Pulmonary Embolism - what the guidelines dont telll.pptx

pulmonary embolism - what the guidelines dont tell

1. HYPOXIC RESPIRATORY FAILURE AS THE PRESENTING FEATURE OF PULMONARY EMBOLISM – THERAPEUTIC OPTIONS Dr Jacob George P MD, DM, DrNB , IDCCM, IFCCM, EDIC Sr Consultant and Head Critical Care Medicine, Caritas Hospital Kottayam

2. Why bother? The most common cause of preventable death in hospitalized patients 80% occur without prior warning signs or symptoms Death due to massive PE is often immediate 2/3 of deaths occur within 30 minutes of embolization Early treatment is highly effective

3. MY PRESENTATION WHY WE GET HYPOXIA IN PE WHAT IS IN THE GUIDELINES. MANAGEMENT OPTIONS OUTSIDE THE GUIDELINES - CONTROVERSIAL

4. Clinical presentation PE is not associated with silent chest always

5. Mechanisms of Hypoxia in Pulmonary embolism V/Q mismatching: Development of high V/Q ratio in areas with occluded pulmonary vessels Development of low V/Q areas caused by redistribution of pulmonary blood flow from obstructed vascular areas to adjacent normal areas Development of bronchoconstriction by various mediators locally released and alveolar hypocapnia Development of alveolar collapse due to surfactant loss Decrease PvO2 due to reduced Cardiac Output Shunt: Surfactant deficiency or opening of pulmonary arteriovenous anastomosis or patent foramen ovale or delayed clearance of alveolar exudates Decreased diffusion capacity: Decrease in pulmonary blood flow.

6. Management of Hypoxia in Pulmonary embolism Increase / Restore pulmonary Blood flow Increasing the CO Increasing the SaO 2

7. Algorithmic approach to PE

8. Prognostic assessment

9. Hemodynamic instability

10. Initial management – Hemodynamic stabilization Cautious with Fluids

11. HIGH RISK PULMONARY EMBOLISM

12. Thrombolysis

13. Resuscitation Oxygen - Administration of supplemental oxygen is indicated in patients with PE and SaO2 <90% NIV or HFNC Intubation should be performed only if the patient is unable to tolerate or cope with non-invasive ventilation

14. WHAT THE GUIDELINES DON’T SAY 1. Lactate 2. Role of HFNC 3. Thrombolysis in intermediate high risk PE 4. Role of Vasopressin

15. Lactate Vanni S, Viviani G, Baioni M, Pepe G, Nazerian P, Socci F, Bartolucci M, Bartolini M, Grifoni S. Prognostic value of plasma lactate levels among patients with acute pulmonary embolism: the thrombo-embolism lactate outcome study. Ann Emerg Med. 2013 Mar;61(3):330-8. doi : 10.1016/j.annemergmed.2012.10.022. TROP I D DIMER BNP

16. Pulmonary Vasodilators

17. Oxygen delivery

18. NIV or Intubation Hypoxia during intubation - KILLS Increases Trans pulmonary pressures Worsens PA Pressures Hastens RV failure and death Effect more commonly seen with MV than NIV Effect is also added by drugs used for intubation May consider zero Peep to reduce the pressures

19. Oxygen delivery HFNC is better tolerated than NIV P rovides a high FiO 2 and minimal PEEP HFNC reduces the work of breathing and respiratory rate and increases the end-expiratory lung volume and pulmonary compliance . HFNC reduces the need for escalation of respiratory support, reduced dyspnea , and improved patient comfort. R apid improvement in respiratory distress in PE patients using HFNC, in terms of oxygenation and respiratory rate.

20. Inhaled NO as Treatment for Acute PE Release of serotonin, histamine, and thromboxane-A2 cause pulmonary artery vasoconstriction Inhaled Nitric Oxide causes pulmonary artery vasodilation and decrease in PVR, Improvement in V/Q matching. May be sufficient to reduce the fraction of blood shunted across an interatrial septal shunt

21.   iNOPE   iNO at a dose of 50 parts per million for 24 hours

22. Maintain circulation Guidelines – Norad + Dobut I may suggest vasopressin Vasopressin increases systemic vascular resistance (SVR) while sparing the pulmonary vasculature.  This can lead to a 45% decrease in the pulmonary-to-systemic vascular resistance (PVR/SVR) ratio compared with treatment without vasopressin.  Vasopressin can also improve right ventricular dilatation, oxygenation, and survival in pulmonary hypertensive crisis.

23. Thrombolysis in the Intermediate group

24. Thrombolysis The Pulmonary Embolism Thrombolysis ( Peitho ) TRIAL M ulti- center , double-blind, placebo-controlled randomized trial. Involved Pharma funding Stratified by centre, Randomised by blocks Inclusion criteria A ge > 18 years confirmed acute pulmonary embolism with an onset of symptoms 15 days or less right ventricular dysfunction positive test for troponin I or troponin T.

25. Peitho Trial Tenecteplase – Weight based + Heparin / LMWH

26. PEITHO TRIAL

27. Peitho Trial – Cause of Death

28. Primary efficacy outcome in non-prespecified subgroups.

29. Peripheral vascular disease = 1 point. Age >65 = 1 point. Prior cerebrovascular accident with residual deficit = 5 points. Prior myocardial infarction = 1 point. Risk of intracranial hemorrhage following systemic thrombolysis: 0 points = 1.2% 1 point = 2.9% 2 points = 3.4% 5 points or more = 18%

30. CONTROVERSIAL TO TAKE HOME 6 /10 patients in the tenecteplase group who had a hemorrhagic stroke were alive 30 days after randomization- case fatality rate of 40% M ild or moderate disability persisted in most of the survivors. If we can avoid the bleeds, Even in sub massive PE- Thrombolysis is far better Those who are tachypnoeic – RR - 24/min Age < 75 years

31. Treatment of submassive pulmonary embolism with tenecteplase or placebo: cardiopulmonary outcomes at 3 months: multicenter double‐blind, placebo‐controlled randomized trial  Journal of Thrombosis and Haemostasis   Volume 12 Issue 4 Pages 459-468 (April 2014) DOI: 10.1111/jth.12521 TOPCOAT

32. TOPCOAT TRIAL P atients with submassive PE may suffer persistent right ventricular dysfunction that can impair their quality of life by causing dyspnea and exercise intolerance Inclusion: adult patients with submassive PE PE diagnosed on CT-PA Normal systolic BP Right ventricular strain (any of the following) hypokinesis on echocardiography elevated Troponin I or T BNP >90pg/ml or NT proBNP >900pg/ml Exclusion: BP<90mmHg, contraindications to thrombolysis

33. Figure 1 Journal of Thrombosis and Haemostasis  2014 12459-468DOI: (10.1111/jth.12521)

34. Figure 3 Journal of Thrombosis and Haemostasis  2014 12459-468DOI: (10.1111/jth.12521)

35. Figure 4 Journal of Thrombosis and Haemostasis  2014 12459-468DOI: (10.1111/jth.12521)

36. Can we get away with a lower dose? MOPETT TRIAL-Moderate pulmonary embolism treated with thrombolysis (from the "MOPETT" Trial) D efined if above criteria met and either of the following: CT-PA involvement of >70% involvement of thrombus in   ≥ 2 lobar or left or right main pulmonary arteries high-probability V/Q scan showing V/Q mismatch in  ≥ 2 lobes

37. A still lower dose?

38. 6-hour intravenous infusion of 25 mg of tPA without a bolus was administered immediately.

39. CONTROVERSIAL TAKE HOME Even in sub massive PE- Thrombolysis is far better A lower dose might be enough Give as a slow infusion, monitoring fibrinogen levels Anticoagulation - Only after stopping fibrinolysis Those who are tachypnoeic – RR - 24/min Age < 75 years

40. Thank you