Page 352 - Clinical Small Animal Internal Medicine

320 Section 4 Respiratory Disease

the technical difficulty of PA catheter placement, it has on PVR, which will already be increased in these patients.
VetBooks.ir been largely supplanted by CTPA in small animals. Caution must be exercised with fluid therapy, because
Ventilation–perfusion (V–Q) scanning has been used
RV overdistension impairs coronary perfusion and LV
for the detection of PTE in small animals. Perfusion
help determine if fluid administration is likely to be
scanning is performed after IV injection of techne­ preload. Echocardiography to determine RV filling may
tium‐labeled macroaggregated albumin ( 99m Tc‐MAA). beneficial.
Inhomogenous pulmonary vascular distribution of activ­ Theophylline may be beneficial as a bronchodilator
ity from the decay of 99m Tc‐MAA is consistent with PTE. and through pulmonary vasodilation, improved dia­
Although radionuclide labeling of inspired air to assess phragmatic contractility, and reduced respiratory muscle
ventilation is possible, typically perfusion scans are com­ fatigue. Positive inotropes such as dobutamine may be
pared against thoracic radiographs to identify pulmo­ necessary in cardiogenic shock, but can increase MPAP
nary pathology. Photopenic wedge‐shaped, pleural‐based and cause arrhythmias. Reflex pulmonary vasoconstric­
defects with a lobar or segmental distribution are classic tion increases PVR in PTE. Inhaled nitric oxide (NO)
for PTE, but entire lung lobes may appear photopenic, or acts as a vasodilator, decreasing MPAP and improving
if multiple small emboli are present, then a mottled pat­ hemodynamics in PTE, but has not been used clinically
tern may result. in small animals as yet, and is cost‐prohibitive. In dogs,
Computed tomography pulmonary angiography has sildenafil has beneficial effects in pulmonary hyperten­
largely replaced V–Q scanning in human medicine. A sion, and in canine PTE models it reduces MPAP through
prospective evaluation of PTE diagnosis (PIOPED II) selective pulmonary arterial vasodilation. In people,
suggested that V–Q scanning was indicated for just a sildenafil has beneficial effects in both acute PTE and the
small subset of the population presenting with suspected treatment of chronic PTE‐induced pulmonary hyperten­
PTE. In light of this, and the limited availability of equip­ sion. Although sildenafil has not been reported in small
ment and expertise, it is likely few V–Q scans will be per­ animal PTE to date, it should be considered if pulmonary
formed in small animals in future. hypertension is documented echocardiographically.
Potential side‐effects include vomiting and systemic
hypotension, and co‐administration with heparin may
Management increase the risk of hemorrhage.

In people, risk stratification based on clinical assess­ Thrombolysis
ment, oxygenation status, anatomic clot size, cardiac
function, and biomarkers underpins successful treat­ Therapeutic thrombolysis is the administration of supra­
ment. Anticoagulant therapy alone is recommended for physiologic doses of plasminogen activators systemically
low‐risk patients, while patients with hypotension sec­ or directly at the thrombus site to accelerate plasmin gen­
ondary to PTE are treated with thrombolytics followed eration and induce thrombus dissolution. Thrombolysis
by anticoagulation. The optimal strategy for manage­ in PTE aims to reverse right heart failure, improve sys­
ment of PTE in small animals is not known because of temic and pulmonary hemodynamics, limit neurohu­
the scarcity of specific information in the veterinary lit­ moral activation, and reduce recurrence. Available drugs
erature. Tailored supportive treatment for PTE patients include alteplase, reteplase, and tenecteplase. These drugs
is easy to recommend. When PTE is definitively diag­ have distinct pharmacokinetics, thrombolytic activities,
nosed or the index of suspicion is sufficiently high then and fibrin specificities. Veterinary experience with throm­
antithrombotic therapy is also warranted. Successful bolytics is limited and is predominantly in the field of
treatment for acute PTE is typically followed by chronic feline aortic thromboembolism (ATE). A recent prospec­
antithrombotic therapy and should be accompanied by tive clinical trial of tissue plasminogen activator (t‐PA) in
management of any underlying predisposing disorder. cats with ATE highlighted the risks of side‐effects associ­
ated with these agents. Although efficacious in >50% cats,
all 11 patients in the study suffered side‐effects, many
Supportive Therapy
attributable to reperfusion injury.
For some patients, PTE is rapidly fatal irrespective of The t‐PA products are fibrin specific, activating
therapy. In normal dogs, thrombi lyze rapidly so sup­ fibrin‐bound plasminogen more rapidly and more effec­
portive therapy buys time for fibrinolysis to occur. All tively than plasminogen in circulation. At pharmaco­
dyspneic patients should receive oxygen therapy. Positive logic concentrations, however, a systemic lytic state
pressure ventilation (PPV) should be considered as a last can still occur and all t‐PA products are associated with
resort if oxygen therapy cannot resolve hypoxemia, with a risk of hemorrhage in humans. Alteplase has the short­
efforts made to minimize the detrimental impact of PPV est half‐life of the available recombinant thrombolytics.