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Glycolate, renal failure caused

O Brien KL et al. Epidemic of pediatric deaths from acute renal failure caused by diethylene glycol poisoning. Journal of the American Medical Association, 1998, 279(15) 175-78. [Pg.138]

Report of the Secretary of Agriculture submitted in response to resolutions in the House of Representatives and Senate (USA). 1937 Journal of the American Medical Association 111 583, 919. Recommended reading. A similar episode occurred as recently as 1990-1992 See Hanif M et al 1995 Fatal renal failure caused by diethylene glycol in paracetamol elixir the Banglandesh epidemic. British Medical Journal 311 88. Note diethylene glycol is cheap. [Pg.74]

Normally, the sum of the cations exceeds the sum of the anions by no more than 12-16 mEq/L (or 8-12 mEq/L if the formula used for estimating the anion gap omits the potassium level). A larger-than expected anion gap is caused by the presence of unmeasured anions (lactate, etc) accompanying metabolic acidosis. This may occur with numerous conditions, such as diabetic ketoacidosis, renal failure, or shock-induced lactic acidosis. Drugs that may induce an elevated anion gap metabolic acidosis (Table 58-1) include aspirin, metformin, methanol, ethylene glycol, isoniazid, and iron. [Pg.1251]

Methocarbamol is effective if administered i.v. at 4.4-22 mg/kg for moderate conditions and 22-55 mg/kg for severe conditions (e.g. tetanus) (Plumb 1995). The dose rate for oral administration should be two to three times the i.v. dose (Curmingham et al 1992) 50-100mg/kg (Muir et al 1984). Methocarbamol frequently causes sedation in horses and should not be administered to pregnant mares. In addition, because of the presence of polyethylene glycol 300 as the vehicle in the parenteral solution, methocarbamol should not be used in animals with renal failure. [Pg.140]

Ethylene glycol has a characteristically sweet smell that makes it irresistible to animals. The bright green or red fluorescein dye is added to warn humans and animals of the inherent danger associated with the ingestion of antifreeze. If antifreeze is swallowed, it causes central nervous system depression followed by respiratory and cardiac distress. If untreated, ingestion leads to cardiac failure, renal failure, and brain damage. [Pg.165]

These unmeasured anions are generated as the result of the consumption of HCOJ by endogenous organic acids such as lactic acid, acetoacetic acid, or / -hydroxybutyric acid or from the ingestion of toxins such as methanol or ethylene glycol. The degree of elevation in the SAG is dependent on the clearance of the anion, as well as the multiple factors that influence HCOJ concentrations. Thus the SAG is a relative rather than an absolute indication of the cause of metabolic acidosis. The SAG may also be elevated in the metabolic acidosis due to renal failure, as the result of the accumulation of various organic anions, phosphates, and sulfates. [Pg.987]

Mupirocin may cause irritation and sensitization at the site of application. Contact with the eyes should be avoided because it causes tearing, burning, and irritation that may take several days to resolve. Systemic reactions to mupirocin occur rarely, if at all. Polyethylene glycol present in the ointment can be absorbed from damaged skin. Application of the ointment to large surface areas should be avoided in patients with moderate to severe renal failure to avoid accumulation of polyethylene glycol. [Pg.473]

This gap is normally 12-16 meq/L. A significant increase may be produced by diabetic ketoacidosis, renal failure, or drug-induced metabolic acidosis. Drugs that may cause metabolic acidosis include ethanol, ethylene glycol, isoniazid, iron, methanol, phenelzine, salicylates, tranylcypromine, and verapamil. [Pg.519]

G. Renal failure. Examples of dmgs and toxins causing renal failure are listed in Table I-28. Renal failure may be caused by a direct nephrotoxic action of the poison or acute massive tubular precipitation of myoglobin (rhabdomyolysis), hemoglobin (hemolysis), or calcium oxalate crystals (ethylene glycol) or it may be secondary to shock caused by blood or fluid loss or cardiovascular collapse. [Pg.39]

Ethylene glycol is the primary ingredient (up to 95%) in antifreeze. It is sometimes intentionally consumed as an alcohol substitute by alcoholics and is tempting to children because of its sweet taste. Intoxication by ethylene glycol itself causes inebriation and mild gastritis in addition, its metabolic products cause metabolic acidosis, renal failure, and death. Other glycols may also produce toxicity (Table 11-24). [Pg.194]

The alcohol in beverages undergoes oxidation reactions to other compounds that are eliminated by the body. When ethylene glycol is oxidized, the products can cause renal failure and may be toxic to the body. [Pg.1]


See other pages where Glycolate, renal failure caused is mentioned: [Pg.650]    [Pg.426]    [Pg.427]    [Pg.1263]    [Pg.1260]    [Pg.1413]    [Pg.195]    [Pg.567]    [Pg.570]    [Pg.160]    [Pg.690]    [Pg.1099]    [Pg.1263]    [Pg.2821]    [Pg.594]    [Pg.936]    [Pg.108]    [Pg.682]    [Pg.36]    [Pg.1073]    [Pg.6]    [Pg.608]    [Pg.260]   
See also in sourсe #XX -- [ Pg.39 ]




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