Page 349 - Clinical Small Animal Internal Medicine

32 Pulmonary Thromboembolism 317

Figure 32.3 Tissue factor‐activated 10 millimeters
VetBooks.ir patient with PTE secondary to PLE. The
thromboelastography tracings from a
black tracing is a markedly
hypercoagulable TEG run at the time of the
patient’s PTE. Note the shortened reaction
(R) and clot formation (K) times and the
increased alpha angle (α), maximum
amplitude (MA), and clot elasticity (G)
values. The patient was treated with low
molecular weight heparin, which
significantly prolonged the R and K times
and reduced the alpha and MA values
(green tracing). A baseline (pink) is
G
MA
displayed for comparison. After stabilizing Events at time of trace R time K time angle (mm) (d/s)
(min)
(min)
(°)
on therapy, a normal‐looking TEG tracing 3.0–8.0 3.1–6.7 28.0–58.9 38.8–59.0 3.2–7.2 k
was produced (orange tracing).
At time of PTE 2.3 0.8 78.6 77.1 16.8k
On LMWH 7.2 9.5 26.1 29.8 2.1 k
PLE stable on Tx 4.2 2.8 54.9 51.4 5.3 k

viscoelastic properties of clotting blood during clot for­ parameters are most predictive of thrombotic risk. The
mation and lysis. These different systems produce com­ ability of these tests to identify hypercoagulability at the
parable but not interchangeable results. These point of care suggests they help identify at‐risk patients
techniques have been validated in small animals and are who require further investigation, particularly once
now commonly used in veterinary medicine. Using properly integrated into diagnostic algorithms.
TEG/ROTEM, hypercoagulability has been identified
in multiple settings in veterinary patients. Plasma‐Based Coagulation Assays
Hypercoagulable patients produce characteristic Tests including the prothrombin time (PT), activated
TEG/ROTEM tracings (Figure 32.3). These patients partial thromboplastin time (aPTT), activated clotting
typically have short reaction and clot formation times, time (ACT), and fibrinogen concentration are of limited
steep alpha angles, and large maximum amplitudes. In value in PTE because they may be normal, and any
people, MA values derived from conventional TEG and abnormalities are nonspecific. Similarly, abnormalities
from a rapid‐TEG assay have been demonstrated to of FDPs have not been widely identified in small animals
predict thrombotic risk in human surgical patients, and with PTE. These molecules indicate plasmin‐mediated
risk of PTE following trauma. It is unclear which (if any) degradation of fibrinogen or fibrin has occurred.
of these parameters best relates to thrombotic risk in Increased FDP concentrations are present in thrombo­
veterinary patients. It is also essential to recognize that sis, but also occur in liver failure, dysfibrinogenemia,
preanalytical variables such as patient hematocrit and excessive fibrinolysis, and DIC, making FDPs less spe­
fibrinogen concentration in addition to sample han­ cific than D‐dimers.
dling and assay parameters contribute to the final TEG/
ROTEM tracings. Complete Blood Counts/Serum Biochemistry
To date, only one study has reported viscoelastic coag­ These tests are not discriminating for PTE, but serum
ulation testing in small animal PTE. That study did not biochemical testing may help identify predisposing con­
identify any correlation between TEG variables and PTE, ditions such as hyperadrenocorticism, protein‐losing
but the sample size was limiting. A recent study evalu­ nephropathy, diabetes mellitus, or hypothyroidism.
ated TEG in dogs with thrombosis in various anatomic Complete blood counts may help identify a nonspecific
locations. This study found that although the TEG G‐ inflammatory leukogram or myeloproliferative disor­
values of dogs with thrombosis were significantly greater ders such as polycythemia or essential thrombocytosis
than controls, half of the dogs’ TEG tracings were clas­ that can predispose to thrombosis. Secondary thrombo­
sified as normocoagulable, suggesting that TEG may not cytosis does not predispose to PTE, although primary
have the discriminant power necessary to diagnose essential thrombocythemia may, particularly if other
PTE. These tests likely have a place in the diagnostic risk factors exist. Thrombocytopenia or schistocytosis,
work‐up of possible PTE patients, but more work is as markers of DIC, may increase the index of suspicion
needed to identify which test protocols and which for PTE.