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Thrombosis and Thrombo -embolisms

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

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Thrombosis and Thrombo -embolisms

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  1. Thrombosis and Thrombo-embolisms Megan Connolly Block 2 6/2011

  2. How 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.

  3. 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.

  4. 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.

  5. Common sites of thrombo-embolus formation: • Aortic trifurcationaortic-iliac bifurcation • Caudal vena cava • Renal arteries • Pulmonary arteries • Mesenteric arteries

  6. 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

  7. 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.

  8. 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.

  9. 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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