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Ann Thorac Surg 2002;73:S363-S365
© 2002 The Society of Thoracic Surgeons
a Hammersmith Hospital, London, United Kingdom
* Address reprint requests to Dr Kohn, Alvarado 209, Mar del Plata 7600, Argentina
Presented at Outcomes 2001, "The Key West Meeting," Key West, FL, May 23–27, 2001.
Over the past decade, advances in technology and surgical technique have resulted in a substantial reduction in mortality related to cardiac surgery performed with cardiopulmonary bypass (CPB). Morbidity has now become the focus of both researchers and the lay press [1, 2]. A postoperative neurologic event secondary to an otherwise technically perfect surgical procedure is the most dreaded outcome for both the surgeon and the patient [3, 4].
Since 1960, an increasing number of reports have documented cognitive deterioration after cardiac surgery with CPB. The incidence of subtle brain injury is alarmingly high compared with similar reports of major, clinically obvious, neurologic deficits.
In the early studies of neurologic outcomes, each research group used different definitions for evidence of brain injury, yet they all demonstrated unacceptably high levels of impaired brain function after cardiac surgery. Sotaniemi [5] reported subtle neurologic changes in 37% of patients the first postoperative year after aortic valve replacement. Dr Shaw’s work from Newcastle, England in the late 1980s [6] was the first to systematically document the alarming high incidence of cognitive deterioration: 79% in the first postoperative week after coronary artery bypass grafting (CABG). Her work initiated the current high level of interest in identifying the etiology of the neurologic injury and devising interventions to prevent or reduce its impact. A recent example is Newman’s 1999 paper [7]. Although a 12% event rate is much less than the previous reported neurologic morbidity (possibly due to the definition of neurologic injury in this study), it is still double the incidence of major neurologic complications. A recent 2001 publication, from the Duke group, reports a 42% incidence of neurologic symptoms 5 years post-CABG surgery from a cohort studied in the early 1990s [8].
There are two things that capture our attention when discussing cognitive dysfunction. First, why is it so common but difficult to document without sophisticated testing? Is there a change in the brain that we cannot define morphologically, or is the injury to the brain so minor that it only takes it a few months to recover completely? Second, is there a difference in the incidence and possibly the etiology of neurologic insult between the early 1980s and late 1990s? During this period of time, the most important changes in cardiac surgery practice have been the universal usage of membrane oxygenators and arterial filters. One can speculate the introduction of these changes coupled with advances in anesthetic technique, although far from explaining all these changes, may well be key factors responsible in the reduction of brain injury after CPB.
Brain injury after cardiopulmonary bypass can generally be ascribed to four etiological factors: macroemboli, microemboli, ischemia, or inflammation [9, 10]. Although, these four factors may explain permanent focal neurologic deficits, more challenging is trying to explain transient neurologic deficits. Computed tomagraphy scanning of the brain, spectroscopy, electroencephalogram, and many other techniques [11–14] have failed to clarify the etiology of this injury.
Magnetic resonance images (MRIs) have demonstrated areas of infarction, punctuate lesions, and cerebral edema after CABG. Although the formation of new lesions has been linked to the incidence of neurologic deficits, no correlation has been found between the site of the lesion and the severity and level of neurologic dysfunction [12]. More recently, diffusion-weighted MRIs (DWIs) have demonstrated an increase in brain water content 1 hour after CPB. No evidence of neurologic deficit was found and the changes reverted by 1 week. The findings were consistent with cerebral swelling due to an increase in extracellular water content. We have previously demonstrated changes in the brain in the acute postoperative stages (within 1 hour) after CABG and vascular surgery using FLAIR [15, 16] and three-dimensional subvoxel image registration and subtraction [17–19]. The changes were also consistent with cerebral swelling.
In an effort to understand these neurologic events, we have designed a double-blind placebo-controlled trial where 27 patients (Table 1) undergoing primary CABG were randomized to receive intraoperative full-dose aprotinin (Trasylol) or a placebo drug. All patients were imaged on a 1.0-T Marconi Medical Systems (Cleveland, Ohio) MRI System using a three-dimensional T1 W rf Spoiled imaging sequence. Images of the brain were obtained preoperatively, within 1 hour of chest closure, and at 3 months and 1 year after surgery. All follow-up images were realigned to the preoperative baseline image using a registration program and measured using a semiautomated quantitation program [17, 18]. Participants were assessed using a battery of 10 neuropsychological tests administered the day before surgery, and 3 months and 1 year postoperatively. Mood state was also assessed on both occasions. Premorbid IQ was assessed preoperatively using the New Adult Reading Test (NART).
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Standardized techniques were used for anesthesia and CPB. Anesthetic premedication included morphine (10 mg) and hyoscine (0.3 mg) administered intramuscularly 2 hours before induction surgery. Anesthesia was induced with midazolam (100 to 200 µg/kg), fentanyl (150 to 200 µg) and pancuronium (50 to 100 µg/kg), and sustained with propofol (5 to 10 mg/kg/h) during CPB.
During the induction of anesthesia, a jugular bulb catheter was inserted in the neck on the same side of the central venous pressure (CVP) line. After conventional median sternotomy and before aortic cannulation, a thorough inspection and palpation of the ascending aorta was performed to avoid plaques or atheromas.
The CPB circuit consisted of a roller pump (Stockert Instr., Munich, Germany), a Bard William Harvey HF-5700 membrane oxygenator, and polyvinylchloride tubing with a 40-µm Pall arterial filter. Pulsatile extracorporeal circulation was used at 2.4 to 2.8 L/m2/min, maintaining a mean arterial pressure between 50 and 70 mm Hg. Moderate hypothermia of 32°C was employed in all patients. Myocardial protection was administered with a Bard cardioplegia delivery system using antegrade cold cardioplegia, mixed with St. Thomas’ crystalloid solution in a 4:1 ratio, with additional 200 mL "hot shot," before cross-clamp removal. Venous top-ends were fashioned using a partial side-biting aortic clamp.
Standard physiologic monitoring (electrocardiogram, arterial pressure, CVP, nasopharyngeal temperature, FiO2, pCO2, pO2, airway pressure, SaO2, and urine output) was used throughout the procedure.
At the visual assessment, 8 patients had infarcts at 3 months and 1 year. Ventricular enlargement was seen in 21 patients in all the postoperative images; 1 patient had a reduction, 1 patient had no changes, and 3 were equivocal. The brain was unchanged on visual analysis for all the studied patients. Increases and reduction of ventricular size were measured ranging between 1.4% to 32.9% and 1.6% to 6% postoperatively (for example, see Fig 1).
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At the 1-year neuropsychological assessment, the number of new infarcts correlated (Pearson’s) with the number of tests showing 1 SD decline (r = 0.6655, p = 0.001). Similarly, we also found a correlation between Z change score and number of new infarcts at 12 months (r = -0.4672, p = 0.028).
Acknowledgments
The author acknowledges with gratitude the support and assistance of several colleagues in the research presented: Professor Graeme Bydder and Dr Angela Oatridge, the Robert Steiner MRI Unit, Dr David Harris and Dr Jeff Lockwood, Department of Anaesthetics, and Professor Ken Taylor, Department of Cardiothoracic Surgery, Hammersmith Hospital, London, United Kingdom; and Professor Stan Newman and Jan Stygall, Department of Neuropsychology, University College, London, United Kingdom.
References
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