Page 383 - Small Animal Internal Medicine, 6th Edition

CHAPTER 22 Disorders of the Pulmonary Parenchyma and Vasculature 355

bacteria, parasites (particularly heartworms), neoplasia, or Blunted pulmonary arteries, in some cases ending with focal
fat. Conditions that have been associated with the develop- or wedge-shaped areas of interstitial or alveolar opacity
VetBooks.ir ment of pulmonary emboli, and the chapters where they are resulting from extravasation of blood or edema, may be
present. Areas of lung without a blood supply can appear
discussed, are listed in Box 22.3.
Clinical Features hyperlucent. Diffuse interstitial and alveolar opacities and
right-sided heart enlargement can occur. Pleural effusion is
In many instances, the predominant presenting sign of present in some cases and is usually mild. Echocardiography
animals with PTE is peracute respiratory distress. Cardiovas- may show secondary changes (e.g., right ventricular enlarge-
cular shock and sudden death can occur. As awareness of ment, increased pulmonary artery pressures), underlying
PTE has increased, the diagnosis is being made with greater disease (e.g., heartworm disease, primary cardiac disease),
frequency in patients with milder and more chronic signs of or residual thrombi.
tachypnea or increased respiratory efforts. Historical or Arterial blood gas analysis can show mild or profound
physical examination findings related to a potential underly- hypoxemia. Tachypnea leads to hypocapnia, except in severe
ing disease increase the index of suspicion for a diagnosis of cases, and the abnormal alveolar-arterial oxygen gradient
PTE. A loud or split second heart sound may be heard on (A-a gradient) supports the presence of a ventilation/
auscultation and is indicative of pulmonary hypertension. perfusion disorder (see Chapter 20). A poor response to
Crackles or wheezes are heard in occasional cases. oxygen supplementation is supportive of a diagnosis of PTE.
Clinicopathologic evidence of a disease known to predis-
Diagnosis pose animals to thromboemboli further heightens suspicion
Routine diagnostic methods do not provide information for this disorder. Unfortunately, routine measurements of
that can be used to make a definitive diagnosis of PTE. A clotting parameters (e.g., prothrombin time, partial throm-
high index of suspicion must be maintained because this boplastin time) are not helpful in making the diagnosis or
disease is frequently overlooked. The diagnosis is suspected even in identifying at-risk patients. Thromboelastography
on the basis of clinical signs, thoracic radiography, arterial (TEG) is a diagnostic tool that results in a graph, indicating
blood gas analysis, echocardiography, and clinicopathologic rate of clot development, clot strength, and subsequent dis-
data. A definitive diagnosis requires contrast-enhanced solution. Interest has been growing for the use of this tech-
computed tomography, pulmonary angiography, selective nique and related techniques in veterinary critical care
angiography, or nuclear perfusion scanning, but contrast- settings. The test cannot be used as a diagnostic tool for PTE
enhanced computed tomography is the routine modality itself but may prove useful in identifying at-risk patients
for diagnosis. (those with measured hypercoagulability), directing treat-
PTE is suspected in dogs and cats with severe dyspnea of ment to affected arms of coagulation, and monitoring the
acute onset, particularly if minimal or no radiographic signs effect of specific treatment on measured coagulability.
of respiratory disease are evident. In many cases of PTE, the In people, measurement of circulating D-dimers (a degra-
lungs appear normal on thoracic radiographs in spite of dation product of cross-linked fibrin) is used as an indicator
severe lower respiratory tract signs. When radiographic of the likelihood of PTE. It is not considered a specific test,
lesions occur, the caudal lobes are most often involved. so its primary value has been in the elimination of PTE from
the differential diagnoses. However, even a negative result
can be misleading in certain disease states and in the pres-
BOX 22.3 ence of small subsegmental emboli.
Measurement of D-dimer concentrations is available for
Abnormalities Potentially Associated With Pulmonary dogs through commercial laboratories. A study of 30 healthy
Thromboembolism* dogs, 67 clinically ill dogs without evidence of thromboem-

Surgery bolic disease, and 20 dogs with thromboembolic disease
Severe trauma provides some guidance for interpretation of results (Nelson
Hyperadrenocorticism, Chapter 50 et al., 2003). A D-dimer concentration > 500 ng/mL was able
Immune-mediated hemolytic anemia, Chapter 82 to predict the diagnosis of thromboembolic disease with
Hyperlipidemia 100% sensitivity but with a specificity of only 70% (i.e.,
Glomerulopathies having 30% false-positive results). A D-dimer concentration
Dirofilariasis and adulticide therapy, Chapter 10 > 1000 ng/mL decreased the sensitivity of the result to 94%
Cardiomyopathy, Chapters 7 and 8 but increased the specificity of the result to 80%. A D-dimer
Endocarditis, Chapter 6 concentration > 2000 ng/mL decreased the sensitivity of the
Pancreatitis, Chapter 37 result to 36% but increased the specificity to 98.5%. Thus the
Disseminated intravascular coagulation, Chapter 87
Hyperviscosity syndromes degree of elevation in D-dimer concentration must be con-
Neoplasia sidered in conjunction with other clinical information.
Computed tomography pulmonary angiography is com-
*Discussions of these abnormalities can be found in the given monly used in people to confirm a diagnosis of PTE and
chapters. is being used routinely for the diagnosis in veterinary