Aortic thrombosis in a dog


An Aortic tromboembolism (ATE) or saddle thrombus is caused by a thrombus, getting lodged in the aorta and blocking blood flow. This decreases or eliminates the flow of blood to the limbs which can cause different degrees of clinical signs. This is common in cats and in ATE a thrombi formed in the left atria or auricle embolize to the aorta.

This condition is less common in dogs and it’s called aortic thrombosis (ATh). Aortic thrombosis is associated with a regional prothrombotic environment in the distal aorta. We know that hypertrophic cardiomyopathy is a common underlying disease for cats with ATE. However, dogs with Ath might have no underlying disease at all (up to 58%) or a neoplasia, endocrinopathy or more commonly protein-losing diseases.

Clinical sings

Clinical signs of cats with ATE tend to be hyperacture and severe, with paraplegia, lack of deep pain perception and lack of femoral pulses a common finding. In dogs with ATh, the clinica presentation can be chronic and insidious complicating tremendously the diagnosis.

The dog will present chronic, mild locomotor abnormalities to non ambulatory paraparesis. Pain and complete absence of femoral pulse is not a typical finding. We might find some discomfort and weak but present femoral pulses

What can you see on this video is the severe weakness. DO you see how the dog is giving weight when trying to walk? He’s not able to support the weight. More than dragging, he’s weak! And this is because of the myopathy,,,,and this is also why you don’t have a patellar reflex, as we don’t have a withdrawal reflex neither. It’s very common that on this cases you find difficult to localize because it’s like a mix between neuro/ortho and the signs can wax and wane a lot!

Diagnosis of Aortic Thrombosis in Dogs

A part from your clinical examination, complete blood work including creatine kinases (CK) is required. Increased CK will raise the suspicion of poor muscle vascularization and subsequent muscle necrosis. Ultrasound imaging will allow visualizing the clot.

Treatment of Aortic Thrombosis in Dogs

Despite an overall guarded prognosis for dogs with ATh, long-term survival occurs in some dogs, suggesting heterogeneity in the clinical presentation of affected dogs.

Commonly reported treatment for ATh in dogs typically involves combinations of antiplatelet (eg, clopidogrel, aspirin) alone or in combination with anticoagulant therapies such as heparin, warfarin, direct oral anticoagulants such as rivaroxaban and apixaban with thrombolysis by tissue plasminogen activator (TPA) being attempted with varying clinical outcomes.

Outcome and treatments of dogs with aortic thrombosis: 100 cases (1997-2014)

Mackenzie Ruehl , Alex M Lynch,  Therese E O’Toole  et AL J Vet Intern Med 2020 Sep;34(5):1759-1767.

Background: Aortic thrombosis (ATh) is an uncommon condition in dogs, with limited understanding of risks factors, outcomes, and treatments.

Objectives/hypothesis: To describe potential risk factors, outcome, and treatments in dogs with ATh.

Animals: Client-owned dogs with a diagnosis of ATh based on ultrasonographic or gross necropsy examination.

Method: Multicentric retrospective study from 2 academic institutions.

Results: One hundred dogs were identified. Anti-thrombin diagnosis, 35/100 dogs were nonambulatory. The dogs were classified as acute (n = 27), chronic (n = 72), or unknown (n = 1). Fifty-four dogs had at least one comorbidity thought to predispose to ATh, and 23 others had multiple comorbidities. The remaining 23 dogs with no obvious comorbidities were classified as cryptogenic. Concurrent illnesses potentially related to the development of ATh included protein-losing nephropathy (PLN) (n = 32), neoplasia (n = 22), exogenous corticosteroid administration (n = 16), endocrine disease (n = 13), and infection (n = 9). Dogs with PLN had lower antithrombin activity than those without PLN (64% and 82%, respectively) (P = .04). Sixty-five dogs were hospitalized with 41 subsequently discharged. Sixteen were treated as outpatient and 19 euthanized at admission. In-hospital treatments varied, but included thrombolytics (n = 12), alone or in combination with thrombectomy (n = 9). Fifty-seven dogs survived to discharge. Sixteen were alive at 180 days. Using regression analysis, ambulation status at the time of presentation was significantly correlated with survival-to-discharge (P < .001).

Conclusions/clinical importance: Dogs with ATh have a poor prognosis, with nonambulatory dogs at the time of presentation having worse outcome. Although the presence of comorbid conditions associated with hypercoagulability is common, an underlying cause for ATh was not always identified.