Chronic poisoning therapy

The frequent occurrence of carbon monoxide poisoning necessitates the availability of rapid and accurate methods for the determination of HbCO in human blood samples. These methods may also be of value in evaluating the results of the usual oxygen therapy in severely poisoned patients, and in the detection of cases of chronic poisoning of moderate degree. A review... 

Cadmium, 925-1022 acute poisoning, 1000 chronic poisoning, 1000 metallothioneins, 1021 poisoning therapy, 1001 toxicology, 999 Cadmium complexes alcohols, 964 amides, 944 amine oxides, 964 amines, 933 amino acids, 938... 

IV. Diagnosis is based on a history of recent overdose or characteristic arrhythmias (eg, bidirectional tachycardia and accelerated junctional rhythm) in a patient receiving chronic therapy. Hyperkalemia suggests acute ingestion but may also be seen with very severe chronic poisoning. Senim potassium levels higher than 5.5 mEq/L are associated with severe poisoning. 

C. Late complications include bone marrow suppression, particularly leukopenia and thrombocytopenia (4-5 days) and alopecia (2-3 weeks). Chronic colchicine therapy may produce myopathy (proximal muscle weakness and elevated creatinine kinase levels) and polyneuropathy. This has also occurred after acute poisoning. 

C. Allergic reactions have not yet been reported with acute intravenous therapy for cyanide poisoning. However, allergic reactions have been reported when used for chronic IM therapy. 

A study of 55 adolescents who had been treated for lead intoxication in early childhood (11-17 years earlier) revealed no evidence of chronic nephropathy, as evidenced by endogenous creatinine clearance, BUN, serum uric acid, and routine urinalysis (Chisolm et al. 1976). PbB levels during the acute poisoning episode ranged from 100 to 650 pg/dL all patients received immediate chelation therapy. At the time of the study, their PbB levels had decreased to less than 40 pg/dL. 

Desferrioxamine has been shown to be effective in the therapy of acute iron poisoning and in the treatment and perhaps in the diagnosis of diseases associated with chronic iron accumulation. A topical formulation is available for ocular siderosis. 

Haemochromatosis leads to an increase in the density of the liver parenchyma, which correlates with the accumulation of iron. CT scans reveal a remarkably dense and bright liver parenchyma with density values of up to +140 HU (so-called white liver). The deposition of 1 g iron results in a rise in density of 1 HU. (20) CT densitometry clearly facilitates effective control of therapeutic success in this storage disease. It is not possible, however, to differentiate pronounced secondary haemo-siderosis. Hyperdense values are also found in longterm gold therapy, in glycogen thesaurismosis and M. Wilson, or in chronic arsenic poisoning. 

In chronic intoxication, the therapeutic objective is removal of the patient from the site of exposure and elimination of the noxa from the body (e. g. detoxification measures, infusions of calcium-disodium EDTA in cases of lead poisoning, etc.). There is no justification whatsoever for therapeutic nihilism. With the aid of dietetic measures (if necessary) and adjuvant therapy (N-acetylcysteine, antioxidants, ursodeoxycholic acid, S-adenosyl-methionine, etc.), the clinical course and hence the prognosis can be favourably influenced. Insufficient regression or inadequate normalization of laboratory parameters and histological changes despite removal of the patient from the area of exposure must arouse suspicion of a further, still existing noxa (alcohol, medicaments, other chemicals). 

Lead nephropathy is important because it is one of the few renal diseases that is preventable. Moreover, lead-induced acute renal dysfunction can sometimes be reversed by chelation therapy [19, 28, 63]. The salutary effect of chelation therapy appears to be on the acute reduction in GFR and the acute elevation of blood pressure associated with elevated blood lead concentration rather than on the long-term effects of cumulative exposure associated with endothelial dysfunction, hypertension, and interstitial nephritis. There is no evidence that such therapy reverses established interstitial nephritis. The partial remission achieved among moonshiners and lead workers appears to represent reversal of the physiologic effects of acute poisoning superimposed on chronic lead nephropathy. No improvement in renal function has been observed once advanced interstitial nephritis is present and the steady-state serum creatinine concentration exceeds about 3 mg/ dL [64]. 

Chen LL, Fang JT, Lin JL. Chronic renal disease patients with severe star fruit poisoning hemoperfusion may be an effective alternative therapy. 2005 43 181 -183... 

Extremely small amounts of Se are required by warm-blooded animals, but Se is also highly toxic in larger amounts. Two livestock diseases known as blind staggers and alkali disease were identified as manifestations of acute and chronic Se poisoning (Robinson, 1933). New Zealand scientists McLean et al. (1959) discovered that muscular dystrophy in lambs and calves could be prevented by Se therapy. Selenium-deficiency areas were later identified in many other countries and it soon became apparent that these areas were of far greater extent than those affected by excessive Se levels. 

Several toxic metals, including arsenic, iron, lead, and mercury, are discussed in Chapters 30 and 35. Their measurement in urine, blood, and hair (in some cases) is valuable to help diagnose acute or chronic metal poisoning. Specific therapy for these toxins is listed in Table 34-1. Because the assessment of acute iron overdose requires emergency laboratory support, it is discussed in this chapter. 

Although chelation therapy effectively reverses acute lead nephropathy and the preclinical renal dysfunction of occupational lead nephropathy, there is no evidence that such therapy reverses established interstitial nephritis due to lead. The partial remissions achieved among moonshiners and symptomatic lead workers may represent reversal of acute poisoning superimposed on chronic lead nephropathy. No improvement in renal function can be expected once ad-... 

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