Post on 15-Nov-2019
P Milsom
Capture of intracardiac material
minimising potential systemic emboliPaget Milsom
Green Lane Cardiothoracic Surgical Unitat
Auckland City Hospital
other significant contributors
S Mitchell A Barber A Merry L Blakey L Tippett S Hach
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Disclosure Form
I have had a financial interest with Dual Vent Circuit Ltd.
This could be perceived as a conflict of interest in the content of the subject of this program.
However the presentation is evidence based and balanced.
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Brain damage - talk outline
MagnitudeCostEtiology
Reduction methods
Trials and reportsNew approach to microemboli reductionReducing Brain Injury in Cardiac Surgery
Relating structural damage to functional outcome
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CABG brain damage - magnitudeRisk of Stroke
• CABG (0.6% - 5.2%)
• Valves (4.2% - 13%) Nussmeier, Jan 96
6.1% adverse neurological event Type 1 & 2
50% severe ↑ mortality and hospital stay
Roach, NEJM Dec 96
60% cognitive defects @ 8 days50% persisting @ 1 year
Taylor, Annal Thorac Surg 1998
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Incidence CNS perioperative injury↑ Complexity surgery → ↑ Adverse outcome
Newman Lancet;2006: 368:694
CABGNon vented 9/486 (1.9%)Vented 58/1549 (3.7%) p < 0.05
1.95 risk ratio 1.8% (0.07 - 3.7%) absolute risk
Roach, Personal communication 1999Combined procedures
16% adverse cerebral outcometype 1 8.4%type 2 7.3%
Wolman Stroke;1999;30:514
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Cost of Cerebral Event
D Hill 1999
174100Total Care Cost (%)
11.13.4Hosp Mort (%)
11.67.0Hosp LOS (days)
131.944.0ICU LOS (hrs)
StrokeNo Stroke
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Etiology of Brain Injury
Known Risk factors for CVABypass TimeAortic atheromaIABP usageDiabetesHistory of hypertensionHistory of pulmonary diseaseUnstable angina↑ age
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Etiology of Brain Injury
Major Risk factors for CVA
Embolism
Hypotension on bypass
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Increased Embolisation = ↑ Risk Neurological Deficit
43> 10008.6< 200Pugsley199435≥ 600< 30Clark 199570≥ 174
30< 106Stump 1996Neurological DeficitEmboli count
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Microemboli Release
80% released after x-clamp removal
continues for 28 mins following establishment of physiological flows
Tingleff et al Ann Thorac Surg 95
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Circuit Operates at Point of Maximum Embolisation
0
200
400
600
800
1000
start stable Up to34ºC
34 - 37ºC pumpwean
workingheart
Med
ian
Embo
li C
ount
CPB Rewarming
Ann Thorac Surg 1998;66:785-91
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New Approach to Microemboli Reduction
Circuit diverts total output of weaning heart
to CPB venous resivoir
↓
Emboli removed by CPB circuit prior to x-clamp removal
Milsom P, Mitchell S, Ann Thorac Surg 1998;66:785-91
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Surgical Considerations with Dual Vent Circuit
Surgical registrar manages root pressure by the variable resistor
De-airing time ≤ conventional methods.
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Microemboli CountConventional v's Milsom Circuit
0
500
1000
1500
2000
5 Surgeons PM Conventional PM Dual Vent Nonvented CABG
Med
ian
Embo
li C
ount
1749 1580
101 9
Ann Thorac Surg 1998;66:785-91
N=58 N=16
N=14 N=4
P Milsom 219AVR + 2 CABG1435AVR130MVR + Tricuspid12
208AVR117AVR + 2 CABG106AVR + 1 CABG90MVR818AVR + 1 CABG7
865AVR62AVR5
167AVR + 1 CABG4562AVR3363MVR2652AVR1IMAProcedurePatient No.
Index of Microembolic Activity after Aortic Declamping
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Summary
Minimises emboliat the time of maximum emboli release
Potentially minimises neurological damage
Dual Vent Circuit
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Reducing Brain Injury in Cardiac Surgery
Paget Milsom, Alan Barber, Alan Merry, Linda Blakey, Lynette Tippett, Sylvia Hach
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Primary Hypothesis
Dual Vent Circuit (DVC)
creates less
DW MRI brain damage (vol)
than
conventional “de-airing”
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Material & Methods
Registered trial Funded jointly by: NHF & Neurological Soc
Cardiac valve surgery patients +/- CABG
150 Prospective randomized - Only the surgical team unblinded to the intervention
√
Post-op 6 wks
Primary endpoint
√√DW MRI (ischaemic volume)
Reliability change index
√Neuropsych testsConsensus statement for assessment after Cardiac Surgery
√MMSE >24 mRS < 2NIHSS
√√√Neurological ExamChangePost-op ≤ 7 daysPre-op>18 years neurologically intact
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The controversy over the relationship between imaging and neuropsych testing
FORKohn 2002Toner 1994Restrepro 2002
AGAINSTVanninen 1998Bendszus 2002Knipp x 4 2004 → 09
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Results
Cohort
40 patients
26 men aged 63yrs (SD 12 yrs)
post-op imaging
37 with (36MRI + 1CT)
3 without (pacemaker, declined, early discharge)
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Pre-op
72 h post-op
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Early post-op results
Images:37 Scans (36 DWI 1CT)16 patient with ischemic lesions
16 / 37 43%13 small < 1cm33 confluent lesions 8 %
Clinical:2 strokes 5.0%
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Patients with and without post-operative ischemia on diffusion weighted MRI
0.0432:195:11CABG+valve : Valve0.14411:1012:4AV:MV/TV0.3672(9)3(19)Diabetes mellitus (%) 0.4834(19)4(25)Dyslipidaemia (%)0.2727 (33)3 (19)Atrial Fibrillation (%)0.1034(19)7(44)IHD (%)0.4958(38)7(44)Hypertension n(%)0.32310.613.5Length of stay (days)0.345144.0158.4CPB time (mins)0.6675.86.5EuroScore0.24059.665.2Age mean (SD)0.58914:711:5Male:Female
PDWI lesion absent
DWI lesion present
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Late Follow-up Procedures
Neuropsych
Neurological
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6 Week Results
Neurocognitive measurement 35 patientsRCI assesseddeficit = ↓ 1 ≥ measure
22 significant decline in ≥ 1 measure 63%
12 significant decline in ≥ 2 measure 34%
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6 Week Results
32 patients combined NP and MRI imaging
15 Patients new DWI lesions
all ↓ > 1 NP measure 100%
17 Patients no DWI lesion
only 6 ↓ > 1 NP measure 35%p<0.0001
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Patients with and without post-operative ischemia or neuropsychological decline
0.00237.49(4 →350)
DWI lesion / absence
0.1036.370.0785.00(0.83 →30)
CABG+valve : Valve
0.3511.010.3041.01CPB time0.6890.970.6381.04EuroScore0.1500.370.8900.91Gender/male0.1021.040.2491.03Age
PORPORPredictor variable
Neuropsychological outcome
DWI outcome
Logistic regression
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The burden of ischaemic damage resulting in decrease ≥ 2 neurocognative measures
6/8 (75%) patients multiple lesions or single lesion 1cm3
2/7 (29%) solitary lesion
3/17 (18%) no lesionp = 0.001
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Conclusions
Minimising brain emboli is a purposeful endeavor
as
Cognitive decline is linked to brain ischemia
and furthermore the
Volume of MRI damage is associated with the magnitude of cognitive decline