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

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Presentation on theme: "Thrombosis and Thrombo-embolisms Megan Connolly Block 2 6/2011."— Presentation transcript:

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

2 How is a thrombus identified ultrasonographically? How is a thrombus identified ultrasonographically? B-mode U/S exam B-mode U/S exam Doppler- helps evaluate the degree of vascular compromise 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. 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. 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. 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 1. Use Doppler to identify an acute thrombus 2. Evaluate the extent and location of visible thrombi 2. Evaluate the extent and location of visible thrombi 3. Check for peripheral flow with color Doppler 3. Check for peripheral flow with color Doppler 4. Look for evidence of neoplasia 4. Look for evidence of neoplasia 5. Assess for the sequelae of thrombosis  ischemia, ascites, etc. 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. 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. Thrombo-embolus - obstruction of a vessel downstream of the site of a clot formation.

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

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9 Pulmonary Thromboembolism Complication of many systemic diseases that predisposes the patient to a hypercoaguable state Heartworm disease Heartworm disease Pulmonary artery thrombosis  pulmonary thrombo-embolism Pulmonary artery thrombosis  pulmonary thrombo-embolism Glomerulonephropathies Glomerulonephropathies Loss of antithrombin III through glomerular basement membrane  hypercoagulation Loss of antithrombin III through glomerular basement membrane  hypercoagulation IMHA IMHA Hyperadrenocorticism Hyperadrenocorticism Secondary to erythrocytosis, hypertension and hypercoaguable state Secondary to erythrocytosis, hypertension and hypercoaguable state DIC DIC Intravascular deposition of fibrin  thrombosis Intravascular deposition of fibrin  thrombosis Neoplasia 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. 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 Sepsis

10 Clinical signs of PTE: 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.

11 Cardiac Thrombi and Aortic Thrombo-embolism Can occur with both HCM, DCM and Restrictive CM. Can occur with both HCM, DCM and Restrictive CM. Stasis of blood  activation of clotting factors  thrombus formation in left atrium, ventricle or both. 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” 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. 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. If obstruction is partial may observe neurological deficits in the hindlimbs or unilateral paresis.

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17 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 bilateral and potentially renal failure.


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