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Eur J Cardiothorac Surg 2004;25:708-715
© 2004 Elsevier Science NL
a Department of Cardiothoracic Surgery, Mount Sinai School of Medicine/New York University, One Gustave L. Levy Place, P.O. Box 1028, New York, NY 10029, USA
b Department of Neurosurgery, Mount Sinai School of Medicine/New York University, One Gustave L. Levy Place, P.O. Box 1028, New York, NY 10029, USA
c Department of Biomathematics, Mount Sinai School of Medicine/New York University, One Gustave L. Levy Place, P.O. Box 1028, New York, NY 10029, USA
Received 15 October 2003; received in revised form 6 January 2004; accepted 8 January 2004.
* Corresponding author. Tel.: +1-212-659-6800; fax: +1-212-659-6818
e-mail: ju.strauch{at}gmx.de
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Abstract |
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 Top Abstract 1. Introduction2. Materials and methods3. Results4. Discussion and conclusionsAppendix A. Conference...References |
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Key Words: Thoracoabdominal aortic replacement • Spinal cord ischemia • Hypothermia • Motor-evoked potentials
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1. Introduction |
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TopAbstract1. Introduction2. Materials and methods3. Results4. Discussion and conclusionsAppendix A. Conference...References |
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The pathogenesis of paraplegia, especially delayed-onset deficit, is not fully understood [5]. Current research has focused increasingly on obtaining a better understanding of the physiology of spinal cord blood supply in the hope of reducing the incidence of this dreaded complication [6]. But it seems likely that the severity of the acute intraoperative ischemic insult plays an equally important role in at least some cases of spinal cord injury, and measures to protect the spinal cord during surgery also deserve renewed scrutiny.
Various adjunctive procedures have been introduced in recent years, and have successfully reduced the incidence of postoperative cord dysfunction. Routine use of distal aortic perfusion is increasingly common if the operation may exceed a very brief duration of aortic cross-clamping. Intraoperative and postoperative monitoring of somatosensory evoked potentials to assess cord function, and use of cerebrospinal fluid (CSF) drainage to improve perfusion are widely accepted. Some centers advocate selective preoperative identification of segmental spinal cord blood supply, and use intraoperative segmental perfusion. Many surgeons implant intercostal arteries liberally postoperatively. Various pharmacological agents have been found helpful in experimental studies, although there is no consensus about their clinical use.
But a significant number of patients still suffer from postoperative paraplegia or paraparesis, despite all these precautions and safeguards [7]. Although hypothermia is widely accepted as a protective method for temporary central nervous system ischemia, and most surgeons allow mild hypothermia to occur passively during aneurysm surgery, only a few surgeons advocate using deep hypothermia routinely during thoracoabdominal aneurysm repair, or actively seek to assure the presence of mild hypothermia to cool the spinal cord [8–11]. Similarly, although recording of motor-evoked potentials (MEPs) has been shown to be the most effective means of monitoring spinal cord function intraoperatively, it is used in only a few centers.
We have embarked on a multifaceted investigation of the pathophysiology of paraplegia in the chronic pig model, using MEPs to monitor spinal cord function intraoperatively. In the current study, we used simple cross-clamping of the descending thoracic aorta to test the hypothesis that mild hypothermia during transient spinal cord ischemia would be neuroprotective. We systematically investigated the relationship between duration of aortic cross-clamping and MEP recovery during hypothermia and normothermia, and its relationship to the development of both immediate and delayed paraplegia. We were surprised to find that mild hypothermia has a dramatic impact in lengthening the interval of aortic ischemia tolerated by pigs without the development of postoperative spinal cord dysfunction.
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2. Materials and methods |
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TopAbstract1. Introduction2. Materials and methods3. Results4. Discussion and conclusionsAppendix A. Conference...References |
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Myogenic MEPs and intracranial pressure (ICP) were monitored, and postoperative recovery was evaluated for 3 days using a Tarlov score.
2.2. Description of body temperature management
After inducing the anesthesia (see protocol below) all animals belonging to the group where mild hypothermia was applied, were cooled down to 32.0 °C rectal body temperature by covering the animals with cold packs of artificial refrigerants. These cold packs of artificial refrigerants were around the whole animal for a period of 30 min reducing the temperature to 32.0 °C. In addition a cooling blanket beneath the animal was used for the whole period of cooling and maintaining the low temperatures and to prevent a temperature drift. The operating room temperature was reduced and kept at 14.0 °C. No local cooling of the vertebral column was done. After passing through the clamping period the animals were warmed up via heating blanket, a heating lamp for a required time, which normally took 90–100 min and highering the operating room temperature to 24.0 °C.
For the normothermia (36.5 °C) experimental group the methods to maintain stable body temperature simply consisted of constant temperature in the operation theatre and a heating blanket below the animal. The small left thoracotomy in the fourth intercostal space and the short time for dissection was without any risk for temperature drifting.
2.3. Perioperative management and anesthesia
All animals received humane care in compliance with the guidelines of ‘Principles of Laboratory Animal Care’ formulated by the National Society for Medical Research and the ‘Guide for the Care and Use of Laboratory Animals’ published by the National Institute of Health (NIH Publication No. 88-23, revised 1985). The protocols for all experiments were approved by the Mount Sinai Institutional Animal Care and Use Committee.
After pretreatment with intramuscular ketamine (15 mg/kg), and atropine (0.03 mg/kg), animals were anesthetized with intravenous sodium thiopenthal (20 mg/kg). After endotracheal intubation, the pigs were ventilated mechanically with FiO2 of 0.5 and isoflurane 1–2% to induce sufficient anesthesia. Inhalation of isoflurane was immediately discontinued, and anesthesia was maintained with an infusion of ketamine 15 mg/kg per h and sufentanil 5 µg/kg per h. This anesthetic regimen has no major effect on MEP responses and has been described previously [12]. Paralysis for intubation was achieved with intravenous pancuronium (0.1 mg/kg), but no further doses were administered subsequently to avoid interfering with measurement of MEPs. The ventilator rate and the tidal volume were adjusted to maintain the arterial carbon dioxide tension at 35–40 mmHg. End-expiratory carbon dioxide, and inspiratory and expiratory isoflurane were monitored continuously (PPG Biomedical Systems, Model 2010-200 R, Lenexa, KS, USA). Arterial oxygen tension was maintained greater than 100 mmHg.
A bladder catheter (Foley 8–10 F) was inserted for online measurement of urine output, and temperature probes were placed in the esophagus and the rectum. Electrocardiographic measurements were recorded continuously. An arterial line was placed in the right brachial artery for pressure monitoring and blood sampling (pH, oxygen tension, carbon dioxide tension, oxygen saturation, base excess, hematocrit, hemoglobin and glucose, lactate, Blood Gas Analyzer, Ciba Corning 865, Chiron Diagnostics, Norwood, MA, USA). For the monitoring of an eventually collateral pathway flow to the lower extremities, a second arterial line was placed in the right side femoral artery.
2.4. Monitoring technique for motor-evoked potentials (MEP)
A 5 cm longitudinal incision was made in the scalp overlying the skull, and the periosteum was removed to expose the sagittal and coronal sutures of the calvarium. Four stainless steel screw electrodes with attached wire leads were screwed into the skull 10 mm lateral to the sagittal suture. Two screws were placed on the left side (8 mm anterior and 8 mm posterior to the coronal suture), and two were equally placed on the right. The wire leads were connected to an electrical stimulator (Digitimer Stimulator Model D 180A, Welwyn, Garden City, United Kingdom). Electromyographic recordings were made from sterile stainless steel needle electrodes placed through the skin over the tibialis muscle in the hind leg and the muscles in the foreleg (see Figs. 1 and 2) . A stimulation train (3 pulses, 200–300 V, 100 µs pulse duration, and 2 ms interstimulus interval) delivered to the skull electrodes was used to elicit MEPs. MEPs were amplified (gain 2000), bandpass filtered (10–1000 Hz), digitized, and stored on an optical disk for subsequent analysis by a Spectrum 32 neurophysiological recording system (Cadwell Laboratories Inc., Kennewick, WA, USA).
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Data acquisition and analysis were performed on a computer with an AD converter and software (LabVIEW, National Instruments, Austin, TX) (Fig. 3) .
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2.6. Operative technique for induction of spinal cord ischemia
The chest was opened via a small left thoracotomy in the fourth intercostal space. The descending aorta was mobilized and encircled with a silastic catheter directly below the left subclavian artery. The first two thoracic segmental arteries, with their single origins, were dissected and exposed but left untouched. The pericardium was opened and the heart exposed. After heparinization (200 IU/kg) and preparation with a 4–0 pursestring suture, the right atrium was cannulated with a 24 F single stage venous cannula. The cannula was connected to a heparinized blood bank for withdrawal and bag infusion (IntraViaTM Container, Baxter Inc., Deerfield, IL, USA). Mean arterial pressure was adjusted to a level of 100–110 mmHg during aortic cross-clamping by exsanguination of 350–400 cc from the circulating blood volume; the blood was reinfused after release of the cross-clamp. This method allowed easy and rapid partial exsanguination for blood pressure control and stabilization and avoided the potentially confounding effects of vasoactive drugs [13]. Just before cross-clamping, a left atrial catheter was inserted for subsequent left heart preload measurement and volume management.
A baseline MEP recording was obtained, and repeated three times while mean arterial blood pressure and anesthesia conditions were stable. Thereafter, the descending aorta was cross-clamped in the prepared area. Measurements for MEP response were taken at 1 min, and then every 5 min after cross-clamping, as well as after cross-clamp release. A period of 180 min was considered adequate to monitor MEP recovery after aortic cross-clamp release.
2.7. Postoperative course
During the observation period—180 min after aortic cross-clamp release—the thoracotomy incision was closed. The scalp incision was closed after the final reading. All animals remained on the operating table with intermittent positive pressure ventilation for a recovery period of 2 h after closing all incisions. Mean arterial pressure was maintained >65 mmHg using 0.9% sodium chloride infusion if required. The animals were then extubated and brought to the recovery room, where food and water were provided starting on POD 1. For continuing observation, the pig was placed in a separate pen as soon as it was alert. Analgesic treatment (buterophenol 0.1 mg/kg) was maintained for all 3 postoperative days.
Neurological examination using the Tarlov score was carried out daily at the same time by an investigator blinded to the grouping. The Tarlov score is as follows: 0, spastic paraplegia and no movements; 1, paraparesis and slight movements; 2, paraparesis and powerful movements in hindlimbs but not able to stand; 3, able to stand but unable to walk; 4, full recovery and normal walking [14]. After assessment of the Tarlov scores on POD 3, the animals were sacrificed using intravenous pentobarbital.
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3. Results |
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TopAbstract1. Introduction2. Materials and methods3. Results4. Discussion and conclusionsAppendix A. Conference...References |
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3.2. Comparability of experimental groups
A comparison of preoperative animal weights (normothermia group 19.6±0.9 kg vs. hypothermia group 19.3±1.1 kg) and age (normothermia group 11.1±0.5 months vs. hypothermia group 10.9±0.7 months) showed no differences between the groups.
As intended by the design of the study, basic hemodynamic data showed no significant differences between groups in heart rate, mean arterial pressure or central venous pressure. No significant hemodynamic, metabolic, or blood gas changes were noted during the procedure, with the exception of rising lactate levels.
There was no significant difference between groups in the volume of blood exsanguinated.
3.3. Motor-evoked potentials (MEP)
Reproducible MEPs could be recorded in all study animals. A response in each animal was obtained with a 200–250 V stimulation intensity. Following total aortic cross-clamping, the MEP signal tracing characteristically disappeared (extended latency and diminished signal amplitude) within the first minute in all animals, and never came back during the period of aortic cross-clamping.
The time to MEP recovery differed between groups (Table 2). After aortic cross-clamping for 20 min at normothermia, it took a statistically significant (P=0.04) longer time with a mean of 43.8±21 min to observe the start of MEP recovery, but only 32.5±11 min under hypothermic conditions. Hypothermia clearly shortens the mean time to MEP recovery after aortic cross-clamping for a given duration.
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3.4. Intracranial pressure (ICP)
Mean ICP baseline values did not show significant differences between normothermic and hypothermic animals. ICP decreased with aortic cross-clamping and diminished over the prolonged duration of cross-clamping, but this phenomenon did not vary with temperature (see Table 2).
3.5. Metabolic changes
As was anticipated and is seen in Table 1, arterial lactate levels rose throughout the procedure, but arterial lactate in normothermic pigs rose faster during cross-clamping, resulting in significantly higher lactate levels than in the hypothermic group with equivalent cross-clamp durations (P<0.0001). Arterial lactate levels for normothermic animals remained at significantly higher levels 3 h after clamp release (P<0.0001): the hypothermic pigs were able to reduce their lactate levels during the 3 h after clamp release, but lactate values tended to be sustained at high levels in the normothermic group. Both groups clearly failed to reach baseline levels during the 3 h of monitoring after clamp release. The data are consistent with the idea that more severe ischemic injury occurs during normothermia, producing higher lactate levels. Venous lactate levels did show the comparable tendency throughout the whole experiment.
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Two of the three animals with 25 min of aortic cross-clamping at normothermia were scored 0 according to Tarlov (spastic paraplegia, no movements) on POD 1, and never regained function, but one emerged from surgery normal (Tarlov 4) on POD 1. All three animals cross-clamped for 30 min at normothermia were paraplegic, with a Tarlov score of 0, on the first postoperative morning.
The three animals that underwent 60 min of aortic cross-clamping at hypothermia (32.0 °C) were initially functioning normally (Tarlov 4) on the morning of postoperative (POD) 1. All three animals became paraplegic (Tarlov 0) between 24 and 48 h after the procedure. This delayed-onset paraplegia showed slight improvement in only one of the three animals, which recovered to a Tarlov score of 2 (paraparesis, powerful movements in hindlimbs, but not able to stand) on POD 3.
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4. Discussion and conclusions |
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TopAbstract1. Introduction2. Materials and methods3. Results4. Discussion and conclusionsAppendix A. Conference...References |
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Hypothermia is widely used in clinical surgery as a protective agent for temporary central nervous system ischemia because it reduces metabolic rate and oxygen requirements. With mild hypothermia (32.0 °C) via surface cooling, we were able to more than double the tolerance of the spinal cord to ischemia in the pig.
Other groups have also seen a beneficial effect of reduction of temperature on the duration of ischemia tolerated by the spinal cord, but in different experimental models. In a study in rabbits, it was estimated that every 1 °C of hypothermia increases spinal cord tolerance to ischemia by about 5 min. In the rabbit study, spinal cord ischemia was produced by temporary occlusion of the abdominal aorta distal to the renal arteries for up to 35 min; temperature was reduced no lower than 34 °C, and magnesium infusion was carried out in most of the animals with longer cross-clamp durations, possibly enhancing the benefit of hypothermia [17]. In a study in dogs, the aorta was cross-clamped for 30 min between the left subclavian artery and the diaphragm while the spinal cord was perfused with Ringer's solution via the intercostal arteries at 20 °C. This resulted in recovery of normal motor function in all six hypothermically perfused dogs, in contrast to the controls, that all became paraplegic following 30 min of aortic cross-clamping at normothermia without spinal cord perfusion [18,19].
We restricted our study protocol to an overall surface cooling, using cold packs of artificial refrigerants which are easy to control: this averts complications related to systemic cooling on cardiopulmonary bypass. No harmful cardiac or hemorrhagic complications were seen during the mild hypothermia of 32.0 °C in our study, even after 70 min of cross-clamping, as previously described by others [6]. No significant effect of hypothermia on blood gases was noted. The mean level of lactate rose more slowly with hypothermia than with normothermia, reaching lower maximal values, with earlier recovery. But even pigs with the highest lactate values recovered fully, suggesting that lactate levels are of little value in predicting paraplegia: this confirms the findings of other groups [20].
A few surgeons recommend deep hypothermia with circulatory arrest during replacement of the thoracoabdominal aorta [8], and others have advocated cooling the cord with cold saline infusion via an intrathecal catheter [21]. Svensson et al. recently reported a low incidence of paraplegia in a clinical study, using mild hypothermia in combination with other adjuncts [22]. In contrast to these more elaborate protocols, the current study suggests that mild systemic hypothermia augmented by complete surface cooling provides significant spinal cord protection without any adverse sequelae.
It has been theorized that delayed paraplegia following aneurysm surgery probably occurs when an acute ischemic insult to the spinal cord intraoperatively is compounded by a lack of adequate perfusion postoperatively. The current experiment suggests that an acute intraoperative ischemic injury alone is sufficient to cause delayed paraplegia without invoking a major role for postoperative hemodynamic compromise. The delayed-onset paraplegia observed in all three animals after 60 min of cross-clamping during hypothermia suggests that an initial ischemic event of borderline severity may induce subclinical neuronal damage initially, without immediate paraplegia. The later clinical deterioration may be a result of spinal cord edema, reperfusion injury-induced toxicity, an episode of inadequate perfusion postoperatively, or apoptosis. All these factors may play a role in delayed-onset paraplegia, and all are likely to be minimized by intraoperative hypothermia.
Whether additional adjunctive measures might have further improved results is open to question. Several studies have described the interaction between arterial blood pressure and CSF pressure within the spinal canal. Experimental cross-clamping of the descending aorta in dogs has been reported to result in a 3–4 mmHg increase in CSF pressure; another study in humans has reported an average increase of 7 mmHg in CSF pressure during aortic cross-clamping [5]. Because of the pig's small size and the possible damage one might inflict by positioning an intrathecal catheter, we did not monitor CSF pressure in our study, although we monitored ICP, which we anticipated should correlate with CSF pressure. We failed to observe an ICP increase during descending aortic cross-clamping and in the 3 h postclamping period, perhaps because severe elevation of arterial pressure was controlled by exsanguination. Our findings confirm the work of Strømholm et al. [23], who describe a decrease in intracranial ventricular volume and ICP during cross-clamping of the descending aorta. Hypothermia reduces ICP, which increases spinal cord perfusion pressure without adjunctive measures. Nevertheless, there is considerable clinical evidence that CSF drainage may further enhance spinal cord perfusion, and that use of steroids and some other pharmacological agents may be beneficial in preventing paraplegia, especially postoperatively.
Monitoring of MEPs is a valuable adjunct in thoracoabdominal aneurysm operations to assess anterior and lateral motor column function. As has been previously described, MEPs are highly sensitive when recorded from the lower extremity muscles even in pigs [3,12,24,25]. The use of MEPs in humans offers the promise of being able to avert neurological compromise through early detection of abnormal signal transmission from the motor cortex to the distal extremities; whether there is a significant diminution in MEP response during surgery will establish whether the borderline contribution of a small segmental vessel is critical to cord viability. The routine monitoring of MEPs under stable anesthesia and analgesia conditions can be accomplished clinically, and the response to reperfusion is immediate restoration of normal amplitudes [12]. Monitoring of SSEPs is less precise and the response to ischemia is slower, but SSEPs can be used postoperatively to alert the clinician to the occurrence of delayed paraplegia.
In the pig, the return of MEPs after ischemia is delayed, but this does not seem to be an effect of temperature, since it is also observed during normothermia. Despite the lag in recovery of MEPs, all our findings during MEP monitoring were borne out by postoperative clinical observations: there was recovery of motor function in all animals that had return of MEP during operation. There were borderline MEP findings initially in some animals that eventually recovered full function, however. We think it is interesting that the time to the start of MEP recovery in the pig seems to depend both upon the duration of aortic cross-clamping and the temperature at which the procedure is carried out.
Our most important observation is that mild hypothermia more than doubles the tolerance of the spinal cord to ischemia in the pig. These results suggest that cooling to 32.0 °C should be encouraged during surgery which carries a risk of spinal cord injury and/or postoperative compromise of spinal cord blood supply.
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Footnotes |
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Appendix A. Conference discussion |
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TopAbstract1. Introduction2. Materials and methods3. Results4. Discussion and conclusionsAppendix A. Conference...References |
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The point that I wanted to make here is that if you're going to use this technique clinically, mild hypothermia won't do it. You really need to go to deep hypothermia for the additional benefits, also for open anastomosis and so forth. At 30 degrees, you get a very high incidence of delayed paraplegia because of induction of the apoptotic pathways.
My question here is whether you did any microscopic studies in the spinal cords and whether you looked for evidence of apoptosis in these animals?
Dr Strauch: No, I'm sorry for this. We didn't perform any histopathology studies in these animals.
Dr T. Carrel (Bern, Switzerland): May I ask the surgeons in the audience how many people use mild hypothermia during descending aortic surgery, just to have a look. (Show of hands.)
I'm a little bit surprised by the design of your study, which I would have judged a little bit simplistic, because I think that this mild hypothermia is already well established and I did not see any additional protection, for example, with spinal cord drainage or anything else. Can you make a statement on this.
Dr Strauch: The study was more or less a study on our way to establish a model to investigate on delayed paraplegia. So it was more or less the basic study to find the model to investigate and to look for delayed paraplegia. But so far, I'm sorry, there is no model for delayed paraplegia.
Dr S. Takamoto (Tokyo, Japan): I'd like to ask about the temperature managing after cross-clamping. You put the pigs in hypothermia by surface cooling, so that this temperature does not accurately indicate the temperature on the spinal cord, right?
Dr Strauch: No, it's a rectal temperature.
Dr Takamoto: It's a rectal temperature.
Dr Strauch: It's a rectal temperature we measured in this protocol. And we cooled down over the period even to 70 minutes by again and again doing topical surface cooling, not more. And the temperature drops down to 31.5, 31.4, not deeper.
Dr Takamoto: And then after this declamping the aorta, how do you manage the temperature?
Dr Strauch: The pig warms up by itself. The pig warms up just by a heating blanket by itself and we wait.
Dr Takamoto: Soon after declamping?
Dr Strauch: Soon after declamping we remove all the ice packs and all the cooling material.
Dr Takamoto: If you keep the low temperature after declamping, I think you can extend the safe time for the paraplegia.
Dr Strauch: That's true. But the study is limited by the motor-evoked potential monitoring process. One time you have to remove, you have to cut anesthesia, and you have to remove your screw electrodes from the skull. So there is no time to observe the pig, probably the whole night, and find the sensitive time interval of delayed paraplegia.
Dr T. Sueda (Hiroshima, Japan): So if you use distal perfusion plus hypothermia, how can we prolong the time limit to prevent spinal cord injury?
Dr Strauch: In humans?
Dr. Sueda: Animal study or humans also.
Dr Strauch: We absolutely didn't use distal perfusion in these animals. It was just straightforward, complete cross-clamping in descending position without any distal perfusion so without any collateral pathways coming from the median sacral artery or the iliac vessels.
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References |
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TopAbstract1. Introduction2. Materials and methods3. Results4. Discussion and conclusionsAppendix A. Conference...References |
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