DESCRIPTION

The odor of certain compounds may be used to identify the poison.

PATHOPHYSIOLOGY

• Olfactory receptors are located in the superior nasal turbinates near the nasal septum; axons from these receptors cross the cribriform plate and join the olfactory bulb.
• The olfactory bulb is connected to the olfactory cortex and other sites within the CNS.
• Primary olfaction for most substances is via the olfactory nerve (cranial nerve I).
• Olfaction for ammonia and acetone is via the trigeminal nerve (cranial nerve V).
• Human olfaction usually cannot distinguish more than four substances simultaneously.
• Olfactory fatigue is a process by which an individual rapidly develops tolerance to an odor (e.g., hydrogen sulfide); within a few minutes, the person can no longer smell the compound, even though it is still present.

RISK FACTORS

Individuals who have impaired olfaction may not be able to identify odors associated with a particular poison; for example, only 55% to 60% of the population can smell cyanide.

Section Outline:

• DESCRIPTION
• PATHOPHYSIOLOGY
• RISK FACTORS

DIFFERENTIAL DIAGNOSIS

Further information on each poison is available in SECTION IV. Characteristic odors and the toxicants associated with them are listed as follows:

• Ammonia. Ammonia or uremia
• Bananas. Amyl acetate
• Bitter almond. Cyanide
• Burning rope. Marijuana
• Cereal. Nystatin
• Charcoal/smoke. Cyanide or carbon monoxide (through smoke inhalation)
• Chlorine. Chlorine or other halogen such as bromine
• Decaying fish. Phosphine
• Fruity. Isopropyl alcohol, acetone, amyl nitrite, butyl nitrite, isobutyl nitrite, diabetic ketoacidosis, alcoholic ketoacidosis, or chloroform
• Garlic. Organophosphates, selenium, arsenic, thallium, tellurium, phosphorus, or phosphine
• Hay. Phosgene
• Mothballs. Naphthalene, paradichlorobenzene, or camphor
• Paint. Toluene
• Peanuts. Vacor
• Pear-like/acrid. Paraldehyde or chloral hydrate
• Peppermint. Methylsalicylate (oil of wintergreen)
• Raw fish/must. Zinc phosphide, aluminum phosphide, or calcium phosphide
• Rotten eggs. Hydrogen sulfide, disulfiram, succimer, carbon disulfide, dimethyl sulfoxide (DMSO), mercaptan or sulfur. Mercaptans are nontoxic agents with an easily detectable odor and are often added to toxic substances as a warning odor; the odor of natural gas is produced by mercaptans.
• Shoe polish. Nitrobenzene or aniline
• Tobacco. Nicotine
• Vinegar. Acetic acid
• Vinyl/"new car." Ethchlorvynol (Placidyl)
• Violets. Urine following turpentine ingestion

SIGNS AND SYMPTOMS

Physical signs may help reveal the poison involved when they occur in conjunction with an odor.

HEENT

• Miosis and garlic odor suggest organophosphate.
• Mucous membrane irritation and mothball odor suggest paradichlorobenzene.
• Mucous membrane irritation and coughing with vinegar odor suggests acetic acid; with acrid smell suggests ammonia; with bleach smell suggests chlorine or other halogen.
• Dermal and mucous membrane irritation, headache, CNS depression, and a banana odor suggest amyl acetate.

Dermatologic

• Skin flushing, headache, tachycardia, abdominal pain, vomiting, and anxiety following ethanol ingestion accompanied by a rotten egg odor suggest disulfiram.
• Rash, nausea, headache and a garlic-onion-oyster smell suggest DMSO.

Pulmonary

• Bronchorrhea, wheezing, progressive respiratory failure, and an odor of garlic or petroleum may indicate organophosphate.
• Dyspnea, cough, mucous membrane irritation, pleuritic chest pain, frothy sputum, pulmonary edema, and cyanosis with the odor of hay suggest phosgene.
• Cough, mucous membrane irritation, altered mental status, and delayed pulmonary edema with the musty odor of fish or raw liver suggest zinc, aluminum, or calcium phosphide (all liberate phosphine gas when exposed to water).

Gastrointestinal

• Hematemesis, abdominal pain, CNS depression, and a fruity acetone-like odor suggest isopropyl alcohol ingestion.
• Nausea, abdominal pain, gastrointestinal bleeding, and a garlic odor may indicate arsenic, thallium, or selenium.
• Luminescent or fluorescent smoking stools combined with hepatic and renal injury after ingestion of a substance with a garlic odor suggest phosphorus.

Hematologic

• Methemoglobinemia or hemolysis and the odor of mothballs suggest exposure to naphthalene.
• Hemolysis and the odor of garlic suggest arsine poisoning.

Fluids and Electrolytes

• An anion gap metabolic acidosis and a peppermint odor on the breath or of the gastric contents suggest oil of wintergreen (methyl salicylate).
• Proteinuria, hematuria, distal renal tubular acidosis, and odor of paint suggest toluene.

Neurologic

Altered mental status may involve the following relationships:

• Bitter almond odor and increased anion gap lactic acidosis suggest pure cyanide toxicity.
• The odor of smoke or burned flesh suggests cyanide or carbon monoxide toxicity.
• The odor of rotten eggs suggests hydrogen sulfide toxicity.
• Odor of paint with hypokalemia, abnormal urinalysis, and perhaps paint on face or hands indicates toluene abuse.
• The odor of burned leaves or rope with bloodshot eyes, somnolence, and mild euphoria suggests marijuana.
• A shoe polish odor associated with hypoventilation, nausea, headache, and occasionally methemoglobinemia suggests nitrobenzene.
• A "new car" vinyl odor on the breath associated with hypoventilation, nystagmus, slurred speech, ataxia, and occasionally coma suggests ethchlorvynol (Placidyl).
• A pear-like odor on the breath associated with CNS depression, hypoventilation, and ventricular dysrhythmias suggests chloral hydrate.

Seizures

• The odor of moth balls associated with nausea, vomiting, and abdominal pain suggests camphor.
• A tobacco odor, salivation, nausea, vomiting, and abdominal pain suggest nicotine.

Peripheral Neuropathy

A chronic exposure to a substance with the odor of rotten eggs suggests carbon disulfide.

Other Neurologic Effects

Inhalation of a substance with a fruity odor associated with tachycardia, hypotension, mucous membrane irritation, nausea, lightheadedness, headache, and occasionally methemoglobinemia suggests amyl, butyl, or isobutyl nitrite.

Endocrine

Ingestion of a rodenticide with a peanut odor associated with new onset diabetes mellitus suggests vacor.

Procedures and Laboratory Tests

• Serum electrolytes, BUN, and creatinine
  • An increased anion gap metabolic acidosis can be seen with exposure to methyl salicylate, paraldehyde, cyanide, carbon monoxide, or hydrogen sulfide; uremia; diabetic ketoacidosis; and seizures produced by water hemlock or other agents.
  • Normal anion gap metabolic acidosis with hypokalemia and low serum bicarbonate may indicate toluene exposure.
  • Hyperglycemia may be produced by PNU (Vacor) or diabetic ketoacidosis.
• Serum lactate. Increased serum lactate can develop with poisoning from cyanide, carbon monoxide, hydrogen sulfide, or seizures, hypotension, or hypoxia from any cause.
• Serum ketones are seen with acetone or isopropyl alcohol poisoning or diabetic ketoacidosis.
• Serum osmolality is increased with ethanol, acetone, isopropyl alcohol, and diabetic ketoacidosis until metabolism has occurred.
• Salicylate level is increased with methyl salicylate poisoning.
• Arterial blood gas analysis may be helpful in evaluating acid-base status and systemic oxygenation.
• Chest radiograph may demonstrate infiltrates and noncardiogenic pulmonary edema that may be delayed following severe exposures to ammonia, chlorine, phosphine, organophosphate, or phosgene.
• Abdominal radiograph. Paradichlorobenzene-containing mothballs are more densely radiopaque when compared with naphthalene-containing mothballs; chloral hydrate is radiopaque.

Section Outline:

• DIFFERENTIAL DIAGNOSIS
• SIGNS AND SYMPTOMS
  • HEENT
  • Dermatologic
  • Pulmonary
  • Gastrointestinal
  • Hematologic
  • Fluids and Electrolytes
  • Neurologic
  • Seizures
  • Peripheral Neuropathy
  • Other Neurologic Effects
  • Endocrine
  • Procedures and Laboratory Tests

• Management should be focused on removal of the patient from the source of the exposure, decontamination, and supportive care.
• Appropriate airway management is vital.
• Dose and time of exposure should be determined for all substances involved.

DIRECTING PATIENT COURSE

The health-care provider should call the poison control center when:

• assistance with odor identification is needed.
• coingestant, drug interaction, or underlying disease presents unusual problems.

DECONTAMINATION

• Inhalational Exposure. Patient should be removed from the source of the exposure; appropriate measures must be taken to protect both rescue personnel and health-care workers.
• Ingestion. The decision to perform gastrointestinal decontamination is based on the suspected toxicant, the time of ingestion, and the clinical status of the patient.
• Dermal Exposure. Exposed areas should be washed by copious irrigation with water; appropriate measures must be taken to protect both rescue personnel and health-care workers.

ANTIDOTES

Specific antidotes are not available for most poisons; thus, the decision to administer an antidote should be based on the suspected toxicant and the clinical status of the patient.

ADJUNCTIVE TREATMENT

• Specific treatment is based on the suspected toxicant.
• Dysrhythmias, blood pressure abnormalities, and electrolyte abnormalities should be corrected as clinically indicated.

Section Outline:

• DIRECTING PATIENT COURSE
• DECONTAMINATION
• ANTIDOTES
• ADJUNCTIVE TREATMENT

PATIENT MONITORING

• Vital signs and cardiac rhythm should be monitored continuously.
• Appropriate airway management is vital; 100% oxygen should be administered.

EXPECTED COURSE AND PROGNOSIS

Complications should be anticipated based on the suspected toxicant and the clinical status of the patient.

EXPECTED COURSE AND PROGNOSIS

Delayed pulmonary edema is a complication of poorly water-soluble inhalants, such as phosgene and phosphine.

Section Outline:

• PATIENT MONITORING
• EXPECTED COURSE AND PROGNOSIS
• EXPECTED COURSE AND PROGNOSIS

• Lack of an odor does not rule out the presence of toxic substances; many toxic substances are odorless, and some individuals have anosmia for specific toxic substances.
• Odors of extremely toxic substances may be masked by odors of less toxic substances; human olfaction usually cannot detect more than four substances at any given time.
• The disappearance of an odor does not mean that the concentration is decreasing; olfactory fatigue may produce a false sense of security and leads to poisoning.
• Other life-threatening causes of an altered mental status should always be ruled out before attributing the effects to ethanol.

Toxic effect of other gases, fumes, or vapors.

See Also: SECTION II, Bradycardia, Hypertension, Hypotension, Tachycardia, and Ventricular Dysrhythmia chapters; and SECTION IV, chapters on individual agents.

RECOMMENDED READING

Chiang W. Otolaryngolic principles. In: Goldfrank LR, Flomenbaum NE, Lewin NA, et al., eds. Goldfrank's toxicologic emergencies, 6th ed. Norwalk, CT: Appleton & Lange, 1998.

Goldfrank LR, Weisman R, Flomenbaum N. Teaching the recognition of odors. Ann Emerg Med 1982;11:684-686.

Author: Edwin K. Kuffner

Reviewer: Katherine M. Hurlbut