Presentation is loading. Please wait.

Presentation is loading. Please wait.

Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M.

Similar presentations


Presentation on theme: "Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M."— Presentation transcript:

1 Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

2 Morbidity & Mortality Conference  It is for the department faculty and residents to peer review case(s) from the inpatient service.  The primary objective is to improve overall patient care focusing on quality of care delivered, performance improvement, patient safety and risk management. This material is confidential and is utilized as defined in Connecticut State statute 19a-17b Section(4) for evaluating and improving the quality of health care rendered

3 Goals:  To review recent cases and identify areas for improvement for (all) clinicians involved  Patient complications & deaths are reviewed with the purpose of educating staff, residents and medical students.  To identify ‘system issues’, which negatively affect patient care  To modify behavior and judgment and to prevent repetition of errors leading to complications.  To assess all six ACGME competencies and Institute of Medicine (IOM) Values in the quality of care delivered  Conferences are non punitive and focus on the goal of improved and safer patient care This material is confidential and is utilized as defined in Connecticut State statute 19a-17b Section(4) for evaluating and improving the quality of health care rendered Morbidity & Mortality Conference

4 Every Defect is a Treasure Every Defect is a Treasure This material is confidential and is utilized as defined in Connecticut State statute 19a-17b Section(4) for evaluating and improving the quality of health care rendered

5 Every Defect is a Treasure Errors are due to: Processes – 80% Individuals – 20% Translate all error into education This material is confidential and is utilized as defined in Connecticut State statute 19a-17b Section(4) for evaluating and improving the quality of health care rendered

6 Learning Objectives- 1. What is the role for DVT prophylaxis in patients with recent intracranial hemorrhage? 2. What are the roles of thrombolytics and heparin in the management of PE? 3. What are the other options in treating PE? Embolectomy EKOS

7 VTE in patients with a history of ICH DVT has been reported in 2-15% of patients with ICH PE occurs in 1-5% of patients Usually 2-4 weeks after onset of acute ICH Risk factors for VTE in patients with h/o ICH Stroke severity Weakness/changes in level of consciousness Female sex African Americans

8 Venous Thromboembolism Prevention in the Setting of Acute/Recent Intracranial Hemorrhage

9 VTE Prevention

10 VTE Prevention -Intermittent Pneumatic Compression Treatment with IPC devices are associated with lower rate of DVT Should be instituted immediately CLOTS 3 Trial Open label, randomized study 2876 patients with stroke. 322 with hemorrhagic stroke IPC use was associated with reduced risk of DVT at 30 days-6.7 % vs 17% No major adverse events IPC devices are associated with a greater incidence of skin breaks

11 VTE Prevention

12 VTE Prevention-Anticoagulation

13 Meta-analysis of four studies Compared anticoagulation therapy with other treatments in patients with ICH Use of anti-coagulation was associated with a significant reduction in Pulmonary Embolism (1.7% vs 2.9% P=0.01) Use of anti-coagulation was associated with a non-significant reduction in DVT formation and mortality Non-significant increase in hematoma enlargement AHA/American Stroke Association: “After documentation of cessation of bleeding, low dose subcutaneous low molecular-weight heparin or unfractionated heparin may be considered for prevention of venous thromboembolism in patients with lack of mobility after 1 to 4 days from onset”

14 Anticoagulation and Thrombolytics in the Management of PE

15 Initial Anticoagulation in PE Subcutaneous LMWH Subcutaneous Fondaparinux Intravenous UFH

16 Initial Anticoagulation in PE SC Low Molecular Weight Heparin (LMWH): Now considered better initial agent over UFH for most hemodynamically stable patients. Secondary to multiple randomized trials and meta-analyses showing: Lower mortality Fewer recurrent thromboembolic events Less major bleeding events Non-superior to Fondaparinux. Monitoring: none required in most patients.

17 Initial Anticoagulation in PE SC Fondaparinux: Recommended for most hemodynamically stable patients. Based on multiple studies against IV UFH: Same effects on mortality, recurrent thromboembolism, major bleeding. Advantages over IV UFH: Once or twice daily administration Fixed dose Less thrombocytopenia No monitoring necessary in most patients

18 Initial Anticoagulation in PE IV Unfractionated Heparin (IV UFH): No longer preferred agent for stable acute PE. Preferred Indications: Persistent hypotension Increased risk of bleeding Thrombolysis being considered Concern about subcutaneous absorption Renal failure Obese patients Monitoring: aPTT

19 Role of Thrombolytics in PE Agents: tPA: Naturally occurring enzyme Binds fibrin to enhance plasminogen activation Streptokinase: Polypeptide derived from beta-hemolytic strep Binds to plasminogen to activate plasmin Urokinase: Occurs naturally in urine Plasminogen activator

20 Role of Thrombolytics in PE Indications: Persistent hypotension /= 40mmHg from baseline. Potential Indications: Severe hypoxemia Large V/Q mismatch Extensive clot burden RV dysfunction Free-floating atrial/ventricular thrombus PFO Cardiopulmonary Resuscitation

21 Role of Thrombolytics in PE

22 Purpose : Compare echo parameters and clinical outcome of heparin vs thrombolysis in first 180 days after SPE w/ RVD. Methods: 72 consecutive patients w/ first episode SPE and symptoms <6 hours w/ CT proven PE and echo proven RVD. Results: Thrombolysis group showed significant early improvement in RV function and this improvement was still observed through the 180 day follow up. Also noted to significant reduction in clinical events during hospitalization.

23 Role of Thrombolytics in PE

24

25 Contraindications: Intracranial neoplasm Intracranial surgery/trauma (< 2 months) Active or recent internal bleeding (< 6 months) Hx Hemorrhagic CVA Non-hemorrhagic stroke (< 2 months) Bleeding diathesis Uncontrolled HTN (>200 sbp/110 dbp) Surgery (< 10 DAYS) Thrombocytopenia ( < 100, 000)

26 Embolectomy in PE

27 Embolectomy: Should be considered when patient presentation warrants thrombolysis but therapy either fails or is contraindicated. Can be done surgically or via catheter: Dependent upon availabilities and expertise at each individual institution.

28 Embolectomy in PE Surgical Embolectomy: Requires cardiopulmonary bypass. Has been prompted by: failure of initial thrombolysis echo evidence of thrombus in: R atrium R ventricle PFO Cardiac arrest pre-surgery can be predictive of mortality during surgery by one small study of 55 pts: 97% survival of those w/o 75% survival of those w/

29 Embolectomy in PE Catheter Embolectomy: Rheolytic (ie. AngioJet): Injection of pressurized saline to macerate emboli. Fragments collected via exhaust lumen. Requires venous cut down. Rotational: Cardiac catheter equipped with a rotating device that continuously fragments/aspirates pieces of the thrombus. Does not require venous cut down. Suction: Uses a large lumen catheter to apply direct negative pressure suction w/ an aspiration syringe. Fragmentation: Thrombus disruption via manually rotating a standard pigtail catheter or balloon angio catheter against the thrombus.

30 Embolectomy in PE

31 Advanced Interventions: Catheter Directed Intervention

32 Indications for catheter based intervention in the setting of acute massive PE should include one of the following Arterial hypotension. defined as systolic arterial pressure ≤ 90 mm Hg, a drop in systolic arterial pressure ≥ 40 mm Hg for ≥ 15 minutes, or ongoing administration of catecholamine for the treatment of systemic arterial hypotension; Cardiogenic shock with peripheral hypoperfusion and hypoxia; Circulatory collapse, including syncope or need for cardiopulmonary resuscitation; Echocardiographic findings indicating right ventricular dilatation and/or pulmonary hypertension; Subtotal or total filling defect in the left and/or right main pulmonary artery determined by chest computed tomography (CT) scan or by conventional pulmonary angiography; or Widened arterial-alveolar O2 gradient (> 50 mm Hg).

33 Advanced Interventions: Catheter Directed Intervention

34 Meta-analysis examining 594 patients from 35 studies Patients with acute massive PE treated with modern CDT Clinical success defined as stabilization of hemodynamics, resolution of hypoxia, and survival Pooled clinical success rate of CDI was 86.5% Risk of minor and major complications were 7.9% and 2.4% respectively

35 Advanced Interventions-EKOS Ultrasound accelerated catheter directed thrombolysis Delivered via an infusion catheter that emits ultrasound energy to accelerate the thrombolytic cascade This is achieved by using the EkoSonic Endovascular System that is manufactured by the EKOS corporation Acoustic energy leads to breakdown of fibrin and increases fibrin porosity without causing distal embolization This facilitates penetration of thrombolytic drugs

36 Advanced Interventions-EKOS

37 Patients were randomized into EKOS group and conventional CDI group who received either tPA or urokinase Complete thrombolysis: More than 90% thrombus removal Near complete lysis: 75-90% removal of thrombus Partial lysis: 50-75% removal Follow-up pulmonary angiography performed hours after initiation of intervention to determine progression of thrombus disruption

38 Advanced Interventions-EKOS

39

40 59 patients with acute main or lower lobe PE and RV/LV ratio of >1 Randomized to receive either ultrasound assisted catheter directed thrombolysis vs. unfractionated heparin alone Primary outcome was the difference in RV/LV ratio from baseline to 24 hours Safety outcomes included death, major or minor bleeding, and recurrent VTE at 90 days

41 Advanced Interventions-EKOS

42 Significant reduction in RV/LV ratio in study group Significant reduction in pulmonary artery and right atrial pressures Significant increase in cardiac index No recurrent VTE or hemodynamic decompensation No major bleeding complications. 3 patients (10%) experienced minor bleeding complications

43 Advanced Interventions-EKOS

44

45

46 References Ogata T, Yasaka M, Wakugawa Y, Inoue T, Ibayashi S, Okada Y. Deep venous thrombosis after acute intracerebral hemorrhage. J Neurol Sci. 2008;272(1-2):83 Christensen MC, Dawson J, Vincent C. Risk of thromboembolic complications after intracerebral hemorrhage according to ethnicity. Adv Ther. 2008;25(9):831. Skaf E, Stein PD, Beemath A, Sanchez J, Bustamante MA, Olson RE. Venous thromboembolism in patients with ischemic and hemorrhagic stroke. Am J Cardiol. 2005;96(12):1731. Orken DN, Kenangil G, Ozkurt H, Guner C, Gundogdu L, Basak M, Forta H. Prevention of deep venous thrombosis and pulmonary embolism in patients with acute intracerebral hemorrhage. Neurologist. 2009;15(6):329. CLOTS (Clots in Legs Or sTockings after Stroke) Trials Collaboration, Dennis M, Sandercock P, Reid J, Graham C, Forbes J, Murray G. Effectiveness of intermittent pneumatic compression in reduction of risk of deep vein thrombosis in patients who have had a stroke (CLOTS 3): a multicentre randomised controlled trial. Lancet. 2013;382(9891):516. Paciaroni M, Agnelli G, Venti M, Alberti A, Acciarresi M, Caso V. Efficacy and safety of anticoagulants in the prevention of venous thromboembolism in patients with acute cerebral hemorrhage: a meta-analysis of controlled studies. J Thromb Haemost. 2011;9(5):893


Download ppt "Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M."

Similar presentations


Ads by Google