with Antipsychotics. The Journal of Clinical Psychiatry. 2001: 62; 4-10.

The Toxicology Takedown #2 – January 2015

A 15-Year-old female presents to the hospital 4 hours after ingestion of her diabetic father’s medication following a family dispute.   Her family is unable to account for 75 x 5 mg glipizide and 29 x 500 mg metformin tablets.  On arrival, she is vomiting and appears anxious and slightly sweaty with Glasgow Coma Score of 14/15.  Her vital signs are pulse rate 90 bpm, blood pressure 110/75 mmHg, respiratory rate 18/min, and temperature of 36.8 C.  A bedside blood glucose level is 54 mg/dl.

What’s the immediate threat to life for this patient?

What’s the mechanism of action of sulfonylurea medications, and how is it problematic in the management in toxicity?

What are the antidotes for sulfonylurea toxicity?

What’s concerning about metformin toxicity?  What is the name of the syndrome that can develop in overdose and how it is managed?

Continue reading

The Toxicology Takedown – December 2014

A 9 month old previously healthy male presents to your Emergency Department as a priority 1 code via EMS after new onset seizure activity at home.  On arrival, EMS mentions severe vomiting and tachypnea followed by seizure activity.  Vital signs are as follows: BP 153/74, HR 164, RR 48, Temp 37.6 and SpO2 87% on NRB.  CBG is 104.  As the child appears to fasciculate in front of you, you quickly reach for your Miller 1 and grab a 4-0 ETT and under RSI with atropine, etomidate and rocuronium you suction a significant amount of clear secretions from the oropharynx before passing the tube.  Breath sounds reveal diffuse rales bilaterally, O2 sats begin to rise, vitals improve and you breathe a sigh of relief.  Stepping back you note a distinct smell of apple juice on the patients clothing and skin.  EMS brings you a container the child was playing with prior to symptom onset depicted in the image.  Parents arrive shortly after and his father explains the container is from a local Vape shop.  He uses the solution in his e-cigarette in attempts to quit smoking.

  1. What are the early signs and symptoms of acute nicotine toxicity?
  1. How do we manage nicotine toxicity in the pediatric population?


Nicotine is the primary alkaloid in the plant (Nicotiana tobaccum) used for most smoking and chewing tobacco products and nicotine-like substances are found in several other plant species (betel nut, Indian tobacco, wild tree tobacco, poison hemlock, mescal bean bush, gold chain tree, and blue cohosh).  In attempts to reduce the harmful effects of cigarette use while still supplementing nicotine, nicotine gums and patches have entered the market.  Another novel nicotine delivery device is the electronic cigarette, which first entered the US market in 2007.  Also known as e-cigarettes, they are battery-powered devices that heat a liquid solution of nicotine.  The solution is vaporized so that no smoke is produced and thus, its use is sometimes referred to as “vaping”.

The main toxicologic concern with e-cigarettes is the highly concentrated nicotine solution used to refill the device.  Given the large amount of nicotine contained in small volumes, they  pose a significant toxic risk to small children. Continue reading

Nicotine Concentrate Overdose

The first reported death from accidental ingestion of a concentrated nicotine product was just reported.
These products can be extremely concentrated, up to 36mg of nicotine per ml. The fatal dose has been reported as low as 0.5 mg/kg, although it usually requires larger doses to be fatal.
Initial symptoms are going to be non-specific and include fatigue, malaise, nausea and vomiting. This progresses  to hypertension and tachycardia. Fasciculations may be present. Later signs of severe intoxication are bradycardia, hypotension, paralysis (including respiratory muscles) and seizures.
Treatment is going to be supportive. With seizure control and respiratory management being paramount. Vasopressors and chronotropes may have limited benefit, so please contact the Tox group as early as possible for a sick patient. 55711 or 800 222 1222