Pulmonary Thromboembolism: Pulmonary Thromboembolism Emily S. Southward DVM University of Missouri – Columbia Veterinary Medical Teaching Hospital


Definition: Definition Pulmonary thromboembolism One clot or many clots that form at distant sites and lodge in the pulmonary vasculature. Pulmonary artery thrombus Clots that form in the pulmonary vasculature. Clots can partially or fully occlude pulmonary vessels.


Virchow’s Triad: Virchow’s Triad Venous stasis. Injury or abnormalities to the vessel wall. Alterations in coagulation properties.


Venous Stasis: Venous Stasis Accumlation of activated procoagulants. Immobilization Inadequate cardiac pump. Promotes thrombus formation.


Vessel Wall Injury: Vessel Wall Injury Acute or chronic injury to vessel endothelium. Leads to activation of platelets and clotting cascade. Promotes thrombus formation.


Vessel Injury: Vessel Injury


Platelet Adhesion: Platelet Adhesion


Aggregation: Aggregation


Alternations in Coagulation: Alternations in Coagulation Increase in procoagulant factors. By trauma to vascular wall or extravascular tissues. Releases tissue thromboplastin and phospholipid. Leads to formation of prothrombin activator. Prothrombin  Thrombin


Alterations in Coagulation: Alterations in Coagulation Decrease in anticoagulant factors. Thrombomodulin Antithrombin III Heparin Alpha2-Marcoglobulin Plasmin Leads to hypercoagulable state by formation of thrombin.


Thrombosis Formation: Thrombosis Formation Platelet nidus at site of injury. Growth by aggregation of platelets and fibrin. Activation of clotting cascade. Larger growth to a red fibrin thrombus. Thrombus fractures and embolizes to other areas of the body.


Predisposing Factors or Diseases for Development of PTE: Predisposing Factors or Diseases for Development of PTE Hypercoagulable state Nephrotic syndrome Immobilization Amyloidosis Early DIC Hyperadrenocorticism Capillary fragility Activation of clotting cascade.


Predisposing Factors or Diseases for Development of PTE: Predisposing Factors or Diseases for Development of PTE Hypercoagulable state Capillary fragility Diabetes Mellitus Immune–mediated hemolyitc anemia Sepsis Hyperadrenocorticism Activation of clotting cascade.


Predisposing Factors or Diseases for Development of PTE: Predisposing Factors or Diseases for Development of PTE Hypercoagulable state Capillary fragility Activation of clotting cascade. Sepsis Pneumonia/pyothorax Heartworm disease Surgery Bacterial endocarditis Neoplasia


Consequences of PTE: Consequences of PTE Respiratory. Increased alveolar dead space. Hyperventilation. Hypoxemia. Ventilation/perfusion inequality. Intrapulmonary shunts.


Normal Alveolus: Normal Alveolus


Increased Alveolar Dead Space: Increased Alveolar Dead Space


Hypoxemia: Hypoxemia Results from ventilation-perfusion inequality, physiologic shunting and increased dead space.


Intrapulmonary Shunts: Intrapulmonary Shunts Blood that has not been to areas of ventilated lung and enters systemic circulation without gas exchange taking place. Poorly oxygenated blood enters the arterial system lowering the PaO2. Not responsive to oxygen therapy.


Ventilation/Perfusion Inequality: Ventilation/Perfusion Inequality V/Q inequality occurs when distribution of blood is altered to the alveoli. O2 increase in the alveoli and CO2 decreases.


Hemodynamic Changes: Hemodynamic Changes Increase in pulmonary vascular resistance. Increased afterload to the right heart. Can lead to circulatory collapse and shock.


Clinical Signs: Clinical Signs Not pathognomonic. Dyspnea. Tachypnea. Hemoptysis. Tachycardia. Hypoxemia. Sudden death.


Diagnosis: Diagnosis CBC/Biochemistry results reflect primary disease process. Hypoxemia common but 10% of patients are normal. Thoracic radiographs can be normal and inconclusive.


Slide25: LaRue MJ and Murtaugh RJ. Pulmonary Thromboembolism in Dogs:47 cases (1986-87). J Amer Vet Med Assoc. 1990 Nov. 15;197(1):1368-1372. Johnson LR et al. Pulmonary Thromboembolism in 29 dogs:1985-1995 J Vet Intern Med. 1999 Jul;13(4):338-345. Flükiger MA and Gomez JA. Radiographic Findings in Dogs with Spontaneous Pulmonary Thrombosis or Embolism. Veterinary Radiology, Vol.25,No.3 124-131.


Advanced Diagnostics: Advanced Diagnostics Pulmonary scintigraphy Pulmonary angiography.


Pulmonary Scintigraphy: Pulmonary Scintigraphy Noninvasive Aids in diagnosis of PTE but not definitive. Two types- ventilation and perfusion scans.


Perfusion Scan: Perfusion Scan Performed first. Normal study rules out PTE. Radionuclide-labelled, macroaggregated albumin in peripheral vein.


Ventilation Scan: Ventilation Scan Inhaled radioactive inert gas-senon-133 or technetium-99m. Patient under general anesthesia. Normal in PTE.


Ventilation/Perfusion Combo: Ventilation/Perfusion Combo With PTE the ventilation scan would be normal and the perfusion scan abnormal. Suggestive of PTE.F Picture from WWW.bschsys.org/DiagnositcImaging/nucmd/htm


Normal Human Perfusion Scan: Normal Human Perfusion Scan


Abnormal Human Perfusion Scan: Abnormal Human Perfusion Scan


Pulmonary Angiography: Pulmonary Angiography Performed if definitive diagnosis or exclusion of PTE is required. Requires sedation or general anesthesia. Greater risks. Intraluminal filling defect and sharp cutoff are diagnostic for PTE.


Pulmonary Embolus: Pulmonary Embolus Human lung. Arrow indicates abrupt termination of a pulmonary artery. Www.brighamrad.Harvard.edu/cases/bwh/images.


Treatment: Treatment Oxygen therapy. Heparinization 200-300 units/kg subcutaneously every 8 hours. Streptokinase or TPA. Mechanical ventilation. Long term- warfarin therapy.


Monitoring: Monitoring Clotting times- want to maintain PTT at 1.5-2.5 times normal or and ACT at 1.2-1.4 times normal. Serial arterial blood gas analysis. Respiratory rate. Central venous pressure. All other basic monitoring.


Complications Of Therapy: Complications Of Therapy Hemorrhage most common. Not predictable. Protamine therapy indicated with hemorrhage due to heparin. Vitamin K or fresh-frozen plasma in warfarin therapy.


Prognosis: Prognosis Guarded. Improves with early detection and treatment. Improves each day the patient survives. At risk for more emboli.


UMC VMTH Cases: UMC VMTH Cases Three in data base. Sadie Magnum Koko


Sadie Bailey: Sadie Bailey 8-year-old FS mixed breed dog. Presented for weight loss, anemia, and anorexia. Weak and lethargic on presentation Hemoabdomen, thrombocytopenia, and neutrophilia with left shift. Developed severe dyspnea and ventricular tachycardia.


Sadie’s Thoracic Films: Sadie’s Thoracic Films


Sadie’s Thoracic Films: Sadie’s Thoracic Films


Sadie’s Necropsy: Sadie’s Necropsy Hepatocellular carcinoma Adrenocortical hyperplasia Pulmonary thrombois – most lobar branches effected. Renal infarction.


Magnum Meeks: Magnum Meeks 8-year-old MC doberman pinscher Presented for dyspnea of two days duration. Protein losing nephropathy.


Magnum’s Thoracic Films: Magnum’s Thoracic Films


Magnum’s Thoracic Films: Magnum’s Thoracic Films


Koko Westerhoff: Koko Westerhoff 12-year-old FS dachshund. Presented for lethargy, anorexia, tachypnea, and possible CHF. History includes diabetes mellitus, IVDD and cataracts. PE- Increased BV lung sounds, mild crackles, tachycardia, and left systolic murmur.


Koko’s Thoracic Films: Koko’s Thoracic Films


Koko’s Thoracic Films: Koko’s Thoracic Films


Koko’s Pefusion Scintigraphy: Koko’s Pefusion Scintigraphy


Koko’s Pefusion Scintigraphy: Koko’s Pefusion Scintigraphy


Koko’s Necropsy: Koko’s Necropsy Muliple small thrombi in the pulmonary vasculature. Cardiomegaly


Thanks: Thanks Dr. Mann Dr. Dodam Dr. Lattimer Dr. Kunz


Questions?: Questions?