mike demeo nikhil kapila april 11, 2014 critical care m&m

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

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

Mike DemeoNikhil Kapila

April 11, 2014

Critical Care M&M

Page 2: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Morbidity & Mortality ConferenceMorbidity & 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

Page 3: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

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 careTo 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

Page 4: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Morbidity & Mortality ConferenceMorbidity & Mortality Conference

Every Defect is a TreasureEvery 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

Page 5: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Every Defect is a TreasureEvery Defect is a TreasureErrors are due to:

Processes – 80% Individuals – 20%

Translate all error into educationThis 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

Page 6: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

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

Page 7: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

VTE in patients with a history of ICHDVT has been reported in 2-15% of patients

with ICHPE occurs in 1-5% of patients

Usually 2-4 weeks after onset of acute ICHRisk factors for VTE in patients with h/o ICH

Stroke severityWeakness/changes in level of consciousness

Female sexAfrican Americans

Page 8: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

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

Page 9: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

VTE Prevention

Page 10: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

VTE Prevention-Intermittent Pneumatic

Compression

Treatment with IPC devices are associated with lower rate of DVT

Should be instituted immediatelyCLOTS 3 Trial

Open label, randomized study2876 patients with stroke. 322 with hemorrhagic

strokeIPC use was associated with reduced risk of DVT at

30 days-6.7 % vs 17%No major adverse eventsIPC devices are associated with a greater incidence

of skin breaks

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

VTE Prevention

Page 12: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

VTE Prevention-Anticoagulation

Page 13: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

VTE Prevention-AnticoagulationMeta-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 enlargementAHA/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”

Page 14: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Anticoagulation and Thrombolytics in the Management of PE

Page 15: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Initial Anticoagulation in PE

Subcutaneous LMWH

Subcutaneous Fondaparinux

Intravenous UFH

Page 16: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

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 mortalityFewer recurrent thromboembolic eventsLess major bleeding events

Non-superior to Fondaparinux.Monitoring: none required in most patients.

Page 17: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

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 administrationFixed doseLess thrombocytopeniaNo monitoring necessary in most patients

Page 18: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Initial Anticoagulation in PE

IV Unfractionated Heparin (IV UFH):No longer preferred agent for stable acute

PE.Preferred Indications:

Persistent hypotensionIncreased risk of bleedingThrombolysis being consideredConcern about subcutaneous absorptionRenal failureObese patients

Monitoring:aPTT

Page 19: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Role of Thrombolytics in PE

Agents:tPA:

Naturally occurring enzymeBinds fibrin to enhance plasminogen activation

Streptokinase:Polypeptide derived from beta-hemolytic strepBinds to plasminogen to activate plasmin

Urokinase:Occurs naturally in urinePlasminogen activator

Page 20: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Role of Thrombolytics in PE

Indications:Persistent hypotension <90 mmHg SBP or

decrease in SBP >/= 40mmHg from baseline.Potential Indications:

Severe hypoxemiaLarge V/Q mismatchExtensive clot burdenRV dysfunctionFree-floating atrial/ventricular thrombusPFOCardiopulmonary Resuscitation

Page 21: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Role of Thrombolytics in PE

Page 22: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Role of Thrombolytics in PE

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.

Page 23: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Role of Thrombolytics in PE

Page 24: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Role of Thrombolytics in PE

Page 25: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Role of Thrombolytics in PEContraindications:

Intracranial neoplasmIntracranial surgery/trauma (< 2 months)Active or recent internal bleeding (< 6

months)Hx Hemorrhagic CVANon-hemorrhagic stroke (< 2 months)Bleeding diathesisUncontrolled HTN (>200 sbp/110 dbp)Surgery (< 10 DAYS) Thrombocytopenia ( < 100, 000)

Page 26: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Embolectomy in PE

Page 27: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Embolectomy in PE

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.

Page 28: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Embolectomy in PE

Surgical Embolectomy:Requires cardiopulmonary bypass.Has been prompted by:

failure of initial thrombolysisecho evidence of thrombus in:

R atriumR ventriclePFO

Cardiac arrest pre-surgery can be predictive of mortality during surgery by one small study of 55 pts:97% survival of those w/o75% survival of those w/

Page 29: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Embolectomy in PECatheter 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.

Page 30: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Embolectomy in PE

Page 31: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Advanced Interventions: Catheter Directed Intervention

Page 32: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Advanced Interventions:Catheter Directed InterventionIndications for catheter based intervention in the setting

of acute massive PE should include one of the followingArterial 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).

Page 33: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Advanced Interventions:Catheter Directed Intervention

Page 34: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Advanced Interventions:Catheter Directed Intervention

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

Page 35: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Advanced Interventions-EKOSUltrasound 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

Page 36: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Advanced Interventions-EKOS

Page 37: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Advanced Interventions-EKOS

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% removalFollow-up pulmonary angiography performed

12-48 hours after initiation of intervention to determine progression of thrombus disruption

Page 38: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Advanced Interventions-EKOS

Page 39: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Advanced Interventions-EKOS

Page 40: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Advanced Interventions-EKOS

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

Page 41: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Advanced Interventions-EKOS

Page 42: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Advanced Interventions-EKOS

Significant reduction in RV/LV ratio in study groupSignificant reduction in pulmonary artery and right atrial pressures Significant increase in cardiac indexNo recurrent VTE or hemodynamic decompensationNo major bleeding complications. 3 patients (10%) experienced minor bleeding complications

Page 43: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Advanced Interventions-EKOS

Page 44: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Advanced Interventions-EKOS

Page 45: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

Advanced Interventions-EKOS

Page 46: Mike Demeo Nikhil Kapila April 11, 2014 Critical Care M&M

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