17 Lead ingestion in a puppy

Initial presentation

Vomiting and seizures

Signalment: 5-month-old entire male West Highland white terrier, body weight 3.1 kg

Case history

The puppy had been vomiting bile and occasionally digested food once a day for 4 weeks.

The owner thought that the puppy’s appetite was reduced and the puppy was reportedly more flatulent. His stools were reported as normal in consistency, but only passed every other day. The puppy’s drinking and urination were unchanged.

The puppy did play with toys and the owner did not know if he could have ingested any of them.

The owner had owned the patient and his litter mate since they were 12 weeks old and the other puppy appeared healthy. The affected puppy was smaller than his littermate. Both puppies were fully vaccinated and had been de-wormed with fenbendazole several weeks prior to presenta­tion. Both puppies were fed a commercial puppy food supplemented with commercial ‘puppy milk’, chicken and rice. They had not travelled out of the United Kingdom.

Physical examination

The puppy was alert and responsive, but quieter than normal for a 6-month-old terrier puppy. His body condition score was 4/9. His mu­cous membranes were pink and moist with a capillary refill time of increases, due to redis­tribution of the lead from bone and tissue. In cases where the blood lead con­centration increases, it is necessary to ensure that the patient is not getting re-exposed to lead. It is also necessary to make sure any lead present in the gastrointestinal (GI) tract has been removed by excretion, which sometimes can be aided by the use of a magnesium or sodium sulphate cathartic or by endoscopy or surgery.

Discussion

Pathophysiology of lead toxicity

Lead is absorbed from the GI tract in varying amounts depending upon the form of the lead, the age of the patient and any intestinal disease present. The acidity of the gastric contents results in ionization of the lead, which is then absorbed from the duodenum, although most of it is passed in the faeces. Lead shot embedded in muscles is not commonly a cause of lead toxicity as it is not well absorbed, although if lead is in the joints it can be released into the body.

Lead is carried on the red blood cells and the unbound form is dis­tributed widely throughout the tissues of the body. It is stored in bone, where it can replace calcium in the bone matrix. It may be released from storage during chelation treatment, fracture repair or lactation.

Lead in the blood is filtered through the kidneys and can accumulate in the renal tubular epithelium.

Lead interferes with calcium ions in the body and alters vitamin D metabolism. It interferes with haem synthesis, affects the stability of the red blood cell membrane causing increased fragility, shortens red blood cell life span and causes decreased oxygen carrying capacity.

The GI signs may be caused by alteration of the smooth muscle con­tractions.

It also causes neuronal damage, decreased cerebral blood flow, cereb­ral oedema, demyelination and decreased nerve conduction.

Clinical signs and laboratory findings

The GI signs seen with lead toxicity most commonly include vomiting, diarrhoea, abdominal discomfort and anorexia. Megaoesophagus may also occur. Neurological signs include ataxia, tremors, agitation, hys­teria, seizures and blindness. Dogs have also been reported to develop aggression, dementia, pica and may even progress to being in a coma. Polyuria and polydipsia have also been reported and appear to occur more in older than in younger animals.

Normoblasts or nRBCs (greater than 40 nRBCs per 100 WBCs) have been found in about half of the blood smears of affected animals, occur­ring more often in dogs than in cats.

Radiography may show a lead foreign body within the GI tract. In chronic cases of lead toxicity, lead lines, which are linear opacities in the epiphysis of the long bones, are seen in lead toxicosis of humans but are not commonly found in dogs and cats.

Diagnosis

The neurological and GI signs associated with lead toxicity are non­specific and have many differential diagnoses. Haematological changes are helpful but not consistently present, so blood lead concentrations should be checked in patients with the clinical signs. However, the blood lead concentrations can fluctuate and are often not consistent with the severity of clinical signs. Blood lead concentrations of 1.45 to 1.7 mmol/l (30-35 μg∕dl) are suggestive of toxicity and levels greater than 2.9 mmol/l (60 μg∕dl) are generally diagnostic of toxicity.

Medical treatment

When necessary, supportive treatment such as diazepam or barbiturates may be needed for control of seizures. Attempts should be made to find and remove the source of lead and it may be necessary to have the water supply checked.

If lead is present in the GI tract, removal is necessary prior to che­lation therapy as calcium edetate increases the absorption of lead from the GI tract. Sulphate-containing cathartics may be given to aid empty­ing the GI tract; these also precipitate the lead as lead sulphate which is poorly absorbed. Larger lead objects may require removal by surgery or endoscopy.

Chelation is used to bind the lead to soluble complexes that are ex­creted in the urine. Most chelators are nephrotoxic, so renal parameters should be checked prior to use and monitored during use. Chelation of animals without signs, such as the litter mate of this puppy, is not re­commended as the chelation may increase the blood lead concentration and result in clinical signs.

Calcium edetate was used as the chelator in this case, after dilution to a 10 mg/ml solution in 5% glucose. Sodium EDTA should not be used as it may cause hypocalcaemia. As the blood lead concentrations may increase during chelation, initial monitoring should be done by clinic­al signs instead of blood lead concentration. The most serious potential side effect of calcium edetate is a reversible nephrotoxicity. GI side ef­fects may also been seen and reportedly these may be reduced by oral zinc supplementation, although no exact dose is available.

British anti-lewisite or dimercaprol is sometimes used as an adjunct therapy with calcium edetate to increase urinary and biliary excretion of lead. It is nephrotoxic and causes pain on injection and potentially may also cause vomiting and hypertension. Penicillamine may be used orally as a chelator but it will also bind zinc, iron and copper and its chelation products may be nephrotoxic.

Succimer is an analogue to dimercaprol which may be given orally. It is less likely to cause nephrotoxicity than the other chelators and does not bind with the nutritionally essential minerals. It probably does not increase the absorption of lead from the intestine and has a lower incid­ence of GI side effects. However, the drug is not widely available in the United Kingdom.

Following chelation, blood lead concentrations may rebound within 2 to 3 weeks due to redistribution of lead from bone and tissue. If this is not associated with clinical signs, further chelation therapy is not required. The animal’s environment should be checked to ensure that there has not been further exposure.

Epidemiology

Younger animals are at greater risk for lead toxicity due to increased blood-brain barrier permeability and up to five times greater absorption rates following ingestion.

Usually the affected animals are less than 5 years of age and about a third of them are less then 1 year old.

Although lead is less commonly used than in previous decades as sources of lead are being replaced, there is still exposure to it. One of the most common sources is oil- and lead-based paints which were used before 1959 and may cause exposure during remodelling of buildings. Other sources include putty, caulking material, roofing materials, bat­teries, lubrication grease, fishing sinkers, lead shot, linoleum, improp­erly fired ceramic bowls, artists’ paints, curtain weights, golf balls, wine cork covers, lead arsenate pesticides and soft water in lead pipes. One dog developed signs after licking water dripping from a tap which con­tained lead. Lead intoxication from water pipe sources may increase in the warmer months and with any cause of increased acidity. Lead con­tamination of soil can also be a source of exposure.

When lead poisoning is diagnosed in a patient where there is not an obvious source (e.g. lead foreign body in the GI tract), the owner should still be informed about the public health risks for human exposure. Chil­dren, like puppies and kittens, are at increased risk for lead poisoning. Local agencies should be contacted to check the water supply and in­vestigate the source of contamination.

Prognosis

In animals showing mild to moderate signs that are treated appropri­ately, the prognosis is good as long as the source of lead is removed. In animals with severe nervous system signs the prognosis may be more guarded.