Suspected Ingestions - Approach

Approach to suspected ingestion

• Ingestion should be suspected in patients who are altered, have a h/o suicidality, are found with prescription or illicit drugs on or near them
• A thorough history should be obtained from patient or witness including meds prescribed to patient and any meds prescribed to roomates
• It is important to determine if the patient's presentation is:
  • preclinical-ingestion occurred recently but no signs or symptoms yet (may be amenable to active charcoal)
  • toxic- from first signs/symptoms to peak of clinical or laboratory manifestations of toxicity (ACS, stabilize patient)
  • resolution- from peak s/s to resolution (focus on mental health, prevention)
  • These stages are based on suspected drug identity and half-life. Extended release drugs may not manifest toxicity for hours
• Monitor the following urgently:
  • Pulse ox (airway compromise, ams)
  • temp (hyper/hypothermia)
  • Telemetry (brady/tachycardia,arrhythmia)
  • ECG (acs with amphetamines)
  • glucose (hypoglycemia ie. salicylates, oral antihypoglycemics)
  • urine pregnancy
  • tox screen and other drugs based on history (ie. dig, lithium)
    
    

Differential of anion gap acidosis

• First remember to adjust the agap based on albumin. Anion gaps are measured based on protein-bound anions, which causes falsely low agap in hypoalbuminemia and falsely high agap with multiple myeloma and other states with elevated paraproteins.
  • Actual Agap= calculated agap + 2.5 (expected albumin - actual albumin)  ie) If a patient has a calculated agap of 17 and a serum albumin of 2, then actual agap = 17 + 2.5 (4-2) or 22
• Differential should include: salicylates, methanol, ethanol, ethylene glycol, ketones (DM, etoh, fasting), lactic acidosis
  • *** Both NSAIDS and salycilates cause anion gap acidosis but only salicylates case the compensatory resp alkalosis.
• Remember that patients may have mixed metabolic, respiratory process as in this patient's case due to vomitting, respiratory depression, salicylates
• In the absence of history, consider checking osmolal gap to further differentiate.
  • Methanol,ethylene glycol, isopropyl alcohol all cause osmolal gaps (isopropyl alcohol does NOT cause anion gap however)
• Methanol toxicity is due to active metabolite formic acid-> blindness, and ethylene glycol is due to active metabolite oxalic acid->renal failure, ca++ ox crystals in urine. Isopropyl alcohol's metabolite is acetone, which may interfere with colorimetric creatinine assays, resulting in falsely elevated values with a normal BUN
  

Anticholinergic ingestion syndrome
Red beet- flushing
Hot hare- hyperthermia, anhydrosis
blind bat- mydriasis
mad hatter-hallucinations, ams
full flask- urinary retention
****Don't forget tachycardia, long qt and qrs
Treatment is supportive: ACS, call poison control hotline
Options to consider are sodium bicarb for cardiac toxicity, physostigmine for moderate/severe agitiation

Other Ingestion Syndromes to consider:
Cholinergic: SLUDGE or salivation, lacrimation, urination, defecations, gastric upset and emesis
Sympathomimetic: tachycardia, diaphoresis, agitation
Opioid: pinpoint pupils, respiratory depression

(Ellen Eaton MD, 8/19/10)