Thrombosis and Thrombo -embolisms

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Thrombosis and Thrombo -embolisms. Megan Connolly Block 2 6/2011. How is a thrombus identified ultrasonographically ? B-mode U/S exam Doppler- helps evaluate the degree of vascular compromise
Thrombosis and Thrombo-embolismsMegan ConnollyBlock 26/2011How is a thrombus identified ultrasonographically?
  • B-mode U/S exam
  • Doppler- helps evaluate the degree of vascular compromise
  • Acute phase thrombi typically appear anechoic. Some faint echogenicity within the vessel may be seen as color flows around the filling defect when using Doppler.
  • After several days the thrombus organizes into a visible structure with intermediate echogenicity.
  • Older thrombi may contract resulting in visualization of flow seen around it.
  • How to evaluate a thrombus
  • 1. Use Doppler to identify an acute thrombus
  • 2. Evaluate the extent and location of visible thrombi
  • 3. Check for peripheral flow with color Doppler
  • 4. Look for evidence of neoplasia
  • 5. Assess for the sequelae of thrombosisischemia, ascites, etc.
  • Thrombosis- formation of a clot/thrombus at a site of blood stasis or vascular injury.
  • Thrombo-embolus- obstruction of a vessel downstream of the site of a clot formation.
  • Common sites of thrombo-embolus formation:
  • Aortic trifurcationaortic-iliac bifurcation
  • Caudal vena cava
  • Renal arteries
  • Pulmonary arteries
  • Mesenteric arteries
  • Pulmonary ThromboembolismComplication of many systemic diseases that predisposes the patient to a hypercoaguable state
  • Heartworm disease
  • Pulmonary artery thrombosis pulmonary thrombo-embolism
  • Glomerulonephropathies
  • Loss of antithrombin III through glomerular basement membrane hypercoagulation
  • IMHA
  • Hyperadrenocorticism
  • Secondary to erythrocytosis, hypertension and hypercoaguable state
  • DIC
  • Intravascular deposition of fibrinthrombosis
  • Neoplasia
  • Caudal vena cava- most common tumor that invades this vessel is an adrenal tumor (pheochromocytomas); tumor thrombus travels down phrenicoabdominal vein to reach the vena cava.
  • Sepsis
  • Clinical signs of PTE:
  • Acute respiratory compromise and a ventilation-perfusion mismatch that can be mild or subclinical depending on the degree of embolization.
  • Difficulty breathing (tachypnea and hyperpnea), coughing (can be productive), wheezing, anorexia, vomiting, lethargy, weightloss.
  • Cardiac Thrombi and Aortic Thrombo-embolism
  • Can occur with both HCM, DCM and Restrictive CM.
  • Stasis of blood activation of clotting factors thrombus formation in left atrium, ventricle or both.
  • Thrombus can dislodge and form an emboli that may obstruct aortic branches (most commonly at the aortic trifurcation). “saddle thrombus”
  • Clinical signs: Pain, cold extremities, cyanotic extremities, lack of palpable femoral pulse, signs of CHF.
  • If obstruction is partial may observe neurological deficits in the hindlimbs or unilateral paresis.
  • Clinical Signs of other Thromboembolisms(difficult to identify via ultrasound)
  • Cerebral TE
  • Change in consciousness, seizures, weakness. If the brain stem area is affected, then cranial nerve dysfunction, cerebellar signs, coma, or weakness may result.
  • Mesenteric artery TE
  • often found with GDV, will cause gastrointestinal signs and abdominal pain.
  • Renal TE or thrombosis leading to renal infarction :
  • decrease in renal function, pyrexia, back pain, proteinuria and hematuria or anuria if bilateraland potentially renal failure.
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