Page 348 - Clinical Small Animal Internal Medicine

316 Section 4 Respiratory Disease

hypercortisolemia. Measuring patient levels of AT
VetBooks.ir activity may allow thrombosis risk stratification. Based
on extrapolations from humans, reductions of AT
activity between 50% and 75% moderately increase risk,
while activities below 30–50% markedly increase
thrombosis risk.
Increased plasma D‐dimer concentrations indicate
plasmin‐mediated cleavage of factor XIII cross‐linked
fibrin. Since D‐dimers require activation of both throm­
bin and plasmin for their formation, they are consid­
ered more specific for thrombosis than fibrin
degradation products (FDPs). Rapid, accurate, bedside
D‐dimer assays are integral to decision making in
humans with possible PTE. People with high clinical
probability scores (previous TE disease, deep vein
thrombosis, dyspnea) undergo thoracic imaging with­
Figure 32.2 A lateral thoracic radiograph from a dog with
pulmonary thromboembolism showing an area of regional out a D‐dimer test. For all other people presenting with
oligemia (Westermark sign) affecting the right caudal lung field. compatible clinical signs, rapid, quantitative D‐dimer
enzyme‐linked immunosorbent assays (ELISAs) are
representing zones of reduced blood flow distal to sites performed prior to selection of further diagnostic test­
of vascular occlusion. This finding, known as the ing. Positive D‐dimer tests prompt thoracic imaging,
Westermark sign (Figure 32.2), is rare but pathogno­ while negative tests suggest no further investigation for
monic for PTE. Pulmonary infarcts appear as distinct PTE is required.
pleural‐based, wedge‐shaped densities. Other potential Similar guidelines for small animals cannot be formu­
abnormalities include uneven vessel diameter, pulmonary lated currently because we lack sufficient data and, more
arterial enlargement, lobar vein or artery attenuation, fundamentally, a convenient and highly accurate D‐
pleural effusion, and right‐sided cardiomegaly. dimer assay is not available for small animals. Although
semiquantitative latex agglutination D‐dimer assays per­
Arterial Blood Gas Analysis form well for disseminated intravascular coagulation
Typical blood gas abnormalities associated with PTE in (DIC) in dogs, their sensitivity and specificity for throm­
dogs are hypoxemia, hypocapnia, and an increased A‐a bosis vary widely depending on the cut‐off used. As such,
gradient. In some cases, this hypoxemia may respond this assay may be best suited to testing patients with a
poorly to oxygen therapy due to intrapulmonary shunt. high index of suspicion for PTE, and a cut‐off of >1000 ng/
These findings are not specific for PTE, however, and mL to minimize false positives. Unfortunately, the latex
should be interpreted in light of other data. Similarly, agglutination assay has limited availability and is labora­
normal blood gas values do not rule out PTE. Using the tory based.
A‐a gradient may be more sensitive than solely looking Point‐of‐care (POC) tests allow determination of ana­
for hypoxemia, since the degree of hypoxemia is propor­ lyte values at the bedside, enabling them to be used for
tional to the extent of thromboembolic occlusion. Arterial clinical decision making in unstable patients. Several
blood gas analysis may be useful in assessing disease canine D‐dimer POC tests have been evaluated for the
severity, monitoring response to therapy, and determin­ detection of D‐dimers in patients with thromboembolic
ing prognosis. The ratio of PaO 2 :PaCO 2 in PTE patients disease. Of these, the NycoCard system performed the
was highly predictive of outcome in a recent human study. best, but all of these assays suffer from a lack of specific­
Blood gas values in cats with PTE have not been reported ity for thromboembolic disease. Irrespective of the assay
to date but are expected to mirror those in dogs. chosen, D‐dimers should be evaluated within 1–2 hours
of the suspected embolic event because in experimental
canine PTE, D‐dimers were increased by 30 minutes,
Risk Profiling
peaked at >2000 ng/mL at 1–2 hours before falling back
Antithrombin and D‐Dimers to control levels after 24 hours.
Antithrombin inhibits coagulation factors IIa, IXa, Xa,
XIa, and XIIa. In patients with active thrombin produc­ Viscoelastic Coagulation Testing
tion, plasma AT activity is reduced by consumption and Whole‐blood tests of coagulation such as thromboelas­
urinary AT loss has been linked to the hypercoagulable tography (TEG), thromboelastometry (ROTEM),
states associated with protein‐losing nephropathy and and the Sonoclot system graphically represent the