mike demeo nikhil kapila april 11, 2014 critical care m&m
TRANSCRIPT
Mike DemeoNikhil 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
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
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
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
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
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
Venous Thromboembolism Prevention in the Setting of Acute/Recent Intracranial Hemorrhage
VTE Prevention
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
VTE Prevention
VTE Prevention-Anticoagulation
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”
Anticoagulation and Thrombolytics in the Management of PE
Initial Anticoagulation in PE
Subcutaneous LMWH
Subcutaneous Fondaparinux
Intravenous UFH
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.
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
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
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
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
Role of Thrombolytics in PE
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.
Role of Thrombolytics in PE
Role of Thrombolytics in PE
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)
Embolectomy in PE
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.
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/
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.
Embolectomy in PE
Advanced Interventions: Catheter Directed Intervention
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).
Advanced Interventions:Catheter Directed Intervention
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
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
Advanced Interventions-EKOS
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
Advanced Interventions-EKOS
Advanced Interventions-EKOS
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
Advanced Interventions-EKOS
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
Advanced Interventions-EKOS
Advanced Interventions-EKOS
Advanced Interventions-EKOS
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