Page 384 - Small Animal Internal Medicine, 6th Edition

356 PART II Respiratory System Disorders

medicine. The diagnosis can never be ruled out on the basis have potential benefit include the long-term administration
of computed tomography because multiple small arteries, of low-molecular-weight heparin, aspirin, or clopidogrel.
VetBooks.ir rather than one or more large vessels, may be obstructed. Aspirin for the prevention of PTE remains controversial
because aspirin-induced alterations in local prostaglandin
Further, changes may be apparent for only a few days after
the event. One limitation of thoracic computed tomography
in dogs and especially in cats is patient size. In addition, and leukotriene metabolism may be detrimental.
veterinary patients will not hold their breath. Patients must Prognosis
be anesthetized and positive-pressure ventilation applied The prognosis depends on the severity of the respiratory
during scanning for maximal resolution. A high-quality signs, the response to supportive care, and the ability to
computed tomography scanner and an experienced radiolo- eliminate the underlying process. In general, a guarded prog-
gist are required for accurate interpretation. nosis is warranted.
Selective angiography is the historic gold standard for the
diagnosis of PTE. Sudden pruning of pulmonary arteries or
intravascular filling defects and extravasation of dye are PULMONARY EDEMA
characteristic findings. Nuclear scans can provide evidence
of PTE with minimal risk to the animal. Unfortunately, this Etiology
technology has limited availability. The same general mechanisms that cause edema elsewhere
Pulmonary specimens for histopathologic evaluation are in the body cause edema in the pulmonary parenchyma.
rarely collected, except at necropsy. However, evidence of Major mechanisms include decreased plasma oncotic pres-
embolism is not always found at necropsy because clots may sure, vascular overload, lymphatic obstruction, and increased
dissolve rapidly after death. Therefore such tissue should be vascular permeability. The disorders that can produce these
collected and preserved immediately after death. The exten- problems are listed in Box 22.4. Most cases of pulmonary
sive vascular network makes it impossible to evaluate all edema resulting primarily from increased vascular permea-
possible sites of embolism, and the characteristic lesions may bility fall within the classification system of acute lung injury
also be missed. (ALI) and acute respiratory distress syndrome (ARDS). ALI
is an excessive inflammatory response of the lung to a pul-
Treatment monary or systemic insult. ARDS describes severe ALI based
All animals with suspected PTE should be given aggressive on degree of hypoxemia. The rapid leakage of high-protein
supportive care and treatment for any underlying, predispos- edema fluid from damaged capillaries is a key feature of ALI.
ing conditions. Oxygen therapy (see Chapter 25) is indicated In some patients that survive the initial edema, epithelial cell
for all patients. Fluids are administered as needed to support proliferation and collagen deposition add to pulmonary dys-
circulation, with care to avoid fluid overload. Theophylline function and can ultimately result in pulmonary fibrosis
may be beneficial in some patients (see Chapter 21). Silde- within a short time (e.g., weeks).
nafil may be helpful for patients with evidence of pulmonary Regardless of cause, edema fluid initially accumulates in
hypertension (see prior discussion of Pulmonary Hyperten- the interstitium. However, because the interstitium is a small
sion in this chapter). compartment, the alveoli are soon involved. When profound
The use of fibrinolytic agents for the treatment of PTE in fluid accumulation occurs, even the airways become filled.
animals has not been well established. Animals with sus- Respiratory function is further affected as a result of the
pected hypercoagulability are likely to benefit from antico- atelectasis and decreased compliance caused by compression
agulant therapy. The goal of such therapy is to prevent the of the alveoli and decreased concentrations of surfactant.
formation of additional thrombi. Anticoagulant therapy is Airway resistance increases as a result of the luminal nar-
administered only to animals in which the diagnosis is highly rowing of small bronchioles. Hypoxemia results from
probable. Dogs with heartworm disease suffering from post- ventilation/perfusion abnormalities.
adulticide therapy reactions usually are not treated with anti-
coagulants (see Chapter 10). Potential surgical candidates Clinical Features
should be treated with great caution. Clotting times must be Animals with pulmonary edema are seen because of cough,
monitored frequently to minimize the risk of severe tachypnea, respiratory distress, or signs of the inciting
hemorrhage. disease. Crackles are heard on auscultation, except in animals
Specific recommendations for the treatment and preven- with mild or early disease. Blood-tinged froth may appear in
tion of thromboembolic disease with anti-coagulant drugs the trachea, pharynx, or nares immediately preceding death
are provided in Chapter 12. Because of the serious problems from pulmonary edema. Respiratory signs can be peracute,
and limitations associated with anticoagulant therapy, elimi- as in ALI/ARDS, or subacute, as in hypoalbuminemia.
nating the predisposing problem must be a major priority. However, a prolonged history of respiratory signs (e.g.,
months) is not consistent with a diagnosis of edema. The list
Prevention of differential diagnoses in Box 22.4 can often be greatly
No methods of preventing PTE in at-risk patients have been narrowed by obtaining a thorough history and performing a
objectively studied in veterinary medicine. Treatments that thorough physical examination.