pulmonary embolism deep venous thrombosis n.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
PULMONARY EMBOLISM DEEP VENOUS THROMBOSIS TERRENCE C. DEMOS, MD PowerPoint Presentation
Download Presentation
PULMONARY EMBOLISM DEEP VENOUS THROMBOSIS TERRENCE C. DEMOS, MD

Loading in 2 Seconds...

play fullscreen
1 / 105

PULMONARY EMBOLISM DEEP VENOUS THROMBOSIS TERRENCE C. DEMOS, MD

1 Vues Download Presentation
Télécharger la présentation

PULMONARY EMBOLISM DEEP VENOUS THROMBOSIS TERRENCE C. DEMOS, MD

- - - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

  1. PULMONARY EMBOLISM • DEEP VENOUS THROMBOSIS • TERRENCE C. DEMOS, MD • DEPARTMENT OF RADIOLOGY

  2. PE AND DVT • HISTORY AND PHYSICAL EXAMINATION • LABORATORY TESTS • CHEST RADIOGRAPHS • NUCLEAR MEDICINE LUNG SCAN • COMPUTED TOMOGRAPHY • SONOGRAPHY • ANGIOGRAPHY • MAGNETIC RESONANCE

  3. PULMONARY EMBOLUSVERSUSLUNG INFARCT • EMBOLUS RESULTS IN HEMORRHAGE • 90% DO NOT RESULT IN INFARCTION AND THE LUNG CLEARS BLOOD WITH NO RESIDUAL EFFECT • 10% HAVE A PERMANENT RESIDUAL DEFORMITY INDICATING INFARCTION

  4. PULMONARY EMBOLI - NO INFARCTLUNGS NORMAL 3 WEEKS LATER

  5. PULMONARY INFARCTSGROSS PATHOLOGY

  6. EVOLUTION OF INFARCT • EARLY- ILL DEFINED LUNG CONSOLIDATION • HEMORRHAGE AND EDEMA • LATER • BETTER DEFINED • PLEURAL BASED • TRUNCATED CONE SHAPE • MELTING SIGN • RETAINS ORIGINAL SHAPE WHILE GETTING SMALLER • OUTCOME • BECOMES LINE OPACITY, THICK PLEURA IN 3-6 WEEKS

  7. EVOLVING PULMONARY INFARCT

  8. PULMONARY INFARCTEVOLUTION

  9. HISTORY • CLASSIC (MASSIVE PE) • PLEURITIC PAIN, DYSPNEA, HEMOPTYSIS (20%) • TACHYPNEA, COUGH, APPREHENSION, FEVER, SYNCOPE • 1990 PIOPED STUDY • FREQUENCY OF SYMPTOMS SAME WHEN (+) OR (-) FOR PE

  10. RISK FACTORS • LOWER EXTREMITY VENOUS STASIS • IMMOBILIZATION • POST OPERATIVE PATIENTS • MALIGNANCY • HEART DISEASE • ESTROGEN CONTAINING COMPOUNDS • CONGENITAL COAGULATION ABNORMALITIES • PROTEIN S DEFICIENCY • PROTEIN C DEFICIENCY • LEIDEN FACTOR • ANTITHROMBIN III DEFICIENCY • ANTIPHOSPHOLIPED SYNDROME

  11. LABORATORY TESTS • LDH, SERUM BILIRUBIN, SGOT • (+) 20% OF PATIENTS WITH PE • FEVER, ELEVATED WBC • 25%PE & PRE-EXISTING HEART/ LUNG DISEASEpO2>80mm Hg • 10% HAD PE AND NORMAL A-a O2 GRADIENT (PIOPED STUDY)

  12. D-DIMER • SEMIQUANTITATIVE LATEX AGGLUTINATION (LA) • 98 PATIENTS WITH SUSPECTED PE STUDIED (D-DIMER, VQ SCAN, ANGIO) • 8/98 PATIENTS WITH NORMAL D-DIMER HAD PE ON ANGIOGRAMS • ENZYME-LINKED IMMUNOSORBENT ASSAY (ELISA) • NEGATIVE PREDICTIVE VALUES 91-98% • CONCLUSION LA D-DIMER SHOULD NOT BE USED TO EVALUATE PATIENTS WITH SUSPECTED PE. • ARCH INTERN MED 1999;159:1569

  13. CHEST RADIOGRAPH • ABNORMAL IN 85% OF PATIENTS • FINDING MOST OFTEN NONSPECIFIC • PLEURAL BASED OPACITY • PLEURAL EFFUSION • LUNG CONSOLIDATION • LOSS OF LUNG VOLUME • RADIOGRAPHS OF LIMITED VALUE • MAJOR IMPORTANCE IS TO IDENTIFY OTHER DISEASE MIMICING PE….. AND TO CORRELATE WITH V/Q SCAN

  14. PULMONARY INFARCTBILATERAL LUNG CONSOLIDATION

  15. MASSIVE PE SPARED UPPER LOBES

  16. PE AND PLEURAL BASED LESION

  17. 31/M POST-OP HERNIORRAPHYTACHYPNEA AND L PLEURITIC PAIN

  18. CHEST RADIOGRAPH • THESE FINDINGS SUGGEST PE, BUT ARE UNCOMMON • ENLARGED HILUS • DUE TO CLOT IN VESSEL • WESTERMARK SIGN • HYPERLUCENCY AND DECREASED VESSELS • PLEURAL BASED ROUNDED OPACITY • HAMPTON’S HUMP

  19. PE WITH ENLARGED HILUS

  20. PE ENLARGED HILUS

  21. WESTERMARK SIGN

  22. HAMPTON’S HUMPV/Q LUNG SCAN

  23. PULMONARY EMBOLISM • VENTILATION PERFUSION LUNG SCAN

  24. PERFUSION VENTILATION LUNG SCANHIGH PROBABILITY

  25. HIGH PROBABILITY (13%) INTERMEDIATE (39%) LOW PROBABILITY (34%) NORMAL (14%) PE > 80% *PE 96% *HIGH CLINICAL SUSPICION PE 20-79% PE 0-19% *PE 4% *LOW CLINICAL SUSPICION PE < 2% V/Q LUNG SCANSENSITIVE BUT NONSPECIFICV/Q MISMATCHES(NONE TO 2 0R MORE LARGE SEGMENTAL)

  26. LOW PROB LUNG SCAN

  27. LOW PROBABILITY LUNG SCAN

  28. IMAGING PLUS CLINICAL PROBABILITY • COMBINE HIGH OR LOW CLINICAL PROBABILITYWITH • HIGH OR LOW PROBABILITY V/Q SCAN • TO • INCREASE THE ACCURACY OF V/Q SCAN AND • DECREASE INDETERMINANT V/Q SCANS • PIOPED STUDY JAMA 1990;263:2753-9

  29. LOW PROB LUNG SCAN

  30. LUNG TRANSPLANTSLOW PROB LUNG SCAN

  31. CENTRAL, LOBAR, SEGMENTAL VESSELS SENSITIVITY > 90% SPECIFICITY > 90% INDETERMINENT 5% SUBSEGMENTAL SENSITIVITY (L0W) CT ANGIOGRAPHY

  32. SADDLE EMBOLUS

  33. SEGMENTAL EMBOLI

  34. SEGMENTAL EMBOLISUBSEGMENTAL EMBOLI

  35. CT ANGIOGRAPHY • HELICAL (GE LightSpeed) CT • 1.25mm collimation, 6:1pitch, 4cc IVcontrast/sec • DIAGNOSTIC CRITERIA • PARTIAL OR COMPLETE FILLING DEFECTS • ( REFORMATTED IMAGES )

  36. POST PARTUM DYSPNEAREFORMATTED IMAGE

  37. CT ANGIOGRAPHY • PITFALLS • POOR VASCULAR ENHANCEMENT • BREATHING AND STREAK ARTIFACTS • DECREASE IN OVERALL ATTENUATION BETWEEN IMAGES • HILAR LYMPH NODES • SITE OF BIFURCATION OF ARTERIES • OBLIQUE VESSELS • PULMONARY VEINS • FLUID FILLED BRONCHI

  38. LYMPHADENOPATHY AND PE

  39. LYMPH NODES VERSUS PE

  40. FLUID FILLED BRONCHIREFORMATTED IMAGE

  41. ASPIRATION FLUID FILLED BRONCHUS

  42. BRONCHI VOLUME AVERAGING SIMULATES EMBOLI

  43. VESSEL BIFURCATIONREFORMATED IMAGE

  44. PULMONARY EMBOLILUNG PARENCHYMAL AND PLEURAL ABNORMALITIES • MOSAIC PATTERN • LARGER VESSELS IN HIGH ATTENUATION AREAS • HEMORRHAGE • GROUND GLASS OPACITY • CONSOLIDATION • PLEURAL BASED • TRIANGULAR TOWARD HILUS • PLEURAL EFFUSION

  45. PELUNG PARENCHYMAL AND PLEURAL ABNORMALITIES

  46. MOSAIC PATTERNSMALL VESSEL OR SMALL AIRWAY DISEASE