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CASE PRESENTATION

CASE PRESENTATION. Idan Khan. Case. 71 y/o male brought in by EMS Very healthy 71 y/o Skiing all day no problems c/o pain / tingling/ weakness to right arm, SOB. Case. Where and what to do??. Case. History Skiing all morning Afternoon at home acute onset SOB (5-10 min) Resolved

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CASE PRESENTATION

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  1. CASE PRESENTATION Idan Khan

  2. Case • 71 y/o male brought in by EMS • Very healthy 71 y/o • Skiing all day no problems • c/o pain / tingling/ weakness to right arm, SOB

  3. Case • Where and what to do??

  4. Case • History • Skiing all morning • Afternoon at home acute onset SOB (5-10 min) • Resolved • Acute onset pain weakness and discoloration to right arm (unable to move arm) • Called EMS

  5. Case • Past Hx • Healthy • Ex-smoker 15 pack yrs • High cholesterol on zocor

  6. Case • EMS • Same hx as previous • O2 sat 80 % RA increased to 92% on NRB • BP 168/98, HR 115, RR 20 • Arm : white / purple

  7. Case • ED Evaluation • Vitals: 159/99, HR 122, RR 20 • O2 sat 83% RA, increased to 96% NRB • Fit looking 71 y/o

  8. Case • PE • A+O x3, speaking in full sentences, didn’t look labored but was tachypnic • H+N: normal • Chest: clear, no rub • CV: • active precordium • S1, S2 no S3 or S4, no murmurs • ? JVD • Abdo: normal

  9. Case • PE (con’t) • Right arm • Purple in colour (from mid upper arm) • Cool to touch • Decreased cap refill • No radial pulse • Motor 4 -/ 5 (left 5/5)

  10. Case • Investigations? • ECG • CXR • ABG???? • Blood work • CBC, LYTES, PT, INR, CK

  11. ECG

  12. X-Ray

  13. Case • CBC: • WBC 11 • Hb 160 • Plt 147 • Lytes • Na 143, Cl 105, K 4.5, CO2 18 • INR 1.0, CK 93

  14. Case • ABG 7.41 / 34 / 217 / 21 A-a gradient: (Alveolar – arterial) Alveolar: FIO2 x (BP – PP H2O) – (1.25 x PCO2) 1 x (665 – 47) – ( 1.25 x 21) = 618 – 26 = 592 Arterial : 217 A-a gradient : 592 – 217 = 375 (extremely elevated) Normal : (5-10) or ( age/4) + 4 - 71/4 + 4 = 22 mmHg

  15. Case • DDX ? • What is your most likely diagnosis??

  16. Case • What to do next? • Pt started on heparin (earlier) • ICU and vascular consulted • Any further investigations/treatment??

  17. PE : Epidemiology • What about PE? • Epidemiology • MC preventable hospital death • MC undiagnosed hospital death • True incidence unknown • 650,000 cases / yr US • 200,000 deaths

  18. PE : Epidemiology • Epidemiology • 1980 • 21% of all ED pts with pleuritic CP had a PE • Mortality • Usually within the first hour • But large # die with subsequent emboli • Acute mortality correlates with RV function • Long term mortality correlates with comorbid illness • Age <40 mortality : 2.5% • Age >40 mortality : 18% (some studies geriatrics 39% even when treated • Overall untreated : 30% mortality • Treated: 5% mortality

  19. PE: Causes • Cause • 90% from lower extremities • Catheter related upper ext PE : up to 15% • PIOPED • 50% immobilization within 3 months of PE • 40% trauma or surgery • Neoplasm • Responsible for 4% of thromboembolic disease • Several studies: idiopathic PE (neoplasm eventually in ~ 9%)

  20. PE: Clinical Features • Clinical Features • Younger pts: • 30% no risk factors • 60% normal vitals • 97% have some combination of : • Dyspnea, tachypnea, or pleuritic CP • Up to 10% will have syncope

  21. PE: Physical Exam • Physical Exam • HR is normal in 70% pts • RR < 20 in 30% pts • Homans sign : flip a coin

  22. PE: ECG • ECG • 20 - 30% normal ECG • 50% NSSTTW changes • RBBB, right axis deviation, ST depression, rarely S1, Q3, T3 • A-fib !

  23. PE: CXR • CXR • 84% pts will have an abn CXR • MS findings” • Atelectasis, blunting of CP angle (effusion),elevated hemidiaphragm • Other signs: • Hamptons Hump • Westermark sign • Fleischner sign

  24. PE: A-a Gradient • A – a Gradient • >1/4 of all pts with PE will have P02 >80 • Some pts can have sat 100% RA • PIOPED • 8-10% pts had normal A-a gradient • A-a gradient nonspecific • Not required in the work-up of PE !!!

  25. Case • What next? • Echo • Moderate TR • Pulmonary artery pressures 90-100! • Hypokinetic RV • Normal LV function • Positive bubble study !

  26. PE: ECHO • ECHO • TTE: 85% sensitive for massive PE • TEE: 90% sen, up to 100% specific • Findings in PE • Increased RV end diastolic pressures • Increased PA pressures • TR • Abn septal movement

  27. PE: CT Scan • CT Scan • Sensitivity: 88-95%, Specificity: 92- 97% • Adv: • Can detect other pathology • Disadv: • Limits visualization to fourth gen pulm arteries • Hard to hold breath for scan!

  28. Case • CT done • Bilateral filling defects (PE’s) • MASSIVE clot in the SVC/ and Right PA

  29. Case • What would you do now? • Pt taken to ICU and underwent thrombolysis

  30. Thrombolysis and PE • Mechanism • Converts plasminogen to plasmin • Breaks down fibrin • Clot dissolution • Agents • tPA, Urokinase, SK • tPA targets clot specific plasminogen/fibrin • Urokinase – human urine or cultured human renal cells

  31. Thrombolysis and PE • Evidence for TT and PE • Case reports and case series in early 1960’s • Improved hemodynamics and perfusion • UPET (Urokinase Pulmonary Embolism Trial, 1970) • 160 pts, heparin vs UK and heparin (12hr infusion) • Hemodynamics/ lung perfusion improved at 24 hrs • No mortality difference

  32. Thrombolysis and PE • Evidence for TT and PE • Sharma et al (pts from UPET and USET) • Measured diffusion capacity and pulmonary blood volume at 2 wks and 1 yr • Improved in the thrombolytic therapy gp • Concluded: TT more complete resolution of clot beyond resolution of perfusion scan or angiography

  33. Thrombolysis and PE • Evidence for TT and PE • Since UPET 8 smaller randomized trials • SK, UK, comparison etc. • All show variable benefit in either blood flow, perfusion but no mortality benefit • PIOPED (13 pts rtPA or heparin) • Pulm vascular resistance : Diff at 1 hr gone at 2 hrs

  34. Thrombolysis and PE • Evidence for TT and PE • Goldhaber et al (1993) • N=101, heparin vs rtPA and heparin • ECHO (3 and 24 hrs) and perfusion scans • rtPA improved RV function and lung perfusion • Trend to decreased recurrence of PE

  35. Thrombolysis and PE • Evidence for TT and PE • Jerges et al 1995 • Small study n=8, massive PE with shock • SK vs heparin • Heparin 4/4 died • rtPA 0/4 died • First evidence of mortality benefit???

  36. Thrombolysis and PE • Evidence for TT and PE • PE registry (1993-1994) n=1001 pts • RV dysfunction/ pulm hypertension (no shock) • rtPA (n=169) vs heparin (n=719) • Mortality: 4.7 vs 11.1% (ARR 3.4%, RRR 31%) • Recurrent PE: 7.7 vs 18.7% (ARR 11%, RRR 59%) • Needs to be validated in a large PRCT

  37. Thrombolysis and PE • Evidence for TT and PE • Long term benefit (Sharma et al) • Right heart cath 7 yrs after PE and either TT or heparin • Heparin gp : higher PA pressures and higher pulmonary vascular resistance • TT gp : values normal

  38. Thrombolysis and PE • Conclusion • TT results in more rapid clot resolution, perfusion and blood flow • No mortality difference in pts without shock (but may be due to small studies) • Possible mortality benefit in pts with shock!

  39. Thrombolysis and PE • Which agent to use?? • SK for 24 hrs, UK for 12 hrs and rtPA for 2 hrs • Goldhaber et al • rtPA 2 hr infusion, UK 24 hr infusion • Earlier clot resolution and improved hemodynamics with rtPA at 2 hrs benefit gone at 24 hrs! • Mortality no diff • Increased hemorrhage in UK (double)

  40. Thrombolysis and PE • Conclusion • All agents seem to be equal • rtPA has faster clot resolution but at 24 hrs no benefit

  41. Thrombolysis and PE • Other conclusions • Intra-arterial TT is no better than systemic therapy (no increased risk of bleeding) • Time of administration: TT better if given early but can have benefit out to 14 days

  42. Thrombolysis and PE • Complications • Major hemorrhage (fatal hem, ICH, hem requiring surgery or transfusion) : ~6% (heparin ~1.5%) • ICH : ~1% (death in ~50% ) • Decreased in SK

  43. Thrombolysis and PE • Indication For Thrombolysis 1) Hemodynamically unstable : shock or evidence of hypoperfusion 2) Hemodynamically stable: RV dysfunction? 3) ?? Large clot burden

  44. Case • In ICU • Thrombolysis with improvement in RV function (demonstrated by repeat echo) • U/S residual clot in superficial femoral and brachial artery • IVC filter placed • Catheter placed tPA – no effect • Thrombectomy right arm • D/C to ward for monitoring • D/C home on lifelong anticoagulation

  45. Case • Paradoxical embolus • Passage of venous embolus into the arterial circulation typically across an intracardiac shunt • Dx can only be inferred • Dx usually made if: • Documented venous thromboembolism • Acute arterial embolization • ECHO evidence of right to left shunt • Exclusion of a left sided source

  46. Case • Paradoxical embolus • MC intra-cardiac defect – PFO • Failed closure of the septum secundum • Frequency of PFO (autopsy) • 29% (probe patent) • 6% (pencil patent)

  47. What if???? • What if pt with antithrombin III deficiency presents with sx compatible with PE • How do you treat this pt.????

  48. THE END

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