Clinical Assessment—History and Physical Examination

After completing this section, you will be able to

• describe what is included in the initial history and physical examination of patients potentially exposed to ethylene glycol, and
• describe how the clinical presentation changes over time.

Ethylene glycol ingestion is a medical emergency requiring prompt recognition and aggressive treatment.

• The clinical presentation changes over time as intoxication progresses.
• Signs and symptoms depend on the amount of ethylene glycol ingested and concurrent use of alcohol.

Therefore, making a correct diagnosis requires a reliable history of the

• time,
• route, and
• intensity of exposure.

In some cases, the patient’s altered mental state can make a detailed history difficult to obtain. Begin appropriate treatment while waiting for laboratory confirmation if ethylene glycol poisoning is strongly suspected (Howland 2015; Johnson et al. 1999; Shah 2013; Stokes and Aueron 1980).

• An exposure history* should be part of the patient history. If you suspect a temporal association between symptoms and exposure to certain products, try to identify the specific chemical ingredients involved.
   
  (*ATSDR has developed other CSEMs, including “Taking an Exposure History” and “Taking a Pediatric Exposure History.” To view these CSEMs, go to http://www.atsdr.cdc.gov/csem/.)

• In all suspected ethylene glycol poisonings, a careful history of possible substance abuse should be taken and a meticulous search in the home should be made for ethylene glycol-containing compounds.
• A history of alcohol use might suggest ingestion of ethylene glycol as an alcohol substitute. Teens might experiment with this compound.
• Regional poison control centers often can assist in identifying the contents of bottles and packages if product labels do not list the chemical ingredients.
• Asking about similar symptoms in family members, pets, friends, and coworkers might be helpful in identifying a common source of exposure.
• Clarify when the ingestion occurred and whether ethanol also was ingested. Most serious poisonings occur from ingestion. Inhalation and dermal exposures rarely cause toxicity. In the absence of treatment, ingestion of approximately 1 g/kg of ethylene glycol is considered lethal. Product labels rarely provide the concentrations of toxic alcohols. As an approximate guide, a 50% v/v solution contains 0.6 g/mL of ethylene glycol (Sivilotti 2018).

A brief initial screening examination, including vital signs, mental status, and pupils, should be performed to identify immediate measures required to stabilize the patient (Sivilotti 2018). The mental status, vital signs, and pupillary examination are the most useful elements. They provide information to classify the patient as being in a state of physiologic excitation or depression (Rhyee 2018; Velez L.I. 2017).

The onset of ethylene glycol toxicity is delayed when ethanol also is ingested. The possibility of concomitant ethanol and toxic alcohol ingestion must be considered (Sivilotti 2018).

A mental status examination includes evaluation of alertness, orientation, cognition, and short–term memory. Peripheral nerve function is evaluated by assessing proprioception, deep tendon reflexes, motor strength, postural stability (Romberg test), and cutaneous sensitivity to vibration, light touch, and pin prick (Fiedler 2007).

The time course for each stage and the severity of illness depend on the amount of ethylene glycol the patient ingested and whether the patient also ingested ethanol. Individual patients might develop any combination of organ or systemic effects (Table 2).

Stage 1 (CNS depression phase)

CNS depression begins soon after exposure, lasting for up to 12 hours after ingestion. This depression appears similar to ethanol intoxication, but without the characteristic odor of alcohol. The inebriation, euphoria, slurred speech, and lethargy result from unmetabolized ethylene glycol.

After glycoaldehyde forms (at 4–12 hours) and metabolic acidosis begins, CNS depression — especially in cases with high-dose exposures — can lead to the following effects:

• Nausea and vomiting
• Seizures
• Coma
• Cerebral edema (in some cases)

An osmolal gap without metabolic acidosis might be seen before significant metabolism of ethylene glycol occurs. As ethylene glycol is metabolized, the osmolal gap, if present, will decrease and an anion gap metabolic acidosis will evolve. Patients seen by a healthcare provider longer after exposure might have renal failure with normal osmolal and anion gaps and no acidosis or measurable ethylene glycol levels (Ford M 1991).

Signs of metabolic acidosis caused by the metabolites might become apparent late in stage 1.

Stage 2 (Cardiopulmonary toxicity phase)

The following cardiorespiratory symptoms might appear 12–24 hours after ingestion:

• Tachycardia
• Tachypnea
• Hypertension or hypotension

The following conditions might develop in this stage:

• Pulmonary edema
• Pneumonitis
• Congestive cardiac failure
• Shock

Formation of oxalic acid might lead to deposition of calcium oxalate crystals in the

• meninges,
• blood vessel walls,
• lung, and
• myocardium.

These crystal deposits can cause tissue injury and can lead to hypocalcemia secondary to calcium oxalate precipitation. Most deaths from ethylene glycol poisoning occur during stage 2.

Stage 3 (Renal toxicity phase)

Kidney damage usually develops 24–72 hours after exposure. Acidosis and acute renal failure might result from deposition of calcium oxalate crystals in the kidneys (McMartin K 2009).

The following conditions characterize the third phase:

• Flank pain
• Costovertebral angle tenderness
• Oliguric renal failure

Prolonged, rarely permanent, kidney failure is distinguished by

• proteinuria,
• hematuria,
• crystalluria, and
• increased serum BUN and creatinine.

Calcium oxalate crystals might appear in the urine soon after exposure, but absence of these crystals does not rule out ethylene glycol poisoning.

Patients might experience delayed (days to weeks after ingestion) neurological deficits. Cranial nerve deficits have occurred after ethylene glycol poisoning — an outcome likely associated with better survival rates. Severe ethylene glycol poisoning was often fatal before widespread use of hemodialysis (Rahman et al. 2012).

• Taking a detailed patient history that includes an exposure history is important in diagnosing ethylene glycol poisoning.
• Prompt recognition and early therapeutic intervention are essential to prevent sequelae of ethylene glycol poisoning.
• Patients poisoned by ethylene glycol might initially appear inebriated, but might lack other signs and symptoms of severe toxic exposure.
• After a characteristic latent period, metabolites of ethylene glycol can cause potentially life-threatening illness.
• Delayed clinical toxicity results from conversion of ethylene glycol to metabolites of greater toxicity.