Page 1679 - Cote clinical veterinary advisor dogs and cats 4th

Pulmonary Thromboembolism 843

Etiology and Pathophysiology inspired oxygen (e.g., 0.21 for room air; in veterinary medicine, and adverse effects
• PTE is secondary to an underlying condition 0.4 for 40% oxygen), P b = barometric appear to be common.
VetBooks.ir • PTE leads to obstruction of a pulmonary com), P H2O = 47 mm Hg, R = 0.8, and • Catheter-directed thrombectomy/thromboly- Diseases and Disorders
○ Tissue plasminogen activator (Alteplase)
pressure (627-643 mm Hg; www.weather.
that causes venous stasis, endothelial damage,
0.25-1 mg/kg/h IV CRI up to 1-2 days
and/or hypercoagulability (Virchow’s triad).
PaO 2 and PaCO 2 are obtained from the
artery or arteriole and reactive pulmonary
arterial blood gas results.
vasoconstriction, reducing blood flow to • Coagulation profile: not useful because sis is possible but requires anesthesia and
specialized equipment.
the affected region of lung. Other forms of coagulation time below reference interval
emboli, including parasites, neoplastic cells, does not indicate a hypercoagulable state Chronic Treatment
fat, or gas, may also cause pulmonary vascular • Treatment of underlying condition
obstruction. Advanced or Confirmatory Testing • Anticoagulant therapy
• Although small PTEs are often clinically • Plasma D-dimer concentration (p. 1334): ○ LMWH: dalteparin or enoxaparin as
silent and resolve rapidly, large or numerous poor specificity, but high concentrations above, or
PTEs cause hypoxemia due to ventilation- are consistent with thromboembolic disease ○ Warfarin 0.05-0.2 mg/kg PO q 24h
perfusion mismatch, sometimes complicated in the dog (>250 ng/mL is 80% sensitive, titrated to attain an international normal-
by pulmonary edema and atelectasis. > 103 mg/mL is 100% sensitive). ized ratio (INR) of 2-3. Not generally
• Because the lung has a dual blood supply • Thromboelastography: can detect a hyper- recommended due to narrow therapeutic
with bronchial arteries from the aorta perfus- coagulable state but does not confirm PTE index and frequent bleeding complications
ing the lung parenchyma with oxygenated • Echocardiography: evidence of PH, right ○ Rivaroxaban and other direct factor Xa or
blood, PTE generally does not cause lung atrial and ventricular enlargement, and thrombin-inhibiting oral anticoagulants
infarction. occasionally, visible thrombus have recently been used in veterinary
• Increased pulmonary vascular resistance • Nuclear ventilation/perfusion scanning: safe medicine, but experience is limited.
due to pulmonary vascular obstruction and and noninvasive but very limited availability • Antiplatelet therapy: aspirin or clopidogrel
pulmonary vasoconstriction may cause PH, • Pulmonary angiography: previous gold as above
which can lead to right-sided heart failure standard for definitive diagnosis. Invasive;
when severe. unstable patient condition may preclude Possible Complications
sedation/anesthesia. • PH and right-sided heart failure
DIAGNOSIS • CT angiography: confirmatory test of choice. • Potentially severe hemorrhage is possible
Noninvasive and can be performed under with any anticoagulant or thrombolytic
Diagnostic Overview sedation without breath holding using newer therapy. This limits the use of warfarin and
Clinical diagnosis is challenging, and definitive multidetector CT scanners. thrombolytics, but risk appears low with
diagnosis requires advanced imaging. Often, a heparin or platelet antagonists.
presumptive diagnosis is based on strong clinical TREATMENT
suspicion from identifying a known risk factor Recommended Monitoring
and diagnostic test results consistent with PTE. Treatment Overview • Respiratory rate, arterial blood gas analysis
PTE can be a life-threatening emergency, and or pulse oximetry, and thoracic radiography
Differential Diagnosis initial treatment focuses on respiratory support. provide relative indications of response to
• Pulmonary parenchymal disease (e.g., If clinical suspicion is strong or a definitive therapy or deterioration of patient condition.
aspiration pneumonia, bronchopneumonia, diagnosis can be made, specific therapy should • Careful monitoring of coagulation times with
pulmonary edema, neoplasia, contusion) be provided. unfractionated heparin or warfarin therapy;
• Upper or lower airway disease (e.g., consider monitoring anti-factor Xa activity,
bronchitis/asthma, neoplasia, obstruction) Acute General Treatment if testing available, with LMWH
• Pleural space disease (e.g., pleural effusion, • Oxygen therapy (p. 1146)
pneumothorax) • Ventilation with positive end-expiratory PROGNOSIS & OUTCOME
• Other causes of PH (p. 838) pressure if warranted (PaO 2 < 60 mm Hg
despite oxygen supplementation) (p. 1185) Varies, depending on thrombus size and degree of
Initial Database • Judicious parenteral fluid therapy to maintain pulmonary vascular occlusion. Thrombi resulting
• Thoracic radiographs: initial test of choice, tissue perfusion without exacerbating right in occlusion of large portions of the pulmonary
although minimally specific and sensitive: heart failure vascular bed are associated with a poor prognosis.
main pulmonary artery dilation, abrupt • Anticoagulant therapy to prevent additional
distal pulmonary artery attenuation, thrombus formation PEARLS & CONSIDERATIONS
regional oligemia (hypovolemia), interstitial ○ Unfractionated heparin 100-150 U/
or alveolar pulmonary pattern (often with kg IV followed by 18-37.5 U/kg/h IV Comments
lobar distribution), right heart enlargement, continuous-rate infusion (CRI) to prolong • PTE should be considered in any patient
pleural effusion. Radiographs can be normal. activated partial thromboplastin time with dyspnea and/or hypoxemia and normal
• CBC, serum biochemistry panel, and uri- (aPTT) to 1.5-2.5 times baseline, or thoracic radiographs.
nalysis: not specific for diagnosis of PTE but ○ Low-molecular-weight heparin (LMWH): • PTE should be suspected in patients with a
important for recognition of predisposing effective doses not established; dalteparin predisposing cause, lower respiratory signs,
diseases. 150 U/kg SQ q 6-12h or enoxaparin increased D-dimer concentrations, and an
○ Mild to moderate thrombocytopenia may 1 mg/kg SQ q 6-12h abnormal A-a gradient.
be recognized or decrease in platelet count • Antiplatelet therapy • Even with management of an underlying
from (recent) prior value. ○ Aspirin 1-2 mg/kg PO q 12-24h (dogs); disease, recurrence is possible, and long-term
• Arterial blood gas analysis: hypoxemia; hypo- 5-20 mg PO q 3 days (cats), or anticoagulant therapy may be necessary.
capnia or normocapnia; metabolic acidosis; ○ Clopidogrel loading dose of 10 mg/kg PO
increased alveolar-arterial (A-a) gradient followed by 2-3 mg/kg PO q 24h (dogs); Prevention
(>15 mm Hg) is sensitive but not specific. 18.75 mg/CAT PO q 24h (cats) Elimination of predisposing conditions is
○ A-a gradient = FiO 2 (P b -P H2O ) − (PaCO 2 /R) • Thrombolytic therapy may be useful in imperative. Prophylactic anticoagulant therapy
− PaO 2 , in which FiO 2 = fraction of acute stage, but experience is very limited may be considered when this is not possible.

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