Pulmonary effects typically occur 12-72 hours after ethylene glycol intake. People exposed to ethylene glycol have experienced Pulmonary edema, adult respiratory distress syndrome (ARDS) and death (Gordon and Hunter 1982; Haupt et al. 1988; Piagnellelli et al. 1999).

Patients with severe Ethylene glycol poisoning usually have the following respiratory effects within 12 hours or more after exposure:

Tachypnea
Excessive ventilation
Kussmaul breathing

This effect usually reflects the physiological compensation for severe metabolic Acidosis, rather than the primary lung disease (Friedman et al. 1962; Godolphin et al. 1980; Parry and Wallach 1974). Autopsy of ethylene glycol victims [(Vale 1979) showed:

Pulmonary edema with diffuse hemorrhagic Exudate

Bronchopneumonia (possibly caused by aspiration)

Calcium oxalate crystal deposition in lung parenchyma

The following serious cardiovascular effects were reported 12-24 hours after ethylene glycol intake (phase 2) (Friedman et al. 1962; Gordon and Hunter 1982; Parry and Wallach 1974; Vale 1979):

Hypertension or Hypotension

Arrhythmias (caused by electrolyte abnormalities)

Congestive heart failure with cardiogenic Pulmonary edema
Circulation failure
Cardiac arrest
Death

Glycol exposure is characterized by metabolic Acidosis with elevated Osmotic pressure gap and elevated anion gap.

Attack within 24 hours after ingestion.

Acidosis is mainly caused by the accumulation of Glycolic acid and Glyoxylic acid. Oxalic acid and lactic acid also play a role.

Ethylene glycol is a small molecule with osmotic activity

Increase plasma Osmotic pressure

Large Osmotic pressure gap may be caused.

Muscle spasm, including muscle twitching, spasm and contraction, can sometimes be caused by Hypocalcemia, which is caused by Oxalate precipitated calcium formed in the process of ethylene glycol (what is glycol) metabolism (Parry and Wallach 1974).

The renal adverse reactions after ethylene glycol intake typically occur in the third stage of ethylene glycol toxicity, which is 24-72 hours after acute exposure (Davis et al. 1997; Hess et al. 2004).

Renal damage manifests as acute oliguric renal failure.

The most common physical manifestation is tenderness in the rib angle (Friedman et al. 1962).

The most typical abnormality is the presence of a large number of "tent like" (Octahedron) or needle like Oxalate crystals in urine (Froberg et al. 2006; Hanson et al. 2002; Huhn and Rosenberg 1995; Let and Gregersen 2005; McMartin K 2009; Olivero 1993; Takayesu et al. 2006).

The absence of Oxalate crystals cannot exclude the diagnosis of Ethylene glycol poisoning (Baum et al. 2000; Boyer et al. 2001; Curtin et al. 1992; Hanson et al. 2002; Haupt et al. 1988).

Other typical Urinalysis abnormalities include:

Low Specific Gravity
Proteinuria
MicroHematuria
Pyuria

Renal dysfunction may be mild, transient, or severe, persistent. Although uncommon, permanent renal insufficiency does occur.