Poisoning elimination enhancement

I. Pharmacology. Folic acid is a B-complex vitamin that is essential for protein synthesis and erythropoiesis. In addition, the administration of folate to patients with methanol poisoning may enhance the elimination of the toxic metabolite formic acid, based on studies in folate-deficient primates. Note Folic acid requires metabolic activation and is not effective for treatment of poisoning by dihydrofolate reductase inhibitors (eg, methotrexate and trimethoprim). Leucovorin (see p 460) is the proper agent in these situations. 

There is no specific antidote and no currently recognized way to enhance elimination. Conventional treatment is entirely supportive. Cholestyramine has been shown to enhance elimination of chlordane and kepone (HSDB 1994), and may enhance elimination after ingestion of endrin. However, its effectiveness in endrin poisoning has not been tested. 

Activated charcoal adsorbs salicylate effectively, and has been given in repeated oral doses (50 g 4 hourly) to enhance clearance, although its effect on outcome is unknown. Fluid and electrolyte replacement are important and special care should be taken to maintain normal potassium concentrations. Patients with signs of poisoning, especially when plasma salicylate concentration exceeds 500 mg/1, should receive specitic elimination therapy. 

Charcoal does not bind iron, lithium, or potassium, and it binds alcohols and cyanide only poorly. It does not appear to be useful in poisoning due to corrosive mineral acids and alkali. Recent studies suggest that oral activated charcoal given alone may be just as effective as gut emptying followed by charcoal. Also, other studies have shown that repeated doses of oral activated charcoal may enhance systemic elimination of some drugs (including carbamazepine, dapsone, and theophylline) by a mechanism referred to as "gut dialysis."... 

Guerra (187) reported shifts in the M—CO bond to lower frequencies due to poisoning of Ir and Os by H2S. Exposure of Rh to H2S enhanced the bond attributed to two CO molecules per metal site and eliminated bridged Rh2-CO species. Thus sulfur appears to affect the adsorption states for CO on some group VIII metals in a manner similar to nickel. 

Acute poisoning is manifested by excitement and peripheral sympathomimetic effects convulsiorrs may occur also, in acute or chronic overuse, a state resembling hyperactive paranoid schizophrenia with hallucinations develops. Hyperthermia occurs with cardiac arrhythmias, vascular collapse and death. Treatment is chlorpromazine with added antihypertensive, e.g. labetalol, if necessary these provide sedation and a- and P-adrenoceptor blockade (not a P-blocker alone), rendering unnecessary the enhancement of elimination by urinary acidification. 

Despite a relatively fast clearance of formaldehyde from the body, toxic effects may develop in exposed individuals, particularly in cases of acute oral poisonings which quickly overwhelm the body s natural mechanisms to metabolize formaldehyde (particularly via formaldehyde dehydrogenase see Figure 2-3). There is no standard method or practice to enhance the elimination of the absorbed dose of formaldehyde (Aaron and Howland 1994 Ellenhom and Barceloux 1988). 

There are no methods known to accelerate the active transport of poisons into urine, and enhancement of glomerular filtration is not a practical means to facilitate elimination of toxicants. However, passive reabsorption from the tubular lumen can be altered. Diuretics inhibit reabsorption by decreasing the concentration gradient of the drug from the lumen to the tubular cell and by increasing flow through the tubule. Furosemide is used most often, but osmotic diuretics also are employed ("see Chapter 28). Forced diuresis should be used with caution, especially in patients with renal, cardiac, or pulmonary complications. 

Management of the poisoned patient consists of maintenance of vital functions, identification of the toxic substance, decontamination procedures, enhancement of elimination, and, in a few instances, the use of a specific antidote. 

D. Enhanced elimination. There is no role for dialysis or hemoperfusion in acute azide poisoning. 

D. Enhanced elimination. There is no role for hemodialysis or hemoperfusion in cyanide poisoning treatment. Hemodialysis may be indicated in patients with renal insufficiency who develop high thiocyanate levels while on extended ni-troprusside therapy. 

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