SMALL ANIMALS

Aortic thrombosis in dogs: 31 cases (2000–2010)
Geri A. Lake-Bakaar, dvm; Eric G. Johnson, dvm, dacvr; Leigh G. Griffiths, vetmb, dacvim, phd
Objective—To describe clinical signs, treatment, and outcome of aortic thrombosis in dogs.
Design—Retrospective case series.
Animals—31 dogs with aortic thrombosis.
Procedures—Records were retrospectively reviewed and data collected regarding signalment, historical signs, physical examination findings, laboratory testing, definitive diagnosis, and presence of concurrent disease.
Results—The records of 31 dogs with clinical or postmortem diagnosis of aortic thrombosis were reviewed. Onset of clinical signs was acute in 14 (45%) dogs, chronic in 15 (48%),
and not documented in 2 (6%). Femoral pulses were subjectively weak in 6 (19%) dogs and
absent in 17 (55%). Frequent laboratory abnormalities included high BUN concentration (n
= 13), creatinine concentration (6), creatine kinase activity (10), and D-dimer concentration
(10) and proteinuria with a urine protein–to–creatinine concentration ratio > 0.5 (12). Concurrent conditions included neoplasia (n = 6), recent administration of corticosteroids (6), and
renal (8) or cardiac (6) disease. Median survival time was significantly longer for dogs with
chronic onset of disease (30 days; range, 0 to 959 days) than for those with acute onset of
clinical signs (1.5 days; range, 0 to 120 days).
Conclusions and Clinical Relevance—Results suggested that aortic thrombosis is a rare
condition in dogs and accounted for only 0.0005% of hospital admissions during the study
period. The clinical signs for dogs with aortic thrombosis differed from those seen in feline
patients with aortic thromboembolism. Median survival time was significantly longer for
dogs with chronic disease than for dogs with acute disease. Despite treatment, outcomes
were typically poor, although protracted periods of survival were achieved in some dogs.
(J Am Vet Med Assoc 2012;241:910–915)

A

ortic thromboembolism occurs commonly in cats
and has been addressed extensively in the literature.1–6 Typical clinical signs in feline patients consist
of acute-onset hind limb paresis, pain, absent femoral
pulses, and nail bed cyanosis.2,3 Although idiopathic
cases have been reported,7 most cats have underlying
cardiac disease, with congestive heart failure reported
in 40% to 66% of cats.2,3,7 Prognosis is typically poor,
with a reported rate of survival to discharge of 0% to
50% and 6-month recurrence rate of 45% to 75%.2,8
Low rectal temperature, bradycardia, and multiple limb
involvement have all been associated with decreased
survival rate.3 Euthanasia is common, occurring in 24%
to 35% of cases.3
Clinical information regarding aortic thrombosis in
dogs is less thoroughly documented in the current literature. In canine patients, aortic thrombosis has been associated with multiple conditions, including hyperadrenocorticism, protein-losing glomerulonephropathy,
infective endocarditis, and neoplasia.9–12 Both acute and
chronic onset of disease has been reported,9 and clinical signs include exercise intolerance, hind limb paresis, absent femoral pulses, cold extremities, and signs of
pain.9,11,13 Survival rate in dogs with aortic thrombosis
From the Departments of Medicine and Epidemiology (Lake-Bakaar,
Griffiths) and Surgical and Radiological Sciences (Johnson), School
of Veterinary Medicine, University of California-Davis, Davis, CA
95616.
The authors thank Dr. Molly Church for pathology images and Dennis Feser for compilation of hospital population data.
Address correspondence to Dr. Griffiths (lggriffiths@ucdavis.edu).
910

Scientific Reports

Abbreviations
ATIII
ATE
INR
PT
t-PA
UPC

Antithrombin III
Aortic thromboembolism
International normalized ratio
Prothrombin time
Tissue plasminogen activator
Urine protein–to–creatinine concentration ratio

has been reported to exceed that of cats with ATE; however, the prognosis and rate of recurrence have not been
fully addressed.9,13
In feline patients, the outcome of therapeutic interventions, including thrombolytic treatment with streptokinase or t-PA or long-term anticoagulant treatment
with acetylsalicylic acid, clopidogrel, warfarin, and
heparin, has been reported.1,5,6,8,14 The literature concerning therapeutic intervention in dogs is sparse and
conflicting.9 Two case reports14,15 of dogs reported streptokinase or t-PA administration to result in partial or
complete thrombus resolution. However, another case
report9 indicated that t-PA treatment was ineffective. To
our knowledge, there are no reports of long-term management of the disease.
The purpose of the study reported here was to describe the clinical signs and diagnostic findings for dogs
with aortic thrombosis and assess associations with
survival data. We also aimed to describe short-term
(thrombolytic drug treatment and rheolytic thrombectomy) and long-term (anticoagulant and antiplatelet
treatment) therapeutic interventions. Clinical decision
JAVMA, Vol 241, No. 7, October 1, 2012

Of the dogs with murmurs. A cardiac murmur was auscultated in 9 (29%) dogs. whereas chronic disease was defined as clinical signs that developed over a period of > 24 hours. the remaining 12 dogs had no evidence of left atrial enlargement (left atrial-to-aortic root diameter ratio < 1. with echocardiographic diagnosis. and 1 (3%) was a sexually intact female.8°C (101. with a median Scientific Reports 911 SMALL ANIMALS making for the management of dogs with aortic thrombosis is critically dependent on a greater understanding of initial clinical signs. October 1. A CBC was evaluated in all dogs. Digitally captured.414 canine patients within the 10-year search period. Three dogs developed tetraparesis (1 had acute disease. Normally distributed variables are reported as mean ± SD. .5 ± 11. Echocardiographic images were retrospectively reviewed (GALB).2 ± 1°F). and 1 had a proximal aortic thrombus. < 10. the echogenicity of the thrombus. still ultrasonographic images and written ultrasonographic reports were reviewed by a board-certified radiologist (EGJ) for the presence or absence of an aortic thrombus on a dedicated workstation.6 lb). Vol 241. Neutrophilia (without stress leukogram) was present in 6 dogs (4 had acute disease and 2 had chronic disease). To avoid excessive manipulation of the data set. outliers. Two dogs had unclear progression of signs.Materials and Methods Case selection—The University of California-Davis Veterinary Medical Teaching Hospital medical record system was searched for records of dogs initially examined between September 2000 and October 2010 with aortic thrombosis identified on abdominal ultrasonography or postmortem examination. In 1 dog. and 1 had disease with unclear progression).6 years. χ2 Analysis was used to analyze breed distributions. physical examination findings. No dogs had spontaneous echocardiographic contrast in the left atrium or ventricle. body weight. and sex). 7.05 were considered significant. The owner or veterinarian perceived signs of pain in 9 (29%) dogs. 1 had a thickened interventricular septum suggestive of infiltrative disease. were not removed from calculations of mean and SD. age. was recorded. The onset of clinical signs was acute in 14 (45%) dogs and chronic in 15 (48%). Thirteen (42%) dogs were castrated males. definitive diagnosis. and mean body weight was 21. 6 were determined to have myxomatous mitral valve degeneration. Thrombocytopenia (< 100.310 neutrophils/µL (reference value. and laboratory results) were tested for normality of distribution via the Kolmogorov-Smirnov test. 1 had chronic disease. 17 (55%) were spayed females. when present. of which 6 had acute disease and 13 chronic. Mean age was 9.6).b equipped with an S5-1 and S8-3 MHz blended transducer were used for all echocardiographic examinations. Acute disease was defined as clinical signs that developed in < 24 hours. survival time was censored on the last date in the record at which the dog was known to be alive. prognostic associations.500 neutrophils/µL). If the last medical record entry indicated that the dog was alive. and presence of concurrent disease. or both via email or telephone. When performed. 1 had a mass associated with the left ventricular free wall. Results From a hospital caseload of 68. The remaining dog had vegetative endocarditis of the mitral valve. were recorded.c Values of P < 0. presence. 1 of which also had a mass in the left ventricle. and cyanotic hind limb nail beds (2 [6%]). and future prospective assessment of treatment options. No breed was found to be overrepresented. CT. bilateral hind limb involvement was present in 19 (68%) dogs. compared with adjacent muscle. For the 9 cases lost to follow-up. The JAVMA. Seven dogs did not have heart murmurs but underwent echocardiography as part of the diagnostic evaluation for thromboembolic disease. MRI. breed. compared with hospital intake. historical signs.2 kg (47. A stress leukogram was present in 9 (29%) dogs. Two of the dogs undergoing echocardiography had mild left atrial enlargement. The majority of dogs were initially examined because of paresis (23 [82%]). and severity of valvular insufficiency and evidence of clot or spontaneous contrast recorded. Gross and histologic necropsy findings were extracted from the record when performed. 2012 Kruskal-Wallis rank sum test was used to evaluate differences in survival data. Statistical analysis—Categorical data (ie. 2 acute events involved the right hind limb and then left hind limb. Two echocardiographic machinesa. and nonnormally distributed variables are reported as median and range.318 ± 2. laboratory testing. and echocardiography was performed in 7 of these. sex. Procedures—Records were retrospectively reviewed and data collected regarding signalment (age. Mean rectal temperature was 38. All chronic cases involved both hind limbs. Twelve of the 15 dogs with chronic signs had bilateral hind limb involvement. as was the presence or absence of patency through or around the thrombus identified via color flow Doppler echocardiography. 1 had a possible vegetative lesion associated with the mitral chordae tendinae. All laboratory testing was performed at the University of California-Davis clinical pathology laboratory. and examination findings) are summarized as percentages and frequencies. an attempt was made to contact the owner. Overall. An aortic thrombus was defined as a discrete intraarterial space-occupying lesion that altered blood flow. with a mean of 13. Single limb involvement was present in acute cases only: right hind limb in 3 dogs and left hind limb in 2 dogs. Paresis or paralysis was characterized in 28 dogs. Continuous data (ie. referring veterinarian. selected at the discretion of the treating clinician. Echocardiography was performed on 14 (45%) dogs. Physical examination findings included absent femoral pulses (17 [55%]). Additionally. results from other diagnostic tests (radiography. 0.4 ± 1.0005%). The location and anatomic extent of the thrombus were determined from this information. Therapeutic interventions. No.3 ± 24. or necropsy) were obtained from the medical record. All statistical evaluations were performed with a statistical software program. 31 cases of aortic thrombosis were identified (prevalence.9 ± 3. breed. subjectively cool extremities (11 [35%]).000 platelets/µL) was present in 3 chronically affected dogs. Of the dogs without heart murmurs.

and both renal arteries. Determination of UPC was performed in 12 nisone/kg [0. Six (19%) dogs had Concentration of ATIII was low in 5 of the 12 dogs received systemic corticosteroids < 1 month prior to tested. The mean albumin concentration was and 4 were hypoechoic in comparison with adjacent 2. ence range. 7.5 normal thromboelastography results.6 seconds (reference range. Ten of 17 neoplastic disease identified on necropsy. the 17 dogs tested (median. Two (6%) dogs > 0. and the other dog reof these dogs. with a mean of 11. October 1.0 to 4.000 platelets/µL). with a median of 472. and diabetes mellitus (1). ated with the left atrium. hind limb paresis. with final didogs had a prolonged partial thromboplastin time. and 1 had glomerulonephritis. 315 to > One dog had a left ventricular thrombus that was sus1. external iliac arteries.5 mg of predamination. dogs had prior chronic renal disease: 3 had proteinNo other remarkable clinical biochemical abnormalities losing nephropathy. with a range Eight (26%) dogs had renal disease. Eight of concentrations had a UPC > 0.45 mg/lb]. were noted. The mean BUN concentration was mented flow through or around the thrombus and 8 did 41.2 mg/dL (reference range.5. reference range. 51 to 399 U/L). chronic disease). and aortic thrombosis. internal iliac. increased α angle. The distal portion of the aorta and external iliac.8 ± 0. D-dipected to be of neoplastic origin (hemangiosarcoma).4 g/dL). and not. Abdominal ultrasonography was performed in 25 dogs. Fibrinogen concentration was elevated in 11 of renal mass (1). with a mean concentration of 69. The thrombus also extends into the internal iliac arteries. dian creatinine kinase activity was 384 U/L. 912 Scientific Reports JAVMA. q 12 h). Five of sonography. 7 to 9. with a agnoses of lymphoma (n = 2).04) longer than that of dogs with acute disease (1. hypercoagulable state as indicated by decreased K-kinetMedian survival time of dogs with chronic disease ics.500 (range. was also recorded in 21 cases. The distal portion of the aorta and external iliac and internal iliac arteries were involved in 1 dog. 423.7 ± 4. 0 to 959 days) was significantly (P = strength). compared with the mean creatinine concentration was 2.2 ± 7. and an aortic thrombus was identified in all dogs.8. range.1%. Seventeen dogs had these dogs had received antemortem abdominal ultraPT and partial thromboplastin time determined. and 4 of these dogs also had hyperadrenocorticism (n = 1). mer concentration was elevated in 9 of the 11 dogs evalOne dog was found to have a chronic thrombus associuated. range. A thrombus in the aorta.000 to 91. Eighteen of the 19 dogs in which urinalysis Two (6%) dogs had immune-mediated thrombocytowas performed had proteinuria at the time of initial expenia (one dog in remission received 0. Six (19%) dogs had seconds (reference range. (referinitial examination.5 and a mean UPC of 5.0 ± 38. hypoadrenocorticism a prior history of chronic renal disease.6 mg/dL the adjacent muscle. A sole thrombus in the left Figure 1—Necropsy specimen from a 13-year-old castrated male Whippet with chronic external iliac artery was identified in 1 dog. 2012 .16 Ten of these dogs had endocarditis.000 platelets/µL) was presformed. Thrombocytosis (> 400. No underlying disease process Four dogs (1 had acute disease and 3 had chronic diswas determined in 2 dogs. adremean of 15. femoral artery. femoral arteries. 5 to 21 mg/dL). and adseconds). 417 mg/dL.000 to or around the thrombus.2 ± 2. internal and external iliac arteries. and left renal artery was found in 1 dog.4 to 12. chronic kidney disease.6 was correct in all of these dogs. 10.000 (reference range. cardiac sarcoma (1).000 platelets/ Of the 25 ultrasonographic examinations perµL). into part of the left exterbrachial artery was performed in 1 dog and nal iliac artery. No.3 seconds). and down the entire right external iliac artery and into a portion of the right identified a thrombus in this artery as well. and femoral arteries were affected in 7 dogs. and G (clot (30 days. 80% to 120%). Six (reference range. Vol 241.2 mg/dL). 11 were isoechoic to adjacent muscle. q 24 h. Four of these of 78 to 52.756 U/L (reference range. The thrombus was located exclusively in the distal portion of the aorta near the iliac arterial bifurcation in 4 dogs. (1). Other concurrent diseases included also had hypoalbuminemia. The left renal artery was also found to contain a portion of the thrombus. and the diagnosis of an aortic thrombus 17 dogs had a prolonged PT.9 nocortical carcinoma (1). The remaining dog (with chronic disease) had 0. One dog had involvement of the distal portion of the aorta.3 to 1. osteosarcoma (1). 51. 3. All of the dogs with low ATIII A necropsy was performed in 10 dogs.1 ± 2. 21 included color flow Doppler examination ent in 4 dogs (3 had acute disease and 1 had chronic of the affected arteries to evaluate for patency through disease). 13 had some docu859. The aorta and external iliac arteries were involved in 10 dogs. The echogenicity of the thrombus. maximum amplitude. 109 to 311 mg/dL). Thromboelastographyd was performed in 5 dogs. Of these. although 1 had a history of ease) had results of thromboelastography consistent with chronic renal disease (Figure 1). 0.23 mg/lb].SMALL ANIMALS of 69. Azotemia was presof the thrombi identified were hyperechoic to the adent in 19 (68%) dogs (6 had acute disease and 13 had jacent muscle. The thrombus fills the An ultrasonographic evaluation of the left caudal portion of the abdominal aorta extending from the renal arteries to the aortic trifurcation.000 mg/dL. and all dogs had proteinuria with a UPC ceived 1 mg/kg [0.7 g/dL (reference range. which was not classified histologically.8 ± 2. The memuscle.

q 24 h Heparin 90 U/kg. acid and 0. q 24 h. Discussion In the present study. There were no clear historical. days. ATE is a disease characterized by acute clinical manifestation2 and recurrence is common. although further investigation is needed to clarify whether this etiology is present in any or all cases. and it is unclear whether the reScientific Reports 913 SMALL ANIMALS Median No.12 By contrast. Improvement of clinical signs was considered to have occurred when improved exercise tolerance or improvement in degree of paresis was recorded. survival time of dogs with chronic clinical signs was significantly (P = 0. SC.8 These survival differences are not explained by differences in the rate of euthanasia (18 dogs were euthanized [10 had acute disease and 8 had chronic disease]). PO.6 mg/kg. Some patients received multiple treatments and are therefore represented in multiple rows.7 mg/kg.5–0. In cats.0045) longer than that of dogs with acute disease (9 days. 3 16 1* 1* 0 1 1 0 NR acid and PO. although protracted survival time was achieved in some dogs in this series.17 but were found to be uncommon in dogs of the present study. hypothermia. or diagnostic differences between dogs that were euthanized and those that were treated.5 (95%) were common findings. Vol 241.8. Data regarding treatment were summarized (Table 1). rather than thromboembolism should be considered in dogs. the possibility of disease due to thrombosis in situ. range. SC. 14 of which were euthanized without treatment (7 had acute disease and 7 had chronic disease). 0 to 5 days). The initial clinical signs for dogs with aortic thrombosis differ from those seen in feline patients with ATE. Eighteen dogs were euthanized (10 had acute disease and 8 had chronic disease).5–0.Table 1—Outcomes of 17 of dogs receiving treatment for aortic thrombosis between 2000 and 2010. Therefore. of duration of No Chronic Acute Adverse Type of treatment Dosage range dogs treatment (d) Resolved Improved change progression recurrence Euthanized effects . hypoalbuminemia (53%). Median survival time for dogs with chronic clinical signs was significantly longer than for dogs with acute signs. Despite treatment. range. Chronic progression was considered to be present when gradual worsening of exercise intolerance.5–0. q 24 h Enoxaparin 1 mg/kg. paresis. SC. 7 to 959 days) was significantly (P = 0. Evaluation of physical examination and diagnostic findings revealed no significant differences between dogs euthanized at initial examination and those that were not. Eight of these dogs had neoplastic or suspected neoplastic disease. 0 to 120 days). severe left atrium enlargement. 9 25 1 2 0 2 3 1 NR acid q 24 h Acetylsalicylic 0. 7. These differences suggest that the pathophysiology underlying acute versus chronic aortic thrombosis in canine patients may be different. No. Reasons for euthanasia were rarely recorded but may have been influenced by suspected poor prognosis. Median survival time for the 14 untreated dogs (7 had acute disease and 7 had chronic disease) was 1 day (range. and clopidogrel 1–2 mg/kg.04) longer than that of dogs with acute clinical signs and was also longer than reported survival time for cats. No untreated dogs were documented as having any improvement in clinical signs or diagnostic findings during their follow-up period. October 1. In this study. 1 to 120 days). severe underlying cardiac disease.0005% of hospital admissions during the 10-year study period. clinical. 2012 were typically poor. and proteinuria with a UPC > 0. cardiac murmur. Resolution of clot was considered to have been achieved when a previously identified thrombus was found to be absent on abdominal ultrasonography. outcomes JAVMA. Acute recurrence was considered to have occurred when acute exacerbation of clinical signs was documented. Nine dogs (3 had acute disease and 6 had chronic disease) were lost to follow-up. Similarly.2 mg/kg/h and 1 2 + 10 0 1 0 0 0 0 NR 90 U/kg. 2 9 0 1 1* 0 0 1*† NR acetylsalicylic q 12–24 h. Only 4 dogs had prior chronic renal disease. q 8 h Warfarin NA 2 103 0 2 0 0 0 0 NR *Indicates the same patient within a horizontal column. mild azotemia (68%). range.2. 2 13 0 0 1 0 0 1 NR q 12–24 h Enoxaparin and 1 mg/kg. NA = Information not available or not applicable. and congestive heart failure are common findings in cats with ATE2. approximately half of dogs of the present study and a previous report9 had chronic disease and recurrence rate was low. †Indicates the same patient within a vertical column.6 mg/kg. Survival data for those dogs in which owners had an intention to treat demonstrated that median survival time of dogs with chronic disease (293 days. or both were documented. 1 4 0 0 1 0 0 0 NR q 8 h Rheolytic NA 2 NA 0 0 1 NA NA 1 Necrotizing treatment pancreatitis. NR = None reported. Acetylsalicylic 0. SC. In the present study. aortic thrombosis was found to be a rare condition in dogs and accounted for only 0. acute renal failure Surgical NA 1 NA 0 1* 0 0 NA 1*† Acute renal removal failure t-PA and heparin 0.

the presence of a hypercoagulable state is a reasonable assumption. in the present study. therefore. Thirteen of 21 (62%) dogs had some flow through or around the thrombus. However. has been used as an additional means for assessment of coagulation and presence of hypercoagulable state through measuring the speed and strength of clot formation. Braintree. In dogs with aortic thrombosis. The authors concluded that anticoagulation treatment should represent the first line of treatment for patients with aortic thrombosis. This finding supports future prospective investigation of long-term treatment modalities for these patients. Additionally. JMP.23 The limitations of this study are inherent to a retrospective study and include lack of standardized examination. a. 2. The clinical relevance of this finding is unknown at this time and is an area that requires further research. resulted in underestimation of survival rate in the dogs with chronic disease. Further prospective study is required to determine the effect of treatment on thrombus resolution and survival rate in canine patients with aortic thrombosis. cardiac lesions were found in 4 of the 7 dogs without murmurs in which echocardiography was performed. Although the number of cases was small. Thromboelastography. Haemonetics Corp.SMALL ANIMALS maining dogs developed renal disease secondary to the aortic thrombus or whether renal disease was a predisposing factor. In the present study.18. It was impossible from still images to evaluate the degree of blood flow. given that most dogs lost to follow-up had chronic disease. without recurrence of the aortic thrombus while they were receiving the medication. This finding supports including echocardiography.22 Conservative medical treatment in human patients typically consists of IV administration of heparin followed by anticoagulation with 914 Scientific Reports orally administered warfarin derivatives (target INR. October 1. Calculation of INR is an important consideration for monitoring warfarin treatment because the reported PT varies between laboratories on the basis of the strength of the tissue thromboplastin reagent used for the test. there is no consensus in the veterinary literature regarding the appropriate treatment of acute or chronic aortic thrombi in dogs. JAVMA. Cary. the results of thromboelastography analysis were consistent with a hypercoagulable state in 4 of the 5 dogs in which the test was performed. underlying predisposing causes should be thoroughly evaluated at the time of initial examination. and the femoral arteries seen in 7 of 25 (28%) dogs. or presence of concurrent underlying neoplastic lesions. Wash. In human patients. Bothell. in conjunction with standard coagulation profiles. this was unlikely to have affected our acute versus chronic survival data and. thrombolytic treatment.21 In this study. SAS Institute Inc. However. with 9 patients (3 with acute disease and 6 with chronic disease) eventually lost to follow-up.23. Currently. accounting for 10 of 25 (40%) of dogs in this study. Both of these patients had acute recurrence after warfarin treatment was discontinued.20 Interestingly. chronic renal disease and low ATIII concentrations have been associated with a hypercoagulable state. however. The finding that only 2 dogs had a renal artery thrombus and that all of the dogs with azotemia and proteinuria had low ATIII concentrations is suggestive of the latter. Mass.5) and has been documented as resulting in complete resolution of the thrombus without recurrence. if anything. 2012 . Protracted survival periods were documented in some canine patients with aortic thrombosis in the present study.0. Particular emphasis should be placed on diagnosis of subclinical cardiac disease. diagnostic.20. version 8.24 Optimal duration of heparin treatment and target INR have not been fully addressed in the literature. surgical intervention is typically reserved for patients with contraindications to long-term anticoagulation or with a mobile thrombus. There was a striking difference in the echogenicities of the thrombi detected with ultrasonography. internal and external iliac arteries. a measure of the tissue thromboplastin activity of the test. NC. Eight of 21 (38%) dogs of the present study had no documented flow through or around the thrombus. as part of routine diagnostic testing for dogs with aortic thrombosis.22 No consensus exists in terms of optimal treatment strategy for human patients with aortic thrombosis. Philips Medical Systems NA. Philips Healthcare. It is unknown from this study how this finding correlates with prognosis. aortic thrombosis occurring in the absence of underlying disease such as atherosclerosis or aortic aneurysm is rarely reported in the literature. regardless of the presence of a murmur. This site was second only to a more extensive thrombus involving the distal portion of the aorta. Hewlett Packard Sonos 5500 echocardiograph machine. This may be related to the age of the thrombi and is likely related to the histologic composition of thrombi. It is also possible that lack of information on survival rate of canine patients with aortic thrombosis may have influenced owner decision to euthanize. Haemonetics TEG analyzer. this finding is of unknown clinical importance at this time. there was inconsistency of patient follow-up. due to high risk of embolism. 7. c. Abdominal ultrasonographic findings suggest that the distal portion of the aorta and external iliac arteries are the most common site of aortic thrombi in dogs. No. our findings suggested that thromboelastography may be a valuable supplemental diagnostic test for the evaluation of these patients at risk for thrombosis as well as potentially for response to treatment.19 Although the pathogenesis of aortic thrombosis in dogs is unknown. Surgical treatment followed by anticoagulation and acetylsalicylic acid treatment has also been reported to result in thrombus resolution without recurrence in human patients. a recent report by Tsilimparis et al22 reviewed outcome for thrombectomy. Phillips IE33. and treatment protocols. resulting in premature euthanasia in some patients. both dogs receiving anticoagulant (warfarin) treatment with a target INR of 2 to 3 had an improvement in clinical signs.5 to 3. In human patients. Vol 241. and systemic anticoagulation alone as treatment options for aortic thrombosis. b. d. Conversion of the patient’s PT value to an INR allows for comparison of results between laboratories: INR = (patient PT/control PT)ISI where ISI is the international sensitivity index. Mass. Andover. renal disease. The echogenicities varied from isoechoic to adjacent muscle to hyperechoic and hypoechoic to adjacent muscle.

J Vet Intern Med 2003.36:713–719. Lees GE.10:245–257. J Am Vet Med Assoc 2004.65:189–192. . Thromboelastography in veterinary medicine.1:221–231. Watts GF. Dhupa N. et al. In: Small animal cardiovascular medicine.295–301. Vol 241. Hogan DF. Thrombolytic therapy in dogs and cats. Lamb CR. et al.22:357–365. Kienle RD. Welch KW. Freeman LM. J Vet Intern Med 2005. Smith SA. Harpster N. Surg Today 2000. Vet Clin North Am Small Anim Pract 2004. 2. Scott-Moncrieff J. October 1. Sadasivan D. Hanack U. No. Use of low molecular weight heparin in cats: 57 cases (1999–2003). Wiinberg B. Retrospective study of streptokinase administration in 46 cats with arterial thromboembolism. Van Winkle T.18:49–50. Hypercoagulability in chronic kidney disease is associated with coagulation activation but not endothelial function. Use of recombinant tissue-plasminogen activator for aortic thrombolysis in a hypoproteinemic dog. et al. J Vasc Surg 2002. 17. Liebman HA. Penderis J. Nishimura M.1:221–231. Elliott J. Semin Thromb Hemost 2010. J Small Anim Pract 2000. Jacob KA. Laste N. Prospective evaluation of tissue plasminogen activator in 11 cats with arterial thromboembolism. J Vet Emerg Crit Care 2001. Resolution of large intraaortic thrombus following anticoagulation therapy. 24. Pion PD. Philadelphia: WB Saunders Co.19:377–385. et al. J Feline Med Surg 1999. 4. Hackner SG. Liu SM. J Vet Emerg Crit Care 1993. 22. Smith SA. Rozanski EA. Adams MJ. et al. non-atherosclertotic descending thoracic aorta—an unusual source of arterial embolism. et al. Thromboelastographic evaluation of hemostatic function in dogs with disseminated intravascular coagulation. Thombson MF. Fraje BJ. Shimada J. 23.3:13–21. 15. Brown SA. Chang YP. 9.34:1245–1371. J S Afr Vet Assoc 1994. J Vet Intern Med 2008. Kittleson MD.225:1237–1241. St Louis: Mosby Inc. Tsilimparis N. Clare A.36:747–756. Eur J Vasc Endovasc Surg 2010.11:1–8. 21. Thrombus in the non-aneurysmal.30:663–666. 7. Morris N. Tobias AH. 5. Therapy for feline aortic thromboembolism. Van Heerden J. Feline distal aortic thromboembolism: a review of 44 cases (1990–1998). Irish AB. 1989. 12. 13. 8. Thromb Res 2008. Thromboembolic disease. Wiinberg B. Anticoagulation is an effective treatment for aortic mural thrombi. Feline distal aortic thromboembolism: a review of 44 cases (1990–1998).12:122–128. Freeman LM. 14. Carter A.540–551. 7. J Am Vet Med Assoc 1998. 19. Iyer AP. J Small Anim Pract 2008. Clinical and pathological features of aortic thromboembolism in 36 dogs.212:539–543. J Am Anim Hosp Assoc 1995. 11. J Vet Emerg Crit Care 2000. et al. Kittleson MD. Feline arterial thromboembolism: an update. Aortic and iliac thrombosis in six dogs. A retrospective study of 100 cases of feline distal aortic thromboembolism: 1977–1993. Boswood A. 10th ed. In: Kirk RW. Jensen AL. Weaver FA. Kristensen AT. Schoeman JP.41:109–113.31:492–500.References JAVMA. 3. Heart Lung Circ 2009. 16. Current veterinary therapy. Assessment and management of proteinuria in dogs and cats: 2004 ACVIM Forum Consensus Statement (Small Animal). et al.49:178–184. Bowdish ME. Arterial thromboembolism in cats: acute crisis in 127 cases (1992–2001) and longterm management with low-dose aspirin in 24 cases. 6. Pisimisis G.123:374–380. White RN. Schoeman J. Kamal U. Rozanski EA.11:111–121. Moore KE. 1998. 18. Clinical and neurological characteristics of aortic thromboembolism in dogs. J Feline Med Surg 2010. Tobias AH. et al. Acute arterial thrombosis with antithrombin III deficiency in nephrotic syndrome: report of a case.17:73–83. J Feline Med Surg 1999. 2012 Scientific Reports 915 SMALL ANIMALS 1. 20. et al. Johansson PI. ed. et al. Smith CE. 10. Goncalves R. Aortic thrombosis in a dog with glomberulonephritis. et al. Ito K.