Lead toxicity in a puppy 


Subedited by Phil Tucak

Estimated reading time: 7 minutes

Eddie, a 19-week-old male miniature fox terrier, presented to our clinic due to his owner’s concerns that his appetite had decreased markedly. His owner had also noted that Eddie was vomiting most mornings, and that an initial partial inappetance mentioned at a previous recent consultation had progressed to the point that he would approach his food bowl, then back away trembling. 

As well as multiple vomits, worryingly he now weighed 300g less than he had at his puppy vaccination appointment four weeks previously. Eddie’s owner mentioned that roofing activity had been going on at their home for the last month, and that Eddie has been seen licking at a dislodged roofing nail cap. 

On physical examination, Eddie was quieter than usual, with tacky gums and slow skin recoil. Temperature and other vital signs were within normal limits. On cranial abdominal palpation, Eddie demonstrated marked nausea and pain. No faeces were palpable in the large intestine. Given Eddie’s signalment and his owner’s observations, a sliding gastric foreign body was suspected. Other differential diagnoses included pancreatitis, renal and hepatic disease and chronic gastritis of unknown cause (IBD, infectious). 


Eddie was admitted to hospital for a total health profile and abdominal radiographs under sedation. 

The biochemistry was within normal limits, and the CBC and electrolyte abnormalities included mild hypochromic microcytosis in the absence of anemia, mild reticulocytosis, mild leucocytosis due to mild lymphocytosis, mild thrombocytopenia and mild hyponatraemia. 

Radiographs were diagnostic of a gastric metallic foreign body consistent with a metal roofing nail cap. The results were conveyed to Eddie’s owner, and the requirement for immediate removal of the gastric foreign body explained. Having been made aware of the associated risks of exploratory surgeries in young patients, Eddie’s owners gave full consent to proceed with coeliotomy and gastrotomy. 


Eddie was pre-medicated with acepromazine 0.04mg/kg (0.07ml), methadone 0.3mg/kg (0.11ml) s/c and cerenia 1ml/10kg (0.37ml) slow i/v, and placed on intravenous Hartmann’s fluids at a surgical rate of 5ml/kg/hr. Eddie was induced with Alfaxan 2mg/kg slowly to effect (0.74ml) i/v and intubated with a cuffed 5.5 ET tube. 

A ventral midline incision was made from the xiphi sternum extending 7cm distally using a standard coeliotomy technique. A single foreign body was identified in the body of the stomach by external palpation. The entire intestinal tract was examined, and no further foreign bodies were located. All intestinal organs including the stomach were observed to be healthy, peristalsis was normal in the stomach and intestines.  

The foreign body was removed using a standard gastrotomy technique finishing with a 2-layer closure of the gastrotomy site using 3-0 PDM continuous in the submucosa/mucosa and 3-0 PDM inverting Cushing suture in the serosal layer. The abdomen was lavaged with 500ml warmed sterile saline and suctioned. Abdominal organs were replaced in their normal position and an omental wrap placed over the gastrotomy site. After changing all drapes, gloves and kit, a standard 3-layer coeliotomy closure was performed finishing with a 3-0 nylon Riverlon interlocking pattern in the skin.


Eddie’s recovery was uneventful and post-operatively he was started on durogesic 25ug patch (with half patch covered) applied to the right hind limb to be removed in 3 days, metrogyl 15mg/kg (12ml) slow i/v BID to transition to oral metrogyl 15mg/kg (50mg) PO BID 14 days once eating, clavulox 7.5mg/kg(0.2ml) s/c SID to transition to oral amoxyclav 16mg/kg (62.5mg) PO BID 14 days once eating, and omeprazole 0.6mg/kg (2.5mg) PO SID 14 days once eating.

The following day Eddie’s incision site was clean and his vitals were normal. However, he remained inappetant, backing away from his food bowl each time he was offered skinless BBQ chicken. An additional injection of cerenia 0.37ml was given slow i/v in the hope that his nausea was a short-term sequelae of his gastrotomy. A smorgasbord of food was left with him overnight.

The following morning Eddie had not touched any of the foods offered. Discussion between the vets working that day identified the very real possibility that Eddie’s inappetance was due to lead poisoning. A baseline PCV was taken (PCV 35/TPP 64) and a blood smear performed in-house. Eddie’s smear demonstrated all the classic haematological signs of clinically significant lead poisoning, namely mild non-regenerative anemia, basophilic stippling of the RBCs, poikilocytosis, hypochromasia, target cells and a high number of nucleated RBCS disproportionate to the degree of polychromasia and adequate PCV4.

As lead binds sulfhydral groups and interferes with many of sulfyhydral containing enzymes, the end result is interference with enzyme function in many body systems including interference with heme synthesis and inhibition of the enzyme 5’ nucleotides which results in increased erythrocyte fragility and the degradation of ribosomes. Haematologically this appears as thin-walled hypochromic RBCs with basophilic stippling due to degraded ribosomes.

By this stage Eddie had completely won our hearts, and a blood sample was submitted at the clinic’s own expense for urgent determination of lead levels. Given such strong evidence, we decided to commence chelation therapy and thiamine therapy immediately. Our decision was supported when Eddie subsequently returned a high blood lead level of 4.41umol/L. Levels greater than 1.7umol/L are deemed likely to be associated with clinical abnormalities (IDEXX laboratories).

Treatment for lead poisoning

It is recommended to administer Thiamine 2 – 4mg/kg per day SC for 5 days to alleviate clinical manifestations and reduce tissue deposition of lead, with the course repeated after a one-week rest period. Chelation therapy for dogs is also recommended, administering Ca-EDTA 110mg/kg/day IV or SC as a divided dose 4 times a day for 2 to 5 days. Ca-EDTA dose is administered in an equal volume of 5% glucose/NaCl. After a 1-week rest period, another 5-day treatment may be required if clinical signs persist.

Being a small animal clinic, and given the short expiry date of chelating agents, neither medication is routinely stocked and had to be sourced from elsewhere. Our local large animal colleagues generously provided us with thiamine which we started administering immediately. A frustratingly fruitless search for Ca-EDTA then ensued, with no providers throughout central and northern Queensland able to assist. Finally, BOVA Compounding were able to supply vials of Ca-EDTA specifically compounded for Eddie.

Within one day of commencing thiamine therapy Eddie began to eat again. He was discharged, and attended the clinic as a daily outpatient for his thiamine injections. A week later he commenced his Ca-EDTA therapy. Over the subsequent weeks of his therapy, Eddie’s cheerful acceptance of receiving up to five injections a day cemented his place in our clinic’s extended family. By the second round of Ca-EDTA he had put on so much weight we had to adjust his dosage. A blood smear was performed on his second last day of chelation therapy which was normal. 

Based on this excellent news, and Eddie’s obvious return to good health, his owner declined repeating his lead assay. She did however, purchase a metal detector to clear the yard of any further lead items, and reported that she had also scanned Eddie twice and was rewarded each time with a negative result.


1. Rockhampton hailstorm – A cautionary tale…      www.swisher.com.au   22 April 2021.

2. Slatter, D. Textbook of Small Animal Surgery. 2nd Edition. WB Saunders Company.  1985 Volume 1. Chapter 33. Abdominal Wall. Bellenger C.R. Coeliotomy pp 400 – 406

3. Slatter, D. Textbook of Small Animal Surgery. 2nd Edition. WB Saunders Company.  1985 Volume 1. Chapter 43. Stomach. Gastric Foreign Bodies. Van Sluys, F. pp 568 – 571

4. Lead poisoning. www.eclinpath.com 2013-2020

5. Lead poisoning in animals. MSD Manual Veterinary Manual. www.msdvetmanual.com

Dr Virginia Grice BSc (Vet) (Hons I) BVSc (Hons I)

lead toxicity in a puppy 

Veterinarian Dr Virginia Grice commenced a Bachelor of Veterinary Science at The University of Sydney in 1990. After completing third year, she spent a year away from veterinary science and completed a Bachelor of Science (Vet). 

Upon graduating in 1995, Dr Grice worked in small animal practice in metropolitan Sydney before relocating with her husband and children to rural north-west NSW where she worked in a mixed rural veterinary practice concentrating on small animal medicine and surgery.  

In 2015, she and her family moved to regional coastal WA where she spent six years working in a small animal practice which also maintained a dedicated focus on birds and wildlife. She was privileged to spend her last three months in WA working as a locum in a busy and supportive small animal emergency clinic. Dr Grice and her family then moved to QLD in January 2021 whereupon she commenced working at High Street Vet Surgery.

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