Confiabilidad del CAI en español

• Age – very young animals are more susceptible.

• Species – goats, swine and chicken are more resistant.

• Pregnant ewes are more susceptible.

• Soluble salts of lead like lead acetate are more toxic than insoluble salts like lead oxide.

• Rate of ingestion – large amounts ingested in one or two days is more toxic.

• Presence of other toxicants and debilitating disease enhances toxicity.

• Debilitated, weak, poorly nourished and emaciated animals are more susceptible than healthy animals.

• Presence of food or ingesta in the stomach or intestine delays absorption and thereby reduced toxicity.

ABSORPTION AND FATE

• Lead almost always enters the body through mouth.

• Only a small portion of lead is absorbed and over 98% is excreted in faeces.

• After absorption, lead binds to haemoglobin in the RBCs and serum albumin. Only 1% of absorbed lead is in free form.

• It is in dynamic equilibrium with lead bound to erythrocytes and serum albumin.

• Absorbed lead is stored mainly in the bones after redistribution and its subsequent mobilization is similar to that of calcium.

• About 95% of the body burden of lead is found in the bone. This trapping of lead in bones is called as 'bone sink for lead'.

• Bone sink is an important detoxification mechanism in chronic exposure to lead in small amounts. Although in long bones highest content of lead is noticed, after recent exposure, it is also found in the flat bones.

• Deposition of lead in the bones and its subsequent mobilization form the bones is similar to calcium.Lead is excreted in faeces, urine and milk.

• Lead crosses both the blood brain barrier and the placental barrier.

MECHANISM OF TOXICITY

• Lead produces toxicity by inhibiting certain enzymes having free sulphydryl groups. This inhibition is particularly noted with the precursors of haeme and leads to a decrease of

haeme synthesis with resultant anaemia.

• Lead poisoning is characterized by accumulation of protoporphyrin IX and non-haeme iron in red blood cells, accumulation of aminolevulinate in plasma and increased excretion of aminolevulinate.

• Lead also inhibits haeme synthetase, which is required for incorporation of iron in the haeme molecule.

• It also prevents the entry of iron from cytosol to mitochondria.

CLINICAL SYMPTOMS

The poisoning can be acute or chronic. But there is no clear demarcation between these. Both are cumulative poisonings.

• Acute poisoning

o Acute poisoning is common in cattle.

o Symptoms are not usually seen until 2-3 days after a fatal dose.

o Calves show signs by starting to bellow and to stagger about with rolling eyes and frothing mouth.

o Animal appears blind, is greatly excited and tries to climb the walls of its stall, during quiet phases remains with the head pushed against a wall and is inert to any external stimuli.

o Muscular spasm, tetany and death will result.

o In less severe cases, dullness and inappetance occur over a period of several days together with evidence of abdominal pain and constipation, sometimes followed by diarrhoea.

• Chronic poisoning

o Chronic poisoning in cattle is characterized by anorexia, constipation, recumbency and death.

o In sheep the clinical signs are similar to those in cattle but tetany is not observed. Pregnant ewes may abort.

o In horses the symptoms rare not well marked.

o Paralysis of the limbs, anorexia, a tucked up appearance, nasal discharge and jaundice have been reported.

o Laryngeal muscle paralysis gives rise to roaring.

o Pigs are considerably resistant to lead poisoning.

o In dogs two sets of clinical signs namely gastrointestinal and nervous symptoms.

o Gastrointestinal symptoms include anorexia, vomiting, colic and diarrhea with general loss of condition.

o Nervous symptoms include anxiety, hysterical barking, salivation and epileptiform convulsions.

o Lead poisoning in cats is not very common because they do not chew foreign objects, lick painted surfaces or eat material other than foodstuff.

o In birds the symptoms are anorexia, ataxia, followed by excitement and loss of condition. Egg production fertility and hatchability decrease. Mortality is high.

In human the important symptoms are blue line in the gums (Burton's line), wrist drop, growth arrest and lead lines in the bones. There is opacity of the extremities of long bones as

evidenced by x-rays. Basophilic stippling of red cells is also seen in humans.

PM LESIONS

• No observable gross lesions.

• Ingested lead containing material may be found in the stomach and intestines.

• There may be gastritis, hyperemia, petichae on various organs and brain edema.

• In horses there may be aspiration pneumonia secondary to laryngeal paralysis.

DIAGNOSIS

• Diagnosis is based on history, clinical symptoms, post mortem lesions and presence of a source of lead and the lead content of the blood and faeces in a living animal.

• Measurement of ALA dehyratase in blood.

• Urine ALA is increased. Level of lead >4 ppm in the liver, 0.2 ppm in whole bloodδ indicates lead poisoning.

• Twice these levels are fatal. Nucleated RBS and basophilic stippling are associated with lead poisoning in dogs. (These are also noticed in autoimmune haemolytic anaemia).

Differential diagnosis

• The symptoms of lead poisoning especially the nervous symptoms resemble the symptoms exhibited in other conditions like hypomagnesemic tetany, nervous form of acetonaemia, tetanus, vitamin A deficiency, listeriosis, barley poisoning, brain abscess or neoplasia and encephalitis.

• In dogs differential diagnosis should be with acute pancreatitis, hepatitis, intestinal parasiticism, heat stroke, encephalitis, rabies and distemper.

TREATMENT

• Di sodium calcium edentate can be used as an antidote for lead poisoning. This chelates lead to make it non-toxic and the complex lead EDTA so formed is rapidly excreted.

• This itself is nephrotoxic. This drug is administered in cattle and horses 110 mg/kg i/v or s/c two doses at 6 hours interval every other day for three treatments.

• In dogs 110 mg/kg subcutaneously as a 1% solution diluted with 0.9% saline or dextrose divided into four doses every other day for three treatments is recommended.

• Intestinal lavage or a cathartic can be administered to eliminate the unabsorbed lead.

• Thiamine 2 – 4 mg/kg subcutaneously in cattle with sodium calcium edentate is found to be useful.

• BAL increases lead excretion in urine and removes lead from the parenchymatous organs.

• It can also reach the brain tissue. Unithiol (DMPS) and succimer (DMSA) are also useful as chelating agents for lead. They can be given orally or rectally. They have excellent margin of safety and sparing effect on chelation of essential minerals like zinc.

• d- penicllamine can be used in dogs given in empty stomach at 110 mg/kg daily for two weeks. This drug may produce undesirable side effects. Hence the dog should be monitored closely during treatment.

• It should not be used in cattle, horses and sheep.

• Whenever chelating agents are used, close monitoring of water intake and urine output is required.

• Vitamin D and calcium borogluconate and sedatives may give additional support. Oral magnesium sulphate will also be useful.

• Magnesium sulphate will prevent further absorption of lead by reducing the solubility of lead.

• Seizures can be controlled with the use of barbiturates and diazepam.

• Cerebral oedema can be controlled using dexamethasone and mannitol. Since lead is an immunosuppressant, broad spectrum antibiotics are required to control secondary bacterial infection.

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