Agency for Toxic Substances and Disease Registry
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Learning Objectives |
Upon completion of this section, you should be able to
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Introduction |
Ingestion of ethylene glycol has significant toxicologic implications if undetected or left untreated. The preceding section described the clinical features of ethylene glycol poisoning in three stages that are based on the time after ingestion. This section depicts the systemic effects associated with significant ethylene glycol exposure. |
Neurologic Effects |
The initial phase of ethylene glycol poisoning is characterized by inebriation caused by unmetabolized ethylene glycol. In acute poisoning cases, the following symptoms are common (Parry and Wallach 1974; Buell, Sterling et al. 1998)
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Possible Sequelae |
Possible sequelae of severe poisonings (Walder and Tyler 1994; Hantson, Vanbinst et al. 2002) include
Cerebral edema and deposition of calcium oxalate crystals in the walls of small blood vessels in the brain contribute to this CNS toxicity (Jobard, Harry et al. 1996; Bey, Walter et al. 2002; Tobe, Braam et al. 2002). Some studies also documented brain dysfunction with corresponding cranial computed tomography findings after ethylene glycol ingestion (Chung and Tuso 1989; Zeiss, Velasco et al. 1989; Morgan, Ford et al. 2000). |
Cranial Nerve Damage |
Recovery in survivors is usually rapid and complete. However, the following cranial nerve palsies have been reported one or more weeks after acute exposure
Such adverse effects are not seen often, but delayed treatment may contribute to their development (Momont and Dahlberg 1989; Broadley, Ferguson et al. 1997; Lewis, Smith et al. 1997; Tobe, Braam et al. 2002). |
Respiratory Effects |
Inhaled ethylene glycol can irritate the respiratory tract.
Pulmonary effects typically occur 12 to 72 hours after ingestion of ethylene glycol. Pulmonary edema and adult respiratory distress syndrome (ARDS) have been reported in ethylene glycol victims (Haupt, Zull et al. 1988; Piagnerelli, Carlier et al. 1999). The following respiratory effects often occur 12 hours or more after exposure in victims of severe ethylene glycol poisoning.
Such effects most often reflect physiological compensation for severe metabolic acidosis rather than primary lung disease (Friedman, Greenberg et al. 1962; Parry and Wallach 1974; Godolphin, Meagher et al. 1980). Autopsies of ethylene glycol victims revealed the following
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Cardiovascular Effects |
The following severe cardiovascular effects have been reported in ingestion victims, during stage 2 (Friedman, Greenberg et al. 1962; Parry and Wallach 1974; Vale 1979):
Severe metabolic and fluid electrolyte abnormalities (Friedman, Greenberg et al. 1962; Parry and Wallach 1974) may cause
Ingestion of antifreeze (Walder and Tyler 1994), (Jobard, Harry et al. 1996; Rasic, Cengic et al. 1999) may affect blood pressure, causing either
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Metabolic Effects |
Severe ethylene glycol poisoning is characterized by metabolic acidosis.
The metabolic acidosis of ethylene glycol poisoning is characterized as normochloremic (Berman, Schreiner et al. 1957; Curtin, Kraner et al. 1992; Hantson, Hassoun et al. 1998; Bey, Walter et al. 2002)with
Ethylene glycol is a small, osmotically active molecule that
Osmolality reflects the number of solute particles in a solution. Numerical measures of osmolality express the number of particles present in a given weight of solvent. Tetany can sometimes occur due to hypocalcemia that results from precipitation of calcium by the oxalate formed during ethylene glycol metabolism (Parry and Wallach 1974). |
Renal Effects |
Kidney damage typically occurs during stage 3 of ethylene glycol intoxication.
Other typical urinalysis abnormalities are
Disturbed renal function may be mild and short-lived or severe and persistent for several months. Permanent renal insufficiency is uncommon but does occur (Berman, Schreiner et al. 1957; Friedman, Greenberg et al. 1962; Parry and Wallach 1974; Buell, Sterling et al. 1998; Hantson, Hassoun et al. 1998). The toxicity of ethylene glycol is linked with two metabolites.
In transformed kidney cells, the oxalate ion induces cytotoxic damage (McMartin and Cenac 2000). Another study, however, stated that glycoaldehyde and glyoxylate are the principal metabolites responsible for ethylene glycol nephrotoxicity (Poldelski, Johnson et al. 2001). |
Carcinogenicity and Teratogenicity |
Data are insufficient to determine whether ethylene glycol causes cancer or developmental defects.
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Other Effects |
Nausea, vomiting (with or without blood), and abdominal pain are frequent early findings following ethylene glycol ingestion (Meditext 2004). Ethylene glycol is only a minor skin and mucous membrane irritant, although a few cases of allergic contact dermatitis have been documented (Clayton GD & Clayton FE 1994). Reported effects on the blood have included leukocytosis, occasional methemoglobinemia, and bone marrow arrest (Verrilli, Deyling et al. 1987; Hantson, Hassoun et al. 1998; Rasic, Cengic et al. 1999). Reported musculoskeletal effects have included muscle tenderness and elevation of creatine kinase (Friedman, Greenberg et al. 1962; Parry and Wallach 1974; Verrilli, Deyling et al. 1987). |
Key Points |
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Progress Check |