Carrascal and Guerrero- Stroke and CABG part II

from the Neurologist

Perioperative risk factors:
1.  CPB use and factors that are uncontrollable including low flow
2.  Type of procedure-- 3 fold risk in patients undergoing open chamber procedure.Combined procedures eg. CABG + valve causes baseline increase from 5 to 16 % or so
3.  Duration-- number of emboli increase by 90.5 % for every hour
4.  Postoperative complications including low CO (due to MI eg.) or postoperative AFIB which is common in first 4 days.

III Preventive Procedures--
 Operatively
A.  Minimize aortic manipulation -- one cross clamp not multiple, or even zero with pediculate anastomoses
B.  Heart Port Clamp-- instead of external clamp, use a saline filled balloon and clamp internally avoiding manipulation
C.  Identify aortic disease with epiaortic ultrasound; if needed use femoral or axillary catheterization and / or profound hypothermia.
D.  Use side hole not end hole cannulas-- less displacement of particle
E.  Use intraaortic filtration-- not shown to be beneficial YET
F.Dispersion aortic cannulas when friable valves are diagnosed
G.  Carotid surgery according to above criteria
H.  Prophylactic resection of atrial appendage in patients with preexisting AF who also need MVR

Reduce microemboli in CPB Circuit
A. heparin bound CPB circuit
B. Membrane rather than bubble oxygenator
C. CO2 sufflation into thoracic wound to decrease air bubbles
D.  Filter in arterial line; leukocyte filter to decrease inflammatory response
E.  Decrease CPB time
F.  Decrease cardiotomy suction to prevent lipid microemboli and improve cognitive; us ultrasound to help
G.  Early slow rewarming 0.2 degrees C per minute
H.  Alphastat protocol for pH and CO2
I.    Reduce perfusionists' interventions which are directly tied to cognitive decline
J.  Avoid collecting/reinfusing mediastinal blood
K.  Emblocker ultrasound transducer on aorta redirects debris to descending aorta, tried in animals so far

Prevention of ischemic injury
A.  Keep MAP> 50
B.  Avoid maneuvers that increase CVP (CPP = MAP-CVP)
C.  Avoid cardiac luxation during off pump procedures which can lower CO
D.  Pulsatile flow not shown to be superior to continuous flow
E.  Substitute Aprinin for amicar or transxemic acid
F.  Avoid profound hemodilution especially in octagenerarians

Metabolic
A.  Avoid hyperglycemia
B.  Keep HCT over 30

Neuroprotection
Summary
Many have been studied none have shown effective

Bypass and stroke Pt !

also see blog post regarding Lou Caplan's opinion regarding the issue http://strokenotes.blogspot.com/search?q=cabg

Carrascal Y, Guerrerro AL.  Neurological damage related to cardiac surgery; pathophysiology, diagnostic tools, and prevention strategies. Using actual knowledge for planning the future.  The Neurologist 2010; 16:152-164.

Summary-- the population undergoing cardiac surgery is older and sicker.  Prevention efforts should include improvements in surgical techniques and cerebral protection, pharmacotherapy, and adequate neuropsychologic assessments. 

Bullet points: Intro
1. 1-6 % of patients have neurologic complications, but number is up to 15 % in high risk group and up to 50 % if you count cognitive dysfunction.  Neurologic complications increase one year mortality tenfold in first year, and doubles ICU care time.  31 % of patients with neurologic damage return home, 75 % with "minor" cognitive damage, 85 % without neurologic damage. 

I.  Mechanism of damage in cardiopulmonary bypass:  emboli (micro or macro), inflammatory response, metabolic response to hypoxemia or vasogenic or cytotoxic edema, and cerebral hypoperfusion

A.  Emboli
1) Macro, > 200 um, related to manipulation of aorta, calcium, valvular debris.  Causes focal deficits. 
2) Micro, <200 um, due to a) air, related to opening chambers of heart, generation in CPB machine, and during patient rewarming   b)  lipids, especially due to cardiotomy suction especially with lipid reinfusion into CPB circuit   c)  cellular aggregate esp platelets     d)  Exogenous material from heart lung machine such as silicon.  Microemboli go to border zone, to basal ganglia and white matter tracts.  TCD detection of microemboli over 60 correlates with a 70 % risk of cognitive damage.  TCD does not detect type of particle.
Intraoperative TEE detects air bubbles in chambers and diseased arteries that can be avoided for cross clamping.  Aortic intimal thickening over 3 mm, especially with rounded, protruberant or ulcerated plaque is associated with a 4.5 x risk of neurologic sequelae.  Post op stroke is 25 % with a mobile plaque, 8 % with a fixed plaque, and 1.8 % if there is no plaque. 

B.  Inflammatory response activation-- duet to CPB, leads to a coagulation cascade and damage to blood brain barrier. 

C.  Disorders in Neuronal Metabolism secondary to hypoxemia or vasogenic or cytotoxic edema-- related to hypothermia during procedure, which has good and bad points, although mild hypothermia seems to benefit.  Severe may lead to brain edema.

D.  Hypoperfusion--

II Detection
A..Biochemical markers of neuropsychological damage-- adenylate kinase (good), CK-BB (bad marker, totally nonspecific), neuronal specific enolase (good marker, raised levels over 35 ng/ml after 48 hours correlates with bad prognosis, S100 B is a white matter marker, good marker more than 24 hours out (early rise occurs during CPB and is not prognostic) Level of > .5 ug/mL at 48 hours have a 78 % mortality compared to 18 % with a level under .5.  S100B < 1.1 24 hours after surgery has a 97 % specificity to exclude stroke. 
B. Imaging- DWi and NIRS (near infrared spectroscopy) show clinically silent events in a MAJORITY of patients or at least 50 %.  Fluroescein retinal angiography can detect clinically silent retinal events.  and disappear 7 days postop
C.  Neuropscyh-- Studies not clear.  Risk factors (incremental) include DM, CRF, ascending aortic atherosclerosis, CVD, PVD, or previous severe neurologic disease. 

III Major risk factors for complications
A. Age
B.  Carotid disease (controversial)-- this author suggests there is a 10 % reduction of stroke risk if the artery is symptomatic and stenosis is > 50 %.  For asymptomatic , procedure only if patient has life expectancy > 5 years, is 40-70, mortality of procedure < 3 %. 
C.  Prior stroke confers 13-15 % risk no matter when the prior stroke
D.  PVD increases risk of perioperative stroke by 4.5 %, and affects 33 % of octagenarians.
E. Severe LV dysfunction and poor EF
F. Indirect risk factors : DM, RF, HTN, COPD
G. Baseline intellectual function
H.  Genetic factors (apoE) unsettled
I Gender-- women do worse

see next post

Reconsidering MI as a contraindication for IV thrombolysis for stroke

De Silva DA et al.  Neurology 2011; 76:1838-1840. 

General points

1.  Some guidelines suggest 90 days not to use t-pa, but risk exists only in those with transmural MI (for cardiac rupture) and in those cases the wall is healed within 7 weeks, or at least healing, with fibrosis and scarring maximized by then,  to  mitigate risk in younger stroke patients without transmural rupture. 

2.  There are only 3 reports of 5 elderly women with tamponade after stroke thrombolysis. 

3.  In cardiac literature, wall rupture occurs in first 48 hours in those with transmural MI. 

Atraumatic convexal subarachnoid hemorrhage

Clinical presentations, imaging patterns and etiologies.  Kumar S. et al.  Neurology 2010; 74: 893-399

Authors include LR Caplan

Convexal SAH is about 8 percent of all SAH.  Authors found 29 patients at Beth Israel, about two thirds were women.  There was a dichotomy in presentation by age.  The under 60's had a strong tendency to present with a severe headache, whereas that was rare in the over 60's, who presented with TIA-like presentations, migraine creeping numbness mimic (even repetitively) or lethargy.  Angiography/MRA/CTA was almost always negative.  The under 60's were most likely to have reversible cerebral vasoconstriction syndrome (formerly Call syndrome), whereas the over 60's were more likely to have amyloid angiopathy. The latter group tends to have recurrent disease, but this study does not have good followup.  Headaches often were prolonged, associated with retching or vomiting, and described as "thunderclap" in younger patients.  Surface eeg's were always negative for seizures among those presenting with repetitive sensory phenomena.  They were more likely to have superficial siderosis on imaging.

The differential of the presentation includes, in addition to the two above causes, cortical vein occlusion, PRES, coagulopathy, cocaine, lupus vasculitis, cavernoma, brain aneurysm, ephedra, HELLP syndrome, post LP headache, and arterial dissection.

Activated prothrombin complex for dabigratan bleed? one opinion

We recently had a 67-year-old man with atrial fibrillation who was
admitted from the EP lab after developing pericardial hemorrhage during
the procedure.  He had been taking dabigatran and had received his last
dose seven hours prior to the procedure.  He was undergoing an ablation
when a transseptal perforation occurred and hypotension ensued.  He had
received  5000 units of heparin prior to the start of the procedure.
Pericardiocentesis was undertaken and 4500 cc of blood was withdrawn.  He
was given two units of FFP  & Protamine 100 mg  with persistent bleeding.
He was then given  FEIBA (activated prothrombin complex) 3159 units (26
units per kilogram over 15 minutes).   One minute after initiating FEIBA
infusion slowing of the bleeding was observed.  Bleeding stopped from
pericardiocentesis within minutes of administration of FEIBA.  His PTT the
prior to the procedure was 53.  ACT prior to administration of heparin was
233. The PTT decreased to 35 after protamine infusion but prior to the
FEIBA administration, and decreased further to 29 following FEIBA. ACT
decreased to 131 following FEIBA.

Our single experience would suggest that FEIBA was effective in reversing
the anticoagulant effect of dabigatran.  I wonder if any others have had
an opportunity to use this treatment and what their experience has been?
Has anyone used other ways of reversing dabigatran and with what success?