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Pulmonary Thromboembolism. Emily S. Southward DVM University of Missouri – Columbia Veterinary Medical Teaching Hospital. Definition. Pulmonary thromboembolism One clot or many clots that form at distant sites and lodge in the pulmonary vasculature. Pulmonary artery thrombus

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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.
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 pte14
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 pte15
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.
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
Performed first.

Normal study rules out PTE.

Radionuclide-labelled, macroaggregated albumin in peripheral vein.

Perfusion Scan
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

Ventilation/Perfusion Combo
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
Human lung.

Arrow indicates abrupt termination of a pulmonary artery.

Www.brighamrad.Harvard.edu/cases/bwh/images.

Pulmonary Embolus
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 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.
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 necropsy
Koko’s Necropsy
  • Muliple small thrombi in the pulmonary vasculature.
  • Cardiomegaly
thanks
Thanks
  • Dr. Mann
  • Dr. Dodam
  • Dr. Lattimer
  • Dr. Kunz