Overdose (OD) is a common ED complaint. Most OD’s are not medically serious, some require supportive care, and for a very few there antidotes or other specific treatments. The risk of self harm from an underlying psychiatric condition should always be considered. Typical presentations are patients with an altered level of consciousness (ALC), delirium, abnormal vital signs, or nearly or completely asymptomatic. Common pitfalls include premature closure – accepting “OD” as the cause of the patient condition without considering other causes and the overuse of low yield tests such as “tox screens”.

 Is this an OD?
Nursing staff, pre-hospital personnel, and the ED MD sometimes misidentify patients with ALC as having an OD without much evidence to support it. The best way to avoid this is simply to ask: why did they come to this conclusion? If the answer doesn’t make sense, consider other causes of ALC (see separate essay).

  • The vital signs, including pulse oximetry should be critically evaluated to look for complications of an OD or hints that another process may be going on.
    • Tachycardia is common in various OD’s but other vital signs are usually normal unless a cardiotoxic substance or med was taken
      • The point here is that vital signs, whether normal or not should be explainable by the effects of the presumed toxin
        • For example: a patient who consumed a lot of alcohol would be expected to have normal vitals. If they are not, ask why?
        • A benzodiazepine OD would be expected to be drowsy, but not tachycardic.
        • Hypoxemia would be expected in a severe narcotic OD but not for most other toxins
    • Look for the following on PE
      • Pinpoint pupils: in the setting of ↓LOC +/- hypoventilation this finding strongly suggests opiate OD.
        • A trial of Narcan (naloxone) can be diagnostic and therapeutic
      • Unequal pupils suggests a structural CNS lesion or an ocular problem
      • Signs of head trauma
      • Track marks
  • All patients with ALC should have a bedside blood glucose test
    • ↓BS may be the cause for the ALC or a secondary effect of a toxin (alcoholics)

 Be aware of common toxidromes
Toxidrome is a term which refers to the combination of signs and symptoms which occur with certain OD’s. Many toxins do not produce a distinct toxidrome. The advantage to being aware of the common toxidromes is two-fold. In an unknown OD a toxidrome may point to a specific toxin and thus provide direction for the workup and treatment. When a specific toxin is strongly suspected, the relevant toxidrome essentially confirms the diagnosis, and if absent should lead to reconsideration.

Common toxidromes include

  • Sympathomimetic/Stimulant
  • Sedative Hypnotic
  • Opiate
  • Anticholinergic
  • Cholinergic
  • Salicylates/Aspirin
Anticholinergic toxidrome
  • Many drugs and plant toxins have anticholinergic properties. Common culprits are antihistamines, tricyclic antidepressants, anti-psychotics, antispasmodics. The prominent features of anticholinergic poisoning are tachycardia and delirium/psychosis. In severe OD the may be a ↓LOC.
    • The phrase "Red as a beet (flushing), dry as a bone (anhidrosis), hot as a hare (hyperthermia), blind as a bat (anticholinergic medications produce pupillary dilation and ineffective accommodation causing blurry vision), mad as a hatter (delirium,  hallucinations), and full as a flask (urinary retention) lists many of the features.
  • Treatment of anticholinergic poisoning is usually just supportive. However, when a patient has severe delirium, physostigmine should be considered.
    • Physostigmine reverses both central and peripheral anticholinergic effects
    • Do not use in cases with significant QT prolongation (TCA poisoning)
    • Symptomatic bradycardia may occur and should be treated with atropine

  Cholinergic toxidrome
Much less common than anticholinergic poisoning, cholinergic toxicity is typically due to insecticide exposure (organophosphates and carbamates). In many ways it is the opposite of anticholinergic toxicity, as you would expect. There are two mnemonics which help in remembering the salient features.

    • SLUDGE/BBB: Salivation, Lacrimation, Urination, Defecation, Gastric Emesis, Bronchorrhea, Bronchospasm, Bradycardia
    • DUMBBBELS: Defection, Lacrimation, Urination, Bronchospasm, Bradycardia, Bronchorrhea, Emesis, Lacrimation, Salivation
  • Patients with more than mild signs and symptoms should be treated.
    • Atropine and Pralidoxime are antidotal treatment
    • A benzodiazepine should be given if needed for sedation or to treat seizures
  • Decontamination and avoiding exposure are often issues

 Sympathomimetic/Stimulant toxidrome
The commonest is cocaine: shorted/smoked/injected. The main effects are cardiac and CNS. Patients with significant toxicity are tachycardic and hypertensive. They are often very anxious and agitated and may have seizures. 

  • Rhabdomyolysis can occur especially if physical restrains have to be used.
  • Look at the urine and if it is discolored (like Coca-Cola) consider rhabdomyolysis.
    • The best test for rhabdomyolysis is a total CK (not cardiac CK isoenzymes).
      • There is no utility in the ED to checking urine or serum myoglobin
Treatment is usually pretty simple: benzodiazepines.
  • Large doses may be needed.
  • The best end point is to titrate until the patient is calmly asleep with their vital signs normalizing
  • Hydration and alkalinization are used to treat significant rhabdomyolysis
    • My threshold to treat is CK >10,000
      • If there is pre-existing renal insufficiency, use a lower threshold to treat.
When possible use pharmacological restraints instead of physical restraints
    • Physical restraint may be needed in order to administer medications, once the meds are effective consider removing the restraints.

 Sedative/Hypnotic toxidrome
Sedative/hypnotic toxicity is most often caused by benzodiazepines (BZD). The prognosis is very good in isolated BZD OD with just supportive care. Antidotal treatment with flumazenil is usually not indicated.

  • Clinically the patient may appear to simply be sleeping, with normal vital signs. When aroused the clinical picture resembles alcohol intoxication with slurred speech, poor coordination and unsteady gait. EOMs often show nystagmus.
  • Isolated BZD OD does not cause respiratory depression or significant cardiovascular effects.
    • BZD + alcohol may cause respiratory depression
  • Active treatment is usually not needed. The patient simply needs observation until they are more alert.
    • Length of time for ED observation vs. hospital admission depends on resource utilization.
      • If the ED is busy and there are lots of floor beds, 2-4h in the ED is reasonable.
      • When there are no floor beds anyway just keep the patient in the ED
      • In typical circumstances my threshold for admission is to give the patient 6 hours to wake up enough to be re-examined and interviewed. After 6 if they are still too sleepy, admit them.
    • If the OD is related to a potential for self harm, an assessment for suicide risk is appropriate.
  • Flumazenil is a BZD antagonist.
    • Flumazenil is not indicated in most BZD toxicity. In a certain sense the treatment may be worse than the disease.
      • It may precipitate withdrawal seizures in patients habituated to BZDs.
      • In cases of co-ingestants which lower the seizure threshold there is also the theoretical concern of precipitating seizures.
Opiate/Opoid toxidrome
While there are certain differences and peculiarities of specific agents, there are some valid generalities about OD from opiates. The classic signs and symptoms are
  • decreased level of conciousness
  • hypoventilation
  • pinpoint pupils
Opiate antagonists
  • Narcan (naloxone) is a specific antagonist to opiates.
    • Use narcan only to reverse respiratory depression or as a diagnostic tool.
  • Do not use narcan reflaxively "just because" a patient has used opiates
    • Narcan causes acute withdrawal in the habituated patient - unpleasant for both the the patient and staff
  • Narcan has a short duration of action - observe patients for at least an hour after giving narcan
    • Longer observation is needed when a long acting agent has been used

Salicylates/Aspirin toxidrome
Salicylate poisoning is a potentially treatable but sometimes fatal OD that produces a fairly distinctive toxidrome when present in significant amounts. The most prominent signs and symptoms are related to the metabolic and respiratory effects: a combined respiratory alkalosis and (later) metabolic acidosis.

  • Presents with tachypnea/hyperpnea
  • Tachycardia usually present
  • Fever may occur
Symptoms of salicylate toxicity:
  • Nausea, vomiting, and diarrhea are common  
  • Tinnitus is common and somewhat specific
  • Altered mental status is not expected except in severe poisoning or if there are coingestants
Salicylate levels
  • When salicylate toxicity is suspected clinically, get a level
    • If the toxicity is severe enough to require treatment, repeat the level every 2h until it is decreasing
  • Significant salicylate OD should be suspected if an unexpected/unexplained increased anion gap is noted on the BMP  OTOH, if the anion gap is not increased, significant toxicity is ruled out
  • ↑AG in a patient with ΔMS suggests toxic alcohol poisoning
The decision to treat is based primarily on the degree of symptoms and the severity of the metabolic abnormalities. Patient with more than minimal toxicity should be treated.
  • Activated charcoal is indicated in patients at low risk of aspiration.
  • Alkalinize the urine with Na bicarb:
    • 3 amps bicarb/liter of D5W @ 200-300cc/h
      • If severely acidotic start with 1-2 amps bolus
  • Dialysis is indicated as follows.
    • Salicylate level >100mg/dL
    • Severely altered mental status
    • Pulmonary edema
    • Renal insufficiency or fluid overload preventing alkalinization (and decreasing clearance)
    • Rising levels and deterioirating clinical status in spite of alkalinization

Track marks are an indicator of IV drug abuse

Frame “A” shows pinpoint pupils, “B” shows dilated pupils

Unequal pupils: In the awake and alert patient with only ocular complaints usually is an eye problem. In a patient with ↓LOC implies a serious CNS lesion.  In a patient with severe headache, think of aneurysm.

Use of the "tox screen" and "routine" lab tests in OD: covered in another essay