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- Author or Editor: Robert H. Poppenga x
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Abstract
Objective—To identify dogs with anticoagulant rodenticide (AR) screens submitted, determine whether detected concentrations of the anticoagulants correlated with severity of clinical signs for dogs with positive results on AR screens, and identify the most common disease processes present and the prognosis for those with negative AR screens.
Design—Retrospective case series.
Animals—123 dogs.
Procedures—History, signalment, clinical signs, physical examination findings, PCV, total solids concentration, prothrombin time, activated partial thromboplastin time, platelet count, AR concentrations, duration of hospitalization, blood products administered, final diagnosis, and outcome were recorded from medical records of dogs that underwent AR toxicology screenings.
Results—75 of 123 (60.9%) dogs tested positive for AR. Dogs tested positive for brodifacoum, diphacinone (also called diphenadione), and chlorophacinone. Dogs with positive AR screenings weighed significantly less, received significantly more fresh frozen plasma, had significantly longer initial prothrombin time, and were significantly more likely to survive, compared with those with negative screens. Anticoagulant rodenticide concentrations ranged from trace amounts to 1,120 parts per billion and were not correlated with any recorded parameter. The most common conditions diagnosed in the 48 dogs with negative screens included neoplasia in 15 (31.3%), immune-mediated disease in 7 (14.6%), and gastrointestinal bleeding in 5 (10.4%) dogs.
Conclusions and Clinical Relevance—AR concentrations were not correlated with severity of clinical signs or the degree of prolongation of coagulation times in this series of patients. Patients with severe coagulopathies but negative results of AR screening had a poor prognosis, with neoplasia as the most common diagnosis. Anticoagulant rodenticide intoxication had the best prognosis, with a survival rate of 98.7% in this study.
Abstract
CASE DESCRIPTION
During the same week, 3 sequential patients (a 10-year-old 8.7-kg spayed female poodle cross [dog 1], 13-year-old 2.6-kg spayed female domestic longhair cat, and 13-year-old 9.0-kg castrated male mixed-breed dog [dog 2]) underwent CT-angiography (day 0) and transarterial embolization (day 1) for nonresectable hepatocellular carcinoma (n = 2) or prostatic carcinoma (1).
CLINICAL FINDINGS
Contrast-induced nephropathy (CIN) was suspected in all animals on the basis of higher serum creatinine concentrations after contrast medium administration (exposure), compared with baseline concentrations before exposure, consistent with CIN definitions. The total dose of contrast medium was < 3 mL/kg for each exposure. For all 3 patients, creatinine concentration peaked at a median of 3 days (range, 2 to 3 days) after the first exposure (day 0), and the median absolute and relative increases in creatinine concentration after exposure (vs baseline concentrations before exposure) were 2.9 mg/dL (range, 2.2 to 3.7 mg/dL) and 410% (range, 260 to 720%), respectively.
TREATMENT AND OUTCOME
The patients received individually tailored supportive care for acute kidney injury. Serum creatinine concentrations began to improve at a median of 4 days (range, 3 to 4 days) and returned to within reference limits at a median of 7 days (range, 3 to 13 days) following initial exposure.
CLINICAL RELEVANCE
CIN should be considered as a potential complication following IV administration of contrast medium. Short-term outcome following CIN can be excellent with supportive care.
OBJECTIVE
To report history, physical examination findings, clinicopathologic abnormalities, treatments, and outcomes of dogs with confirmed α-amanitin toxicosis resulting from ingestion of α-amanitin–containing mushrooms, and to report whether any differences were significant between survivors and nonsurvivors.
ANIMALS
59 dogs.
PROCEDURES
Medical records of all dogs with confirmed α-amanitin toxicosis presented to a northern California emergency and specialty veterinary hospital between January 2006 and July 2019 were reviewed for signalment; body weight; history; physical examination findings including rectal temperature at presentation; results of serum biochemical analyses, coagulation tests, and a test for the detection of α-amanitin in urine; treatments; and outcomes. Differences for each were compared between survivors and nonsurvivors.
RESULTS
Among the 59 dogs, 36 were < 1 year of age; 56 had variable clinical signs that included vomiting, diarrhea, anorexia, and weakness or lethargy; and 22 had rectal temperatures > 39.2°C (102.5°F) at presentation. Cases were seen throughout the calendar year. At presentation, alanine aminotransferase activity was mildly to markedly increased in 97% of dogs, hypoglycemia was noted in 78%, and coagulation times were prolonged in 91%. Most dogs that rapidly decompensated died; however, 13 dogs survived to hospital discharge and completely recovered.
CONCLUSIONS AND CLINICAL RELEVANCE
Ability to recognize dogs with α-amanitin toxicosis on the basis of clinical signs, physical examination findings, and clinicopathologic test results is essential because mushroom ingestion is rarely observed and immediate treatment is necessary. Dogs that have marked hypoglycemia or coagulopathy may have a poor prognosis.
Abstract
CASE DESCRIPTION
In Latvia in 2014, acquired idiopathic megaesophagus (AIME) was observed in increased numbers of dogs that consumed varieties of 1 brand of dog food. Within 2 years, 253 dogs were affected. In Australia in November 2017, 6 working dogs that consumed 1 diet of another brand of dog food developed AIME. In total, 145 Australian dogs were affected.
CLINICAL FINDINGS
AIME was diagnosed predominantly in large-breed male dogs (> 25 kg [55 lb]). Regurgitation, weight loss, and occasionally signs consistent with aspiration pneumonia (coughing, dyspnea, or fever) were noted. Most Latvian dogs had mild to severe peripheral polyneuropathies as evidenced by laryngeal paralysis, dysphonia, weakness, and histopathologic findings consistent with distal axonopathy. In Australian dogs, peripheral polyneuropathies were not identified, and histopathologic findings suggested that the innervation of the esophagus and pharynx was disrupted locally, although limited samples were available.
TREATMENT AND OUTCOME
Investigations in both countries included clinical, epidemiological, neuropathologic, and case-control studies. Strong associations between the dog foods and the presence of AIME were confirmed; however, toxicological analyses did not identify a root cause. In Latvia, the implicated dietary ingredients and formulations were unknown, whereas in Australia, extensive investigations were conducted into the food, its ingredients, the supply chain, and the manufacturing facilities, but a cause was not identified.
CLINICAL RELEVANCE
A panel of international multidisciplinary experts concluded that the cause of AIME in both outbreaks was likely multifactorial, with the possibility of individualized sensitivities. Without a sentinel group, the outbreak in Australia may not have been recognized for months to years, as happened in Latvia. A better surveillance system for early identification of pet illnesses, including those associated with pet foods, is needed. (J Am Vet Med Assoc 2021;259:172–183)
