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
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
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NIHSS calculator at farmacologiaclinica.info Website
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