Page 260 - Small Animal Internal Medicine, 6th Edition

232 PART I Cardiovascular System Disorders

Management strategies used for TE disease in dogs are (at a dose of 2-4 mg/kg PO q24h) is more effective than
outlined in Box 12.3. Although fibrinolytic therapy is avail- aspirin for in vitro platelet inhibition. At this dose, effective
VetBooks.ir able, its use is limited by dosage uncertainties, the need for levels of clopidogrel are achieved within 3 days; alternatively,
an oral loading dose (10 mg/kg) can provide antithrombotic
intensive care, and the potential for serious complications.
Systemic thrombolysis with rt-PA and streptokinase have
there is no convincing evidence of clinical superiority of
been reported in dogs, with variable success. Locally directed effect in dogs within 90 minutes. However, unlike in cats,
thrombolysis (catheter delivery of rt-PA directly to the side clopidogrel over aspirin. In a subsequent prospective study
of thrombosis) is feasible in dogs and may reduce systemic of dogs with IMHA, there was no difference in outcome
effects of thrombolytics. Interventional radiology techniques between dogs given clopidogrel, ultra–low-dose aspirin, or
can also be used to break down or remove thrombi percuta- both, although sample size was low. Both drugs are well-
neously via catheter-directed thrombectomy and embolec- tolerated in dogs, with minimal GI effects of aspirin at such
tomy. These techniques have not been effective in cats with low doses; aspirin is less expensive than clopidogrel. Thus
ATE but might hold promise in dogs of larger size. Arterial although many clinicians prefer clopidogrel based on its
stenting has been used successfully in some dogs with aortic superior platelet inhibition in vitro, low-dose aspirin remains
thromboembolism. The consequences of reperfusion injury a reasonable, inexpensive alternative in dogs.
and distal embolization of clot fragments remain serious Anticoagulants are recommended in addition to anti-
concerns with any form of thrombolytic therapy. platelet drugs in dogs with aortic thrombosis. In the acute
Fluid therapy is used (in patients without CHF) to expand setting, unfractionated heparin remains the mainstay of
vascular volume, support blood pressure, and correct elec- treatment. A common initial dose is 100 IU/kg IV bolus fol-
trolyte and acid/base abnormalities depending on individual lowed by 600 to 800 IU/kg/day (as a CRI or divided into q8h
patient needs. Hypothermia that persists after circulating intermittent boluses), although the ideal dose has not been
volume is restored can be addressed with external warming. established. Monitoring recommendations are similar to
Concurrent CHF is rarely a concern because cardiac disease those for cats, with the goal of prolonging aPTT to 1.5-2.5×
is an uncommon cause of aortic thrombosis in dogs; acute baseline value. However, recent evidence suggests that moni-
respiratory signs are more likely to signal pain or pulmonary toring anti-FXa activity might better assess anticoagulant
thromboembolism. In cases where heart disease is present, effects of unfractionated heparin and may improve survival.
treatment for CHF or arrhythmias is provided as indicated After initial stabilization, or for dogs with more chronic
(see Chapters 3 and 4 and other relevant chapters). clinical signs, dogs are transitioned to more long-term anti-
Analgesic therapy is important in cases of acute ATE, coagulation with LMWH, warfarin, or a factor Xa inhibitor
which is particularly painful especially for the first 24 to 36 (see later).
hours (see Box 12.3). Chronic in situ aortic thrombosis is In general, the prognosis for aortic thrombosis in dogs is
less painful, and analgesics may or may not be indicated. guarded to poor, with 50% to 60% of dogs surviving to dis-
Loosely bandaging the affected limb(s) to prevent self- charge. Rear limb function improvement could be seen
mutilation might be necessary. Renal function, serum elec- within several days of initiating therapy; however, 2 or more
trolyte concentrations, and ECG rhythm are monitored weeks are required in most cases. Prognosis for dogs that are
frequently to help detect acute hyperkalemia associated with ambulatory on presentation, and those with chronic clinical
reperfusion (see Chapter 2, p. 47). signs, is much better than for dogs with acute-onset signs or
Antiplatelet and anticoagulant therapies are indicated to that are nonambulatory on presentation.
prevent growth of the existing clot and decrease additional
thrombus formation. Drug options are the same as in cats, PROPHYLAXIS AGAINST
and no standard therapeutic protocol has been established. AORTIC THROMBOSIS
Given that aortic thrombi in dogs generally develop in situ Strategies to prevent recurrence of ATE in dogs are similar
in the distal aorta (an area of high-shear blood flow), platelet to those used in cats. Generally, a combination of an anti-
inhibitors are thought to be particularly important. As in platelet (clopidogrel or aspirin) and anticoagulant is used.
cats, clopidogrel and aspirin are the most commonly used Options for long-term anticoagulants include LMWH, war-
antiplatelet medications. There are few studies evaluating farin, and factor Xa inhibitors. LMWHs (such as daltepa-
efficacy of antiplatelet drugs in dogs, and none specifically rin and enoxaparin) require SC administration, and their
in dogs with aortic thrombosis. In dogs with IMHA, a disease expense makes them cost-prohibitive for medium- to large-
known to predispose dogs to TE disease (though more com- breed dogs. Therefore although LMWH has essentially
monly pulmonary thromboemboli), a retrospective study replaced warfarin as the anticoagulant of choice in cats
suggested that dogs that received ultra–low-dose aspirin with ATE, warfarin remains a reasonable treatment option
(0.5 mg/kg PO q24h) in addition to other therapies had for dogs with aortic thrombosis because of their larger
improved survival compared with dogs that did not receive body size.
aspirin. Although this study does not prove efficacy of aspirin Warfarin inhibits the enzyme (vitamin K epoxide re-
in preventing TE disease, it did establish safety of ultra–low- ductase) responsible for activating the vitamin K–dependent
dose aspirin in a patient population concurrently receiving clotting factors (II, VII, IX, and X), as well as proteins C and S.
immunosuppressive doses of glucocorticoids. Clopidogrel Initial warfarin treatment causes transient hypercoagulability