Podcasts

Join Now

Aortic thrombotic disease in dogs | VETgirl Veterinary Continuing Education Podcasts

Need Help?

In today’s VETgirl online veterinary continuing education podcast, we discuss aortic thrombotic disease (what we’ll call ATD from now on). We know that patients with ATD develop this due to Virchow’s Triad – the combination of vascular endothelial injury, altered blood coagulability and changes in blood flow. Common underlying causes resulting in vascular endothelial injury include trauma, dirofilarial infection, hypotension, vasculitis, inflammation, acidosis, hypoxemia, dextrose fluid administration, arteriosclerosis (more in humans), and immune mechanisms. Altered blood coagulability may be due to platelet dysfunction (or hyperfunction), or any factor along the coagulation cascade or fibrinolytic system that has gone awry. Lastly, changes in blood flow may be due to blood stasis (e.g., an enlarged atrium), compressive lesions, trauma, or turbulence.

As an emergency specialist, I’ve seen ATD too many times in my feline patients: as feline arterial thromboembolism (FATE). Unfortunately, almost 90% of the time, underlying cardiac disease is the cause of FATE, and it may be the first indicator of heart disease. In the veterinary literature, ATD has been well described in our feline populations; in fact, we know that 12-21% of cats with hypertrophic cardiomyopathy have developed ATD as a secondary complication.1 However, ATD has not been as thoroughly investigated in our canine population. Reported causes of ATD in dogs include sepsis, DIC, pancreatitis, hyperadrenocorticism, protein-losing conditions (e.g., PLN, PLE), IMHA, heart disease, neoplastic emboli, nephrotic syndrome, dirofilariasis, hypothyroidism, and even diabetes mellitus.2-4 We know from previous studies that protein-losing nephropathy results in antithrombin loss and platelet hyperreactivity that together create a prothrombotic state. Hyperadrenocorticism also produces a state of low antithrombin and increased factors in the blood associated with coagulation, which results in production of a prothrombotic state. Hypertension is known to affect the endothelial lining of the blood vessel where coagulation commences, and affects platelet function as well. Hypothyroidism has been associated with hypercoagulability and hypofibrinolysis. Various neoplasias have also been associated with creating a prothrombotic state within the body both at the site of tumor formation and within the bloodstream.

So, today we’ll review ATD in dogs. Now, if you learn one thing from this VETgirl podcast, it’s that dogs tend not to present with the classic “saddle thrombus” signs of acute hind limb paralysis with exaggerated pain, as cats do. ATD in dogs can be more difficult to diagnose, as it tends to present with more subtle clinical signs such as hind limb dysfunction. Van Winkle et al found that dogs with ATD had physical examination findings of absent femoral pulses, weak femoral pulses, cold extremities, hindlimb pain, or even loss of digital sensation or abnormal reflexes. In a pilot study done by Dauenhauer (and me) at University of Minnesota, 80% of dogs presented for lameness, 73% for weakness, 50% for perceived pain, and clinical signs ranged from acute, peracute to chronic.

So, Winter and Budke from Auburn and Texas A&M wanted to shine some light on possible causes of ATD in dogs (5). In a study called Multicenter evaluation of signalment and comorbid conditions associated with aortic thrombotic disease in dogs, they retrospectively evaluated information from 291 dogs that were diagnosed with aortic thrombus at any of 27 North American veterinary medical teaching hospitals that contributed to the veterinary medical database between 1985 and 2011. This ended up being a prevalence of 0.03% of dogs with ATD out the 984,973 dogs that they used in the database. Control dogs that did not have any recorded evidence of ATD (n=1,445) were used for comparison. In this study, 52% of the dogs were male, and 48% were female. No prevalence was found when evaluating sex, age, or body weight in the study group of dogs with ATD. Only breed type was found to have a significant association with the incidence of ATD diagnosis. The most common breeds represented in the ATD group were mixed breeds (21.6%). Interestingly, Labrador Retrievers accounted for (10%) of the ATD group, followed by Shetland Sheepdogs (6.2%), Golden Retrievers (5.5%), and Toy Poodles (3.1%). Approximately 2/3 of the dogs in the ATD group were found to have underlying diseases, with protein-losing nephropathy (PLN) being the most common (22%), followed by neoplasia of various types (12%), hyperadrenocorticism (5.25%), systemic hypertension (5.2%), and hypothyroidism (5.2%).

While this was a retrospective study, there are some important findings to take away from this study. First, it was interesting to note that the dog breed may be a predilection for developing prothrombotic diseases. This study found that the Shetland sheepdog is an over-represented breed in the ATD group and the authors theorize this may be related to the breed’s predilection for subclinical systemic hypertension. It would be interesting to follow this study with an assessment of all the underlying diseases represented in the ATD dogs to determine if any one underlying disease is more likely to result in a secondary ATD development. From this study and from other similar studies on canine ATD, PLN seems to be the most common of the underlying disease processes. However, one of the limitations of this study is that dogs in the ATD group didn’t all receive echocardiograms, so it was difficult to rule in or out the possibility of subclinical cardiac disease as a root cause for the ATD development.

It should be noted that an older study (1993) published in JVECC retrospectively evaluated 36 dogs in a postmortem study, and found that the majority of ATD was associated with a cardiac cause such as endocarditis or atrial thrombi. This older study found that the underlying disease prevalence (19% for cardiac cause) was followed closely in prevalence by PLN (14%); this older study also did not find any predilection associated with age or sex.(2) Likewise, an older case series by Boswood et al found that half their ATD dogs (n=3) had concurrent hyperadrenocorticism; however, this study was underpowered with only 6 dogs in their ATD group.(3) Two other studies (4,6) likewise found that PLN was the most prevalent of underlying diseases to cause ATD. These studies also suggested that advanced age was a precipitating factor as well, which our current study findings argue against age as a factor.

It should be noted that in this Winter and Budke study (5) 34% of ATD dogs in this study were found not to have an identifiable underlying disease process. They hypothesized that this was similar to human studies, where no obvious underlying disease that precipitated thrombotic disease was found; however, they found abnormal aortic diameters in the distal portion of the aorta that are theorized precipitated thrombus formation.(7) This specific measurement was not investigated in this dog study, and no associations can be made at this time.

So, what can we take away from this VETgirl podcast?
This study pulled information from a database that included information provided by 27 veterinary hospitals. Due to the diversity of patient demographics, this data is likely to be a more appropriate representation of the incidence of ATD in dogs, and may explain variations between study findings, as the other studies were underpowered in ATD subjects. The limitation of this study was that cardiac disease could not be definitively ruled out, as not all dogs received an echocardiogram to ensure that subclinical preexisting heart disease was not a precipitating factor of ATD development. More importantly, clinicians should be aware that ATD in dogs is not similar to ATD in cats – it can be from cardiac disease, but other underlying metabolic causes need to be ruled out. A diagnosis or suspicion of ATD in a canine patient should trigger the clinician to search for an underlying prothrombotic disease such as PLN, neoplasia, systemic hypertension, hyperadrenocorticism, and hypothyroidism. Unlike in cats, cardiac disease was not found to be a common underlying disease in dogs with ATD. But when in doubt, get that echo just in case too.

References:
1. Luis Fuentes V. Arterial thromboembolism: risks, realities, and a rational first-line approach. J Feline Med Surg 2012;14:459–470.
2. Van Winkle TJ, Hackner SG, Liu SM. Clinical and pathological features of aortic thromboembolism in 36 dogs. J Vet Emerg Crit Care 1993;3:13–21.
3. Boswood A, Lamb CR, White RN. Aortic and iliac thrombosis in six dogs. J Small Anim Pract 2000;41:109–114.Davies C, Forrester
4. Gonçalves R, Penderis J, Chang YP, et al. Clinical and neurological characteristics of aortic thromboembolism in dogs. J Small Anim Pract 2008;49:178–184.
5. Winter RL, Budke CM. Multicenter evaluation of signalment and comorbid conditions associated with aortic thrombotic disease in dogs. JAVMA 251(4):438- 442.
6. Winter RL, Sedacca CD, Adams A, et al. Aortic thrombosis in dogs: presentation, therapy, and outcome in 26 cases. J Vet Cardiol 2012;14:333–342.
7. van den Bosch MAAJ, van der Graaf Y, Eikelboom BC, et al. Distal aortic diameter and peripheral arterial occlusive disease. J Vasc Surg 2001;34:1085–1089.

Abbreviations:
ATD=Aortic thrombotic disease
PLN=Protein-losing nephropathy

Only VETgirl members can leave comments. Sign In or Join VETgirl now!