Lead (Pb) is a heavy metal that can be found in its metallic form or as a salt. It can be found in old house paints, products for art work, upholstery accessories, welding, battery components, golf balls, oil used in petrol-run engines/machinery, lead casts and tiles.
Lead poisoning (saturnism) occurs through:
- Licking paints;
- Eating food stored in lead-containing recipients;
- Drinking water carried in lead pipes (generally lined with a protective layer of insoluble lead-carbonate, which can be damaged after repeated repairs);
- Eating vegetables grown in contaminated fields
- Ingestion of engine oil, battery parts or old, lead-based wallpaper;
- Environmental pollution from exhaust fumes.
MECHANISM OF ACTION
Lead interferes with the metabolic pathways involved in the synthesis of haemoglobin and with normal maturation of red blood cells. The fragility of red cells increases, while their capacity to carry oxygen decreases.
High concentrations of lead can cause cerebral oedema and damage to the central nervous system; in the peripheral nervous system it can cause demyelinisation and slowing of nerve conduction.
TOXICITY
The LD50 of a single oral dose of lead in the dog is 800-1000 mg/kg.
CLINICAL SIGNS
Acute poisoning (dog):
- Gastrointestinal signs: loss of appetite, vomiting, diarrhoea with colic and abdominal pain, tense abdomen
- Neurological signs (later): convulsions, hyperexcitability, opisthotonus, teeth grinding, vocalisation, circling, blindness, paresis and sometimes paralysis
Chronic poisoning (rare in animals, the signs are transitory and the evolution is slow):
- Loss of appetite, meteorism, abdominal pain, diarrhoea or constipation, loss of weight.
DIAGNOSIS
Blood tests
The blood count can be normal. Sometimes nucleated red blood cells without polychromasia can be found in the peripheral blood. Anaemia only occurs in cases of chronic poisoning.
Low numbers of red cells with basophilic stippling should raise the suspicion of lead poisoning, while 40 or more basophilic stippled red blood cells per 10,000 red cells is considered pathognomonic.
Ninety percent of absorbed lead circulates bound to red blood cells, so an assay of the concentration of lead in whole blood (collected into test-tubes containing heparin or EDTA) is the laboratory test most commonly used to diagnose intoxication by lead. Blood levels of lead greater than 0.6 ppm are diagnostic, whereas values between 0.35 and 0.6 are diagnostic if accompanied by signs. There is not always a correspondence between blood levels and signs; indeed, there is a high percentage of false negative results in cases of chronic poisoning.
Urine analysis
The urine may contain hyaline casts or granular casts. Occasionally proteins and glucose may be detected following lead-induced renal damage.
The urinary levels of lead are evaluated by giving the patient Ca EDTA (a chelating agent). The level of lead is measured before the administration of the chelator and then again 24 hours after its administration. Levels greater than 0.82 ppm at 24 hours after chelation therapy are diagnostic of lead poisoning.
Tissue analysis
Renal or hepatic levels of lead greater than 10 ppm are diagnostic of lead poisoning, while levels above 35 ppm in the faeces are indicative of exposure to lead.
TREATMENT
- Dimercaprol (BAL) by deep i.m. injection, 2-3 mg/kg every 4-6 hours in the first 24 hours, then every 8 hours in the subsequent 24 hours. If administered before Ca EDTA it enables the effects of this latter to be controlled, because of the increased excretion of the lead;
- Ca EDTA, 25-50 mg/kg i.v., dissolved in physiological saline or glucose. The dose can be repeated two or three times at intervals of 24 hours. Treatment should not be prolonged for more than 5 days and should be integrated with zinc, since this element is lost during treatment with Ca EDTA;
- Cardiorespiratory stimulants;
- Broad-spectrum antibiotics, since lead can be immunodepressant;
- Liver protectants and diet appropriate for an animal with liver impairment.
PROGNOSIS
If lead poisoning is diagnosed and treated promptly, the prognosis is good.
Suggested readings
- Hamir AN, Sullivan ND, Handson PD, Barr S.An outbreak of lead poisoning in dogs. Aust Vet J 1985;62:21-3.
- Huerter L. Lead toxicosis in a puppy. Can Vet J 2000;41:565-7.
- Knecht CD, Crabtree J, Katherman A. Clinical, clinicopathologic, and electroencephalographic features of lead poisoning in dogs. J Am Vet Med Assoc 1979;175:196-201.
- Williams JH, Williams MC. Lead poisoning in a dog. J S Afr Vet Assoc 1990;61:178-81.
- Van Alstine WG, Wickliffe LW, Everson RJ, DeNicola DB.Acute lead toxicosis in a household of cats. J Vet Diagn Invest 1993;5:496-8.
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