| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Ann Thorac Surg 1995;59:1356-1358
© 1995 The Society of Thoracic Surgeons
University College, London, United Kingdom
Abstract
The central nervous system complications arising during or shortly after coronary artery bypass grafting are due to cerebral ischemia associated with hypotension and to embolism. Hemodynamic compromise produces a spectrum of disturbance of consciousness and mentation ranging from brain death and coma through the chronic vegetative state to mild confusion. Watershed infarction may add to this picture focal deficits such as visual disorientation and cortical field defects or bibrachial weakness (the ``man in a barrel'' syndrome). Macroembolism accounts for most perioperative strokes and is related to cardiac arrhythmias, to intracardiac thrombus, and particularly to the severity and friable nature of any aortic atheroma. Microembolism can cause focal problems in the watershed territory but is normally responsible for diffuse changes as seen in the neuropsychologic sequelae of coronary artery bypass grafting. Coexistent carotid artery disease rarely contributes to the postoperative neurologic changes.
Central nervous system complications of cardiopulmonary bypass are due to a variety of pathologic changes. Ischemia predominates, as cerebral, subdural, or subarachnoid hemorrhage related to post-pump coagulation factor changes is rare [1]. Ischemia results from the diffuse results of hypotension or the more focal effects of embolism.
Diffuse Hypoxia/Ischemia From Loss of Cardiac Output or Profound Hypotension
If circulatory arrest is sudden in onset and recovery, damage to the brain is generalized through the neocortex and cerebellum but more variable in the central gray matter. Motor nuclei in the brain stem, the hypothalamus, and the anterior horn cells are least vulnerable. Such severe diffuse hypoxia/ischemia can produce brain death (characterized by unresponsive coma, apnea, fixed pupils, no eye movements, and loss of cough, gag, swallow reflexes) or coma with fixed pupils, apnea, myoclonic jerks, and seizures. A patient in a coma may be left in a chronic vegetative state if brain stem damage is subtotal. Sleep-wake cycles return, and the patient may show chewing, teeth-grinding, and scratching movements. Roving eye movements and grasp reflexes add to the distress of relatives who see them as evidence of returning normality. Less severe diffuse changes produce a confused, agitated patient with roving eye movements and restless limbs in whom memory impairment may be striking. The mildest effects include subtle memory disturbances and soft neurologic signs such as the appearance of primitive reflexes.
Neuropathologic studies in such patients show selective laminar necrosis and edema. Layer 3 is most vulnerable, layers 5 and 6 are next, and layers 2 and 4 are least vulnerable. Magnetic resonance imaging may occasionally show this in life [2]. The minimal lesion affects the CA1 sector of the hippocampus and the neocortex. Less severe hemodynamic crises, where there is a prolonged period of reduced flow rather than cessation, causes laminar necrosis or frank infarction in the watershed or distal field territories. These are the areas where blood supply is tenuous at the end of the longest arterial branches, that is, at the boundary between one major intracerebral vessel and the next, and hence are regions the most vulnerable to infarction if perfusion pressure falls. The territories concerned fall between those of the middle and posterior cerebral arteries in the parietooccipital cortex and between the anterior and middle cerebral arteries in the frontal lobe. There are also watersheds in the posterior circulation, for example, between the areas of supply of the superior cerebellar and posterior inferior cerebellar arteries. The infarcts, which are often hemorrhagic, are cone shaped with a base on the pial surface. They can be symmetrical or unilateral. In the latter case, critical stenosis of a major cervical artery may predispose one hemisphere to watershed damage at levels of perfusion pressure that per se were sufficient to preserve neuronal vulnerability on the other side.
The clinical picture of watershed infarction can be distinctive [3]. The most common lesion is in the parietooccipital cortex. The patient may awake from operation with no vision because of cortical blindness. After a day or 2, this begins to recover, but the patient has an inferior altitudinal field defect caused by the greater ischemic challenge to the upper parts of the calcarine cortex. He or she has great difficulty with visually guided movements and in distance judgment. The patient may lose the blink response to visual threat and will lose optokinetic nystagmus provoked by a rotating drum or striped tape.
If the more anterior part of this watershed area is damaged, the arm and hand areas of the motor strip may be infarcted. The patient has normal movement of the face and legs but can have totally (or partially) paralyzed arms. This condition has been likened to ``a man in a barrel.''
In the frontal lobe, watershed damage may produce the picture of a frontal lobe syndrome with leg weakness, and a disorder of voluntary eye movements. It is difficult to detect subtle signs of watershed cerebellar ischemia postoperatively, but in some convalescent patients, dizziness and lateral displacement instability may reflect it [4].
Infarction in the basal ganglia may also occur because of profound hypotension. This is not strictly a boundary zone but is the territory at risk at the end of small perforating vessels. The anterior thalami and outer parts of the caudate nucleus and putamen rather than the globus pallidus are most affected. On awakening from coma, the patient may show a picture of mutism and rigidity.
Watershed ischemia in the spinal cord usually affects thoracic regions between the fields of supply of the descending spinal arteries and arteries of Adamkiewicz. Urinary retention and flaccid paralysis of the legs are accompanied by a sensory level. (Embolic infarction of the cord, in contrast, often spares the dorsal columns with preserved joint position sense in paralyzed legs because of the separate blood supply to the posterior third of the cord.)
Focal Cerebral Damage From Embolic Stroke
The more common form of stroke in the perioperative period shows all the hallmarks of being embolic in origin rather than hemodynamic (that is, watershed resulting from asymmetrical perfusion failure). The incidence is about 5% with 2% to 3% being major. The evidence of their embolic origin follows. (1) Most are postoperative, occurring at times when there is adequate systemic blood pressure, rather than intraoperative. (2) Risks of perioperative stroke prove to be increased in the presence of atrial rhythm disorders [5], left ventricular thrombi [6], and severe aortic atheroma [7] (all markers of embolic sources). (3) Computed tomographic scans of patients with such strokes rarely show watershed infarction; rather, the lesions reflect territorial infarcts, for example, of the whole territory of the middle cerebral artery. (4) The risk of perioperative stroke shows little relationship to carotid artery stenosis or prior stroke unless recent.
The fate of emboli in the cerebral circulation is size dependent. Large emboli occlude the middle cerebral artery. (It is uncommon for the anterior cerebral artery to be occluded unless the middle cerebral is also obstructed). Smaller emboli enter branches of the middle cerebral artery and produce more discrete infarcts with, for example, isolated dysphasia or a ``cortical hand,'' which shows global weakness and lack of skilled movement. Sensory testing may reveal high-level difficulties like the inability to recognize objects or ``read'' numbers written on the palm, assuming crude sensation is intact.
Microemboli enter finer vessels of course. Particles of 200 µm preferentially enter watershed territories, as they are kept more to the center of the long vessels. A shower of such particles can cause the pattern of bilateral watershed infarction [8]. Small emboli are also thought to explain the occasional postoperative deafness caused by cochlear artery occlusion (labyrinthine function is preserved).
The smallest emboli are widely distributed and are more likely than diffuse hypoxia to be the cause of rather general neuropsychologic changes. Thus the severity of neuropsychologic changes correlates with the number of transcranial Doppler signals thought to represent the passage of emboli, and the incidence of both those signals and neuropsychologic impairment is reduced by additional arterial line filtration during operation [9]. Other evidence suggesting that microemboli cause neuropsychologic deficit includes correlation between the number of emboli and the incidence of the deficit, and reduction in deficits with membrane (but not bubble) oxygenators.
Perhaps hemodynamic mechanisms are most likely to play a role in patients with prior stroke having cardiopulmonary bypass. This theoretical possibility is the rationale for the clinical practice of searching for and treating tight carotid stenosis before or with operation. Rorick and Furlan [10] have shown that operative exacerbation of recent preoperative focal deficits seems to be related to perfusion problems. New strokes in patients with more remote preoperative strokes, on the other hand, tend to be in different sites and to relate to embolic risk factors like atrial fibrillation.
The phenomenon of operative extension of recent infarction probably relates to the loss of cerebral autoregulation after stroke. Cerebral blood flow is normally immune to changes in perfusion pressure over a wide range, for example, mean pressure from 50 to 150 mm Hg. The curve is shifted to the right in chronic hypertension, thereby making such patients more vulnerable to falls in cerebral blood flow when modestly hypotensive. After cerebral infarction, blood flow becomes pressure passive, so any fall in blood pressure threatens to extend the zone of infarction, especially in the territory of a blocked vessel where collaterals are already maximally dilated. Although it is normally taught that autoregulation recovers in the weeks immediately after a stroke, experimental data in the baboon show persistent defective autoregulation 3 years later [11]. Autoregulation is probably intact during bypass, though it will be compromised by high carbon dioxide tension levels. Autoregulation may be less efficient in old age, which may be one factor in the increased vulnerability to central nervous system ischemia at operation in the elderly.
The possible relevance of carotid narrowing to the risks of hemodynamic stroke suggested that carotid stenosis would be a risk factor for perioperative stroke. Patients with cervical bruits, Doppler evidence of carotid stenosis, or angiographic findings suggesting major stenosis or occlusion were followed to estimate whether the factors were predictive of increased stroke risk. The consensus [12] is that though the risk is increased, it remains small in absolute terms and does not normally warrant the added morbidity and mortality of carotid endarterectomy. Symptomatic cerebrovascular disease may be a different case with the risk of aggravating existing infarction and dislodging preexisting mural thrombi. We may be able to refine decision making in this context with the use of preoperative transcranial Doppler monitoring of embolic potential of carotid and aortic disease [13], and carbon dioxide reactivity testing for vulnerability to hypotension [14].
Footnotes
Presented at the Conference on CNS Dysfunction After Cardiac Surgery: Defining the Problem, Fort Lauderdale, FL, Dec 10–11, 1994.
Address reprint requests to Mr Harrison, Middlesex Hospital, Mortimer St, London, United Kingdom W1N 8AA.
References
This article has been cited by other articles:
|
|
 |
|
  N. Stroobant, G. van Nooten, D. De Bacquer, Y. Van Belleghem, and G. Vingerhoets Neuropsychological functioning 3-5 years after coronary artery bypass grafting: does the pump make a difference? Eur. J. Cardiothorac. Surg., August 1, 2008; 34(2): 396 - 401. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. I. Tagarakis, F. Tsolaki-Tagaraki, M. Tsolaki, A. Diegeler, N. B. Tsilimingas, and A. Papassotiropoulos The Role of Apolipoprotein E in Cognitive Decline and Delirium after Bypass Heart Operations American Journal of Alzheimer's Disease and Other Dementias, July 1, 2007; 22(3): 223 - 228. [Abstract] [PDF]
|
|
|
|
 |
|
 J.-C. Tardif, M. Carrier, D. E. Kandzari, R. Emery, R. Cote, T. Heinonen, M. Zettler, V. Hasselblad, M.-C. Guertin, R. A. Harrington, et al. Effects of pyridoxal-5'-phosphate (MC-1) in patients undergoing high-risk coronary artery bypass surgery: Results of the MEND-CABG randomized study J. Thorac. Cardiovasc. Surg., June 1, 2007; 133(6): 1604 - 1611. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Bar-Yosef, M. Anders, G. B. Mackensen, L. K. Ti, J. P. Mathew, B. Phillips-Bute, R. H. Messier, H. P. Grocott, and the Neurological Outcome Research Group and CARE I Aortic Atheroma Burden and Cognitive Dysfunction After Coronary Artery Bypass Graft Surgery Ann. Thorac. Surg., November 1, 2004; 78(5): 1556 - 1562. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. S. Likosky, B. J. Leavitt, C. A. S. Marrin, D. J. Malenka, A. G. Reeves, R. M. Weintraub, L. R. Caplan, Y. R. Baribeau, D. C. Charlesworth, C. S. Ross, et al. Intra- and postoperative predictors of stroke after coronary artery bypass grafting Ann. Thorac. Surg., August 1, 2003; 76(2): 428 - 434. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. C. Charlesworth, D. S. Likosky, C. A. S. Marrin, C. T. Maloney, H. B. Quinton, J. R. Morton, B. J. Leavitt, R. A. Clough, and G. T. O'Connor Development and validation of a prediction model for strokes after coronary artery bypass grafting Ann. Thorac. Surg., August 1, 2003; 76(2): 436 - 443. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Stroobant, G. Van Nooten, Y. V. Belleghem, and G. Vingerhoets Short-term and long-term neurocognitive outcome in on-pump versus off-pump CABG Eur. J. Cardiothorac. Surg., October 1, 2002; 22(4): 559 - 564. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Ascione, B. C. Reeves, M. H. Chamberlain, A. K. Ghosh, K. H.H. Lim, and G. D. Angelini Predictors of stroke in the modern era of coronary artery bypass grafting: a case control study Ann. Thorac. Surg., August 1, 2002; 74(2): 474 - 480. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. J. Wityk, M. A. Goldsborough, A. Hillis, N. Beauchamp, P. B. Barker, L. M. Borowicz Jr, and G. M. McKhann Diffusion- and Perfusion-Weighted Brain Magnetic Resonance Imaging in Patients With Neurologic Complications After Cardiac Surgery Arch Neurol, April 1, 2001; 58(4): 571 - 576. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Diegeler, R. Hirsch, F. Schneider, L.-O. Schilling, V. Falk, T. Rauch, and F. W. Mohr Neuromonitoring and neurocognitive outcome in off-pump versus conventional coronary bypass operation Ann. Thorac. Surg., April 1, 2000; 69(4): 1162 - 1166. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. A. Eagle, R. A. Guyton, R. Davidoff, G. A. Ewy, J. Fonger, T. J. Gardner, J. P. Gott, H. C. Herrmann, R. A. Marlow, W. C. Nugent, et al. ACC/AHA guidelines for coronary artery bypass graft surgery: A report of the American College of Cardiology/ American Heart Association task force on Practice Guidelines (Committee to revise the 1991 Guidelines for Coronary Artery Bypass Graft Surgery) J. Am. Coll. Cardiol., October 1, 1999; 34(4): 1262 - 1347. [Full Text] [PDF]
|
|
|
|
|
|
L. Noyez, D. P.B. Janssen, J. A.M. van Druten, S. H. Skotnicki, and L. K. Lacquet Coronary bypass surgery: what is changing?: Analysis of 3834 patients undergoing primary isolated myocardial revascularization Eur. J. Cardiothorac. Surg., April 1, 1999; 13(4): 365 - 369. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. P.B. Janssen, L. Noyez, J. A.M. van Druten, S. H. Skotnicki, and L. K. Lacquet Predictors of neurological morbidity after coronary artery bypass surgery Eur. J. Cardiothorac. Surg., February 1, 1999; 15(2): 166 - 172. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Birincioglu, K. Arda, H. Bardakci, K. Ozberk, M. Bayazlt, T. Cumhur, O. Tasdemir, and K. Bayazit Carotid Disease in Patients Scheduled for Coronary Artery Bypass: Analysis of 678 Patients Angiology, January 1, 1999; 50(1): 9 - 19. [Abstract] [PDF]
|
|
|
|
 |
|
 A. Jacobs, M. Neveling, M. Horst, M. Ghaemi, J. Kessler, H. Eichstaedt, J. Rudolf, P. Model, H. Bonner, E. R. de Vivie, et al. Alterations of Neuropsychological Function and Cerebral Glucose Metabolism After Cardiac Surgery Are Not Related Only to Intraoperative Microembolic Events Stroke, March 1, 1998; 29(3): 660 - 667. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J S Davies, M F Scanlon, and P E Belchetz Lesson of the week: Hypopituitarism after coronary artery bypass grafting • Commentary: Hypoadrenalism should also be considered in cases of persistent hyponatraemia BMJ, February 28, 1998; 316(7132): 682 - 682. [Full Text]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
