Pulmonary Thromboembolism

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  • What is a pulmonary thromboembolism? By definition it is a clot or many clots that lodge in the pulmonary vasculature. When this occurs this can result in a partial or complete occlusion of the vessel.
  • In the 19th century Verchow discovered three factors that can lead to venous thrombosis. The first factor is venous stasis. When venous stasis occurs, there is a tendency for blood to clot. After the blood clots, parts of the clots can break off and lodge other places in the body including the pulmonary vasculature. The second factor is injury to the vessel wall. When injury occurs to the endothelium of the vessel wall, platelets aggregate to help heal the injury of the vessel walls. Clots can form here and break off. The third factor is a change in coagulation properties of the blood. This is a state that allows for blood to clot when clots are not needed. These clots can lodge elsewhere in the body. These three factors exist and can occur in many disease states.
  • How does the thrombus form? A platelet nidus forms or a large amount of platelets in one area. A thrombus forms with these platelets as other coagulation factors are activated. As it continues to grow it forms a red fibrin thrombus. The large red thrombus can fracture and embolize to other areas of the body.
  • As mentioned before there are a number of diseases that predispose the patient to the development of pulmonary thromboembolism. These diseases can cause alterations in Verchow’s triad. This list is not exhaustive. Any chronic disease process can lead to the development of PTE.
  • As mentioned before there are a number of diseases that predispose the patient to the development of pulmonary thromboembolism. These diseases can cause alterations in Verchow’s triad. This list is not exhaustive. Any chronic disease process can lead to the development of PTE.
  • As mentioned before there are a number of diseases that predispose the patient to the development of pulmonary thromboembolism. These diseases can cause alterations in Verchow’s triad. This list is not exhaustive. Any chronic disease process can lead to the development of PTE.
  • There are many respiratory changes that can take place with the onset of PTE. Some of these are listed above. Hyperventilation can be due to possible pain and hypoxemia.
  • Hypoxemia can result from ventilation-perfusion mismatch, alveolar dead space, and physiological shunting.
  • Intrapulmonary or physiological shunting is defined as blood that enters into the arterial blood system without passing through ventilated lung. Poorly oxgenated blood enters the systemic circulation lowering the PaO2. Intrapulmonary shunts are not responsive to oxygen therapy due to the fact that the blood undergoing gas exchange.
  • Ventilation-perfusion mismatch can be complicated to understand. Increase in ventilation-perfusion mismatch occurs when blood flow is altered to the alveoli. When blood flow is altered to alveoli via a thrombus, that blood can not undergo gas exchange. Consequences in the alveoli are increases in O2 and a decrease in CO2. So, ventilation does not match perfusion.
  • Pulmonary thromboembolism causes and increase in pressure in the lungs, possible pulmonary hypertension and an increase in pulmonary vascular resistance. This increase in pulmonary vascular resistance leads to an increase in afterload to the right hard. The right heart has to work harder and harder to pump blood to the lungs. This can eventually lead to circulatory collapse and shock.
  • With all of these changes taking place in the lungs and vasculature, what are the clinical signs associated with PTE. Unfortunately none of the signs associated with PTE are pathopneumonic. The clinical signs are listed above. When these signs are encountered in a patient in the presence of a clinical disease associated with a risk of PTE, PTE should be on the differential list.
  • Blood panels changes are not reliably consistent in PTE. Hypoxemia is common but 10% of patients have normal oxygen levels. Thoracic radiographs are frequently normal and inconclusive. So how does one diagnose PTE?
  • Advanced diagnostics are needed to diagnose PTE. Pulmonary scintingraphy and pulmonary angiography are advanced diagnostics used to diagnose PTE in patients suspected of having PTE.
  • There are two types of pulmonary scintingraphy, ventilation and perfusion scintingraphy. These are non-invasive procedures that give infromation about ventilation and perfusion of the lungs. The perfusion scan is usually performed first.
  • A radionuclide-labelled, macroaggregated albumin in injected into a peripheral vein and the albumin travels in the blood to the pulmonary vessels. A normal perfusion scan rules out PTE. An abnormal scan can not rule out PTE.
  • A ventilation scan is performed after the perfusion scan if needed. The patient breaths a radioactive aerosol, such as technetium-99m and then images are taken.
  • A normal ventilation scan and abnormal perfusion scan is suggestive of a pulmonary thromboembolism.
  • These are images of a normal perfusion scan in a human.
  • This is an abnormal perfusion scan in a human.
  • Pulmonary angiography is the gold standard of diagnosis of PTE. This provides a definitive diagnosis or exclusion of PTE. The procedure requires sedation or general anesthesia. A contrast media is placed in circulation and it travels to the pulmonary vasculature. Radiographs are taken. An intraluminal defect or sharp cutoff in the pulmonary vasculature is diagnostic for PTE. There are increased risks and complications associated with this procedure.
  • This is an image of a PTE in a human lung. The arrow shows abrupt termination of a pulmonary artery.
  • Treatment of this disease can be difficult. Treatment includes the therapies mentioned above. Heparinization is to prevent further clots from forming. The goal is to maintain PTT at 1.5 to 2.5 times normal or ACT 1.2 to 1.4 times normal. Streptokinase is used to dissolve the clot or clots that are already present. Mechanical ventilation may be required to ensure adequate oxygenation and ventilation. Warfarin may be needed as long term therapy to prevent further clots from forming.
  • Monitoring should include bleeding times, blood gases, respiratory rate and all other basic monitoring.
  • Complications of therapy are not predictable but hemorrhage is the most common. Patients, once discharged should have regular and frequent check ups.
  • Prognosis with PTE is always guarded but improves with early detection and treatment. Each day the patient survives, improves prognosis. The patient is at risk for more emboli.
  • Pulmonary Thromboembolism

    1. 1. PulmonaryPulmonary ThromboembolismThromboembolism Emily S. Southward DVMEmily S. Southward DVM University of Missouri – ColumbiaUniversity of Missouri – Columbia Veterinary Medical TeachingVeterinary Medical Teaching HospitalHospital
    2. 2. DefinitionDefinition  Pulmonary thromboembolismPulmonary thromboembolism – One clot or many clots that form atOne clot or many clots that form at distant sites and lodge in the pulmonarydistant sites and lodge in the pulmonary vasculature.vasculature.  Pulmonary artery thrombusPulmonary artery thrombus – Clots that form in the pulmonaryClots that form in the pulmonary vasculature.vasculature.  Clots can partially or fully occludeClots can partially or fully occlude pulmonary vessels.pulmonary vessels.
    3. 3. Virchow’s TriadVirchow’s Triad  Venous stasis.Venous stasis.  Injury or abnormalities to the vesselInjury or abnormalities to the vessel wall.wall.  Alterations in coagulation properties.Alterations in coagulation properties.
    4. 4. Venous StasisVenous Stasis  Accumlation of activatedAccumlation of activated procoagulants.procoagulants. – ImmobilizationImmobilization – Inadequate cardiac pump.Inadequate cardiac pump.  Promotes thrombus formation.Promotes thrombus formation.
    5. 5. Vessel Wall InjuryVessel Wall Injury  Acute or chronic injury to vesselAcute or chronic injury to vessel endothelium.endothelium.  Leads to activation of platelets andLeads to activation of platelets and clotting cascade.clotting cascade.  Promotes thrombus formation.Promotes thrombus formation.
    6. 6. Vessel InjuryVessel Injury
    7. 7. Platelet AdhesionPlatelet Adhesion
    8. 8. AggregationAggregation
    9. 9. Alternations in CoagulationAlternations in Coagulation  Increase in procoagulant factors.Increase in procoagulant factors. – By trauma to vascular wall orBy trauma to vascular wall or extravascular tissues.extravascular tissues. – Releases tissue thromboplastin andReleases tissue thromboplastin and phospholipid.phospholipid. – Leads to formation of prothrombinLeads to formation of prothrombin activator.activator. – ProthrombinProthrombin  ThrombinThrombin
    10. 10. Alterations in CoagulationAlterations in Coagulation  Decrease in anticoagulant factors.Decrease in anticoagulant factors. – ThrombomodulinThrombomodulin – Antithrombin IIIAntithrombin III – HeparinHeparin – AlphaAlpha22-Marcoglobulin-Marcoglobulin – PlasminPlasmin  Leads to hypercoagulable state byLeads to hypercoagulable state by formation of thrombin.formation of thrombin.
    11. 11. Thrombosis FormationThrombosis Formation  Platelet nidus at site of injury.Platelet nidus at site of injury.  Growth by aggregation of plateletsGrowth by aggregation of platelets and fibrin.and fibrin.  Activation of clotting cascade.Activation of clotting cascade.  Larger growth to a red fibrinLarger growth to a red fibrin thrombus.thrombus.  Thrombus fractures and embolizes toThrombus fractures and embolizes to other areas of the body.other areas of the body.
    12. 12. Predisposing Factors or DiseasesPredisposing Factors or Diseases for Development of PTEfor Development of PTE  Hypercoagulable stateHypercoagulable state – Nephrotic syndromeNephrotic syndrome – ImmobilizationImmobilization – AmyloidosisAmyloidosis – Early DICEarly DIC – HyperadrenocorticismHyperadrenocorticism  Capillary fragilityCapillary fragility  Activation of clotting cascade.Activation of clotting cascade.
    13. 13. Predisposing Factors or DiseasesPredisposing Factors or Diseases for Development of PTEfor Development of PTE  Hypercoagulable stateHypercoagulable state  Capillary fragilityCapillary fragility – Diabetes MellitusDiabetes Mellitus – Immune–mediated hemolyitc anemiaImmune–mediated hemolyitc anemia – SepsisSepsis – HyperadrenocorticismHyperadrenocorticism  Activation of clotting cascade.Activation of clotting cascade.
    14. 14. Predisposing Factors or DiseasesPredisposing Factors or Diseases for Development of PTEfor Development of PTE  Hypercoagulable stateHypercoagulable state  Capillary fragilityCapillary fragility  Activation of clotting cascade.Activation of clotting cascade. – SepsisSepsis – Pneumonia/pyothoraxPneumonia/pyothorax – Heartworm diseaseHeartworm disease – SurgerySurgery – Bacterial endocarditisBacterial endocarditis – NeoplasiaNeoplasia
    15. 15. Consequences of PTEConsequences of PTE  Respiratory.Respiratory. – Increased alveolar dead space.Increased alveolar dead space. – Hyperventilation.Hyperventilation. – Hypoxemia.Hypoxemia. – Ventilation/perfusion inequality.Ventilation/perfusion inequality. – Intrapulmonary shunts.Intrapulmonary shunts.
    16. 16. Normal AlveolusNormal Alveolus
    17. 17. Increased Alveolar Dead SpaceIncreased Alveolar Dead Space
    18. 18. HypoxemiaHypoxemia Results from ventilation-Results from ventilation- perfusion inequality, physiologicperfusion inequality, physiologic shunting and increased deadshunting and increased dead space.space.
    19. 19. Intrapulmonary ShuntsIntrapulmonary Shunts  Blood that has not been to areas ofBlood that has not been to areas of ventilated lung and enters systemicventilated lung and enters systemic circulation without gas exchangecirculation without gas exchange taking place.taking place.  Poorly oxygenated blood enters thePoorly oxygenated blood enters the arterial system lowering the PaOarterial system lowering the PaO22..  Not responsive to oxygen therapy.Not responsive to oxygen therapy.
    20. 20. Ventilation/Perfusion InequalityVentilation/Perfusion Inequality  V/Q inequality occurs whenV/Q inequality occurs when distribution of blood is altered to thedistribution of blood is altered to the alveoli.alveoli.  OO22 increase in the alveoli and COincrease in the alveoli and CO22 decreases.decreases.
    21. 21. Hemodynamic ChangesHemodynamic Changes  Increase in pulmonary vascularIncrease in pulmonary vascular resistance.resistance.  Increased afterload to the rightIncreased afterload to the right heart.heart.  Can lead to circulatory collapse andCan lead to circulatory collapse and shock.shock.
    22. 22. Clinical SignsClinical Signs  Not pathognomonic.Not pathognomonic. – Dyspnea.Dyspnea. – Tachypnea.Tachypnea. – Hemoptysis.Hemoptysis. – Tachycardia.Tachycardia. – Hypoxemia.Hypoxemia. – Sudden death.Sudden death.
    23. 23. DiagnosisDiagnosis  CBC/Biochemistry results reflectCBC/Biochemistry results reflect primary disease process.primary disease process.  Hypoxemia common but 10% ofHypoxemia common but 10% of patients are normal.patients are normal.  Thoracic radiographs can be normalThoracic radiographs can be normal and inconclusive.and inconclusive.
    24. 24.  LaRue MJ and Murtaugh RJ. PulmonaryLaRue MJ and Murtaugh RJ. Pulmonary Thromboembolism in Dogs:47 cases (1986-87).Thromboembolism in Dogs:47 cases (1986-87). JJ Amer Vet Med Assoc.Amer Vet Med Assoc. 1990 Nov. 15;197(1):1368-1990 Nov. 15;197(1):1368- 1372.1372.  Johnson LRJohnson LR et al.et al. Pulmonary Thromboembolism inPulmonary Thromboembolism in 29 dogs:1985-199529 dogs:1985-1995 J Vet Intern Med.J Vet Intern Med. 19991999 Jul;13(4):338-345.Jul;13(4):338-345.  Flükiger MA and Gomez JA. Radiographic FindingsFlükiger MA and Gomez JA. Radiographic Findings in Dogs with Spontaneous Pulmonary Thrombosisin Dogs with Spontaneous Pulmonary Thrombosis or Embolism.or Embolism. Veterinary Radiology,Veterinary Radiology, Vol.25,No.3Vol.25,No.3 124-131.124-131.
    25. 25. Advanced DiagnosticsAdvanced Diagnostics  Pulmonary scintigraphyPulmonary scintigraphy  Pulmonary angiography.Pulmonary angiography.
    26. 26. Pulmonary ScintigraphyPulmonary Scintigraphy  NoninvasiveNoninvasive  Aids in diagnosis of PTE but notAids in diagnosis of PTE but not definitive.definitive.  Two types- ventilation and perfusionTwo types- ventilation and perfusion scans.scans.
    27. 27. Perfusion ScanPerfusion Scan  Performed first.Performed first.  Normal study rulesNormal study rules out PTE.out PTE.  Radionuclide-Radionuclide- labelled,labelled, macroaggregatedmacroaggregated albumin inalbumin in peripheral vein.peripheral vein.
    28. 28. Ventilation ScanVentilation Scan  Inhaled radioactiveInhaled radioactive inert gas-senon-inert gas-senon- 133 or technetium-133 or technetium- 99m.99m.  Patient underPatient under general anesthesia.general anesthesia.  Normal in PTE.Normal in PTE.
    29. 29. Ventilation/Perfusion ComboVentilation/Perfusion Combo  With PTE theWith PTE the ventilation scanventilation scan would be normalwould be normal and the perfusionand the perfusion scan abnormal.scan abnormal.  Suggestive of PTE.Suggestive of PTE.FF  Picture fromPicture from WWW.bschsys.org/DiagnositcImaging/nucmdWWW.bschsys.org/DiagnositcImaging/nucmd /htm/htm
    30. 30. Normal Human Perfusion ScanNormal Human Perfusion Scan
    31. 31. Abnormal Human PerfusionAbnormal Human Perfusion ScanScan
    32. 32. Pulmonary AngiographyPulmonary Angiography  Performed if definitive diagnosis orPerformed if definitive diagnosis or exclusion of PTE is required.exclusion of PTE is required.  Requires sedation or generalRequires sedation or general anesthesia.anesthesia.  Greater risks.Greater risks.  Intraluminal filling defect and sharpIntraluminal filling defect and sharp cutoff are diagnostic for PTE.cutoff are diagnostic for PTE.
    33. 33. Pulmonary EmbolusPulmonary Embolus  Human lung.Human lung.  Arrow indicatesArrow indicates abrupt terminationabrupt termination of a pulmonaryof a pulmonary artery.artery.  Www.brighamrad.Harvard.edu/cases/bWww.brighamrad.Harvard.edu/cases/b wh/images.wh/images.
    34. 34. TreatmentTreatment  Oxygen therapy.Oxygen therapy.  Heparinization 200-300 units/kgHeparinization 200-300 units/kg subcutaneously every 8 hours.subcutaneously every 8 hours.  Streptokinase or TPA.Streptokinase or TPA.  Mechanical ventilation.Mechanical ventilation.  Long term- warfarin therapy.Long term- warfarin therapy.
    35. 35. MonitoringMonitoring  Clotting times- want to maintain PTTClotting times- want to maintain PTT at 1.5-2.5 times normal or and ACTat 1.5-2.5 times normal or and ACT at 1.2-1.4 times normal.at 1.2-1.4 times normal.  Serial arterial blood gas analysis.Serial arterial blood gas analysis.  Respiratory rate.Respiratory rate.  Central venous pressure.Central venous pressure.  All other basic monitoring.All other basic monitoring.
    36. 36. Complications Of TherapyComplications Of Therapy  Hemorrhage most common.Hemorrhage most common.  Not predictable.Not predictable.  Protamine therapy indicated withProtamine therapy indicated with hemorrhage due to heparin.hemorrhage due to heparin.  Vitamin K or fresh-frozen plasma inVitamin K or fresh-frozen plasma in warfarin therapy.warfarin therapy.
    37. 37. PrognosisPrognosis  Guarded.Guarded.  Improves with early detection andImproves with early detection and treatment.treatment.  Improves each day the patientImproves each day the patient survives.survives.  At risk for more emboli.At risk for more emboli.
    38. 38. UMC VMTH CasesUMC VMTH Cases  Three in data base.Three in data base. – SadieSadie – MagnumMagnum – KokoKoko
    39. 39. Sadie BaileySadie Bailey  8-year-old FS mixed breed dog.8-year-old FS mixed breed dog.  Presented for weight loss, anemia,Presented for weight loss, anemia, and anorexia.and anorexia.  Weak and lethargic on presentationWeak and lethargic on presentation  Hemoabdomen, thrombocytopenia,Hemoabdomen, thrombocytopenia, and neutrophilia with left shift.and neutrophilia with left shift.  Developed severe dyspnea andDeveloped severe dyspnea and ventricular tachycardia.ventricular tachycardia.
    40. 40. Sadie’s Thoracic FilmsSadie’s Thoracic Films
    41. 41. Sadie’s Thoracic FilmsSadie’s Thoracic Films
    42. 42. Sadie’s NecropsySadie’s Necropsy  Hepatocellular carcinomaHepatocellular carcinoma  Adrenocortical hyperplasiaAdrenocortical hyperplasia  Pulmonary thrombois – most lobarPulmonary thrombois – most lobar branches effected.branches effected.  Renal infarction.Renal infarction.
    43. 43. Magnum MeeksMagnum Meeks  8-year-old MC doberman pinscher8-year-old MC doberman pinscher  Presented for dyspnea of two daysPresented for dyspnea of two days duration.duration.  Protein losing nephropathy.Protein losing nephropathy.
    44. 44. Magnum’s Thoracic FilmsMagnum’s Thoracic Films
    45. 45. Magnum’s Thoracic FilmsMagnum’s Thoracic Films
    46. 46. Koko WesterhoffKoko Westerhoff  12-year-old FS dachshund.12-year-old FS dachshund.  Presented for lethargy, anorexia,Presented for lethargy, anorexia, tachypnea, and possible CHF.tachypnea, and possible CHF.  History includes diabetes mellitus,History includes diabetes mellitus, IVDD and cataracts.IVDD and cataracts.  PE- Increased BV lung sounds, mildPE- Increased BV lung sounds, mild crackles, tachycardia, and leftcrackles, tachycardia, and left systolic murmur.systolic murmur.
    47. 47. Koko’s Thoracic FilmsKoko’s Thoracic Films
    48. 48. Koko’s Thoracic FilmsKoko’s Thoracic Films
    49. 49. Koko’s Pefusion ScintigraphyKoko’s Pefusion Scintigraphy
    50. 50. Koko’s Pefusion ScintigraphyKoko’s Pefusion Scintigraphy
    51. 51. Koko’s NecropsyKoko’s Necropsy  Muliple small thrombi in theMuliple small thrombi in the pulmonary vasculature.pulmonary vasculature.  CardiomegalyCardiomegaly
    52. 52. ThanksThanks  Dr. MannDr. Mann  Dr. DodamDr. Dodam  Dr. LattimerDr. Lattimer  Dr. KunzDr. Kunz
    53. 53. Questions?Questions?

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