THERMAL MANAGEMENT CONTROL FOR CARDIAC SURGERY PATIENTS.

ABSTRACT

Frank stroke and less easily measured neurological damage are still being noted as complications following cardiac surgical procedures. Observation of patient temperature variances made by physicians treating non-cardiac patients as well as those seen with experiments using laboratory animals may help us to better understand how to avoid some of these negative outcomes. There is also published clinical evidence that careful control of brain temperature during extracorporeal circulation may alter the degree of negative results. The purpose of this report is to glean some of the significant findings that have been reported and to suggest how they may best be applied to cardiopulmonary bypass procedures.

There has been an extensive history of documented stroke [1,2] and neuro- psychiatric problems [3,4] following open heart procedures since the beginning of the use of extracorporeal circulation. Articles about stroke [5] and neuropsychological problems [6,7] following bypass are still being written because a large portion of patients continue to be affected. One of the variables that is commonly measured and assessed, in this connection, is temperature [8,9,10]. Temperature management of the brain may be a key point in controlling the extent of damage following a stroke or other more subtle neural embarrassment.

A simple study [11] was performed to determine if there might be a correlation between the temperature of a stroke victim on admission to a hospital and the severity of the resultant stroke. By observing a total of 390 patients that were admitted within 6 hours of the onset of symptoms, the authors found an increased relative risk of a poorer outcome of 2.2 for each Centigrade degree of temperature elevation noted. It was also shown [12] that if a fever were to develop in a stroke patient anytime within the first 7 days from the onset of symptoms, the outcome would be worsened. The median maximal temperature attained was a mere 37.9 degrees C in the febrile portion of the 183 study patients. The higher the maximal temperature attained, the poorer the result.

One large study [13] of 297 patients admitted with cerebral hemispheric infarctions resulted when care was taken to observe the axilla temperature every 2 hours for the first 72 hours of hospitalization. It was noted that 60.8% of the patients achieved hyperthermia of at least 37.5 degrees C during the study period. The patients that died early had a significantly higher level of admission hyperthermia. The mortality at 3 months was 1.0% for the normothermic patients and 15.8% for those with any hyperthermia. The patients that developed hyperthermia early in the study period had a high mortality rate than those that became febrile later. There was noted to be a correlation between the time of fever onset and the size of the infarction as well as the resultant neurological deficit with the patients suffering earliest doing the worst.

Efforts have been extended toward controlling [14] the body temperature of patients after there were admitted to the hospital with stroke symptoms. Patients were put in a cold room, treated with drugs to prevent shivering and to provide anesthesia, and had a cooling blanket employed to reduce the inter-cranial temperature to 33 degrees C. Once the core temperature was attained, the patients were kept there for a period of 48 to 78 hours and then they were passively rewarmed over a period of 24 hours. These 25 patients demonstrated a reduction in intra-cranial pressures with the cooling, a reduction in the size of the eventual infarction, and a lowered mortality rate from what was expected. Rewarming of the patients was accompanied by a rise in the intra-cranial pressure and the brain temperature was consistently higher in all 25 patients than what was noted with a concurrent bladder temperature. The authors suggest that the higher brain temperatures may be due to either a high metabolic rate in the brain or that the decreased cerebral blood flow caused by the stroke may not be able to remove heat created by local metabolism. An additional insight is gained by noting that the primary complication of these patients (other than the stroke) was pneumonia, which was often first observed during the rewarming phase.

Patients, undergoing hypothermic and normothermic open-heart procedures, were evaluated [15] by observing real time cerebral venous oxygen saturation levels. The warming of the systemic blood caused a reduction in the cerebral saturations during the rewarming phase with the hypothermic patients and at the onset of bypass with the normothermic patients as their temperature was "elevated" to 37 degrees C. The cerebral venous saturations were consistently lower during rewarming than during cooling despite having the same systemic temperature demonstrating the likelihood that the brain was warming faster than the rest of the body. The cerebral venous saturations fell when the aorta was clamped and rose when the heart began to beat again even in the normothermic group. The role, therefore, of pulsatile flow is shown to have a direct positive influence on the blood flow to the brain. There were high saturation levels during hypothermia and this might suggest that the brains were being over-perfused by normal perfusion blood flows. As there was no direct temperature monitoring in the brain, the group repeated part of the study [16] when a new probe allowed simultaneous measurements of the cerebral venous blood. They found that 10 of 10 patients achieved a cerebral venous temperature in excess of 39 degrees C for an average duration of 15 minutes when the water temperature of the heat exchanger was set to 41 degrees C. One further paper [17] had demonstrated that during rewarming from hypothermia, 23% of patients had jugular venous saturations of less than 50%. The patients that had the lowest reading during the rewarming phase had also shown lower saturations during the hypothermic period and suggest that some of them were at a higher risk for inadequate brain blood flow due to previous anatomy, low hematocrit, or insufficient perfusion flows.

In the animal laboratory, some important work has been performed and reported by a group of investigators. First, [18] dogs were warmed to target temperatures of 37, 38, or 39 degrees C and allowed to equilibrate for 20 minutes. A period of 12.5 minutes of complete cerebral ischemia was followed by reperfusion for one hour at the target temperature. Neurologic assessments were made at 24, 48, and 72 hours after the study. All of the normal dogs were alive and well, all of the highest temperature dogs were dead or comatose, and those with modest hyperthermia were noted to recover in between the two extremes. Next, [19] a paper was written that explained the lack of good investigation into the role of temperature management in humans and offered the following suggestions. Find evidence in humans that might replicate the animal work showing the devastating effects of hyperthermia with ischemia. Create better ways to monitor the temperature of the human brain especially for patients at risk. Finally, management techniques should be developed to take advantage of temperature control of the brain while minimizing the alterations in systemic temperature. A pair [20,21] of articles describes a potential methodology that could easily be used in humans. Dogs were placed on bypass and either cooled to 28 degrees C with rewarming to 38 degrees C or kept normothermic. Air that had been cooled to 13 degrees C was blown over the heads of the dogs during the perfusion run. It was demonstrated that the brain temperatures could be kept from 1.1 to 3.3 degrees C colder than the core temperature in all the experiments. If pentobarbital was used as the anesthetic, the brain temperatures were found to be from 4.2 to 6.5 degrees C colder than the core temperature for those that were rewarmed.

The causes of stroke and other neurological changes following open-heart surgery have generally fallen into two categories: embolic events or ischemic periods of poor perfusion. Clearly, all steps should be taken to minimize the occurrence of such episodes. One idea that we have used [22] is to pre-filter the IV solutions that enter the heart-lung machine down to the 0.2 micron level. The recognition that foreign material is found in IV solutions and that if it is allowed to enter the arterial side of the patient, it will cause temporary arteriole vasoconstriction in addition to blocking capillary beds and thus enhance inadequate distal perfusion, may be the key to this practice. One of the most important findings in our early work was a reduction in the maximal core temperature reached in the post-operative period. It is certainly possible that the debris activated the body's defenses and triggered a febrile response. When the detritus in the IV solution was eliminated, so did the fever that was always seen with our patients. The neurologic recovery of our patients continues to be remarkable despite the lack of a good scientific study. A second idea [23,24] is to divert the shed blood, with its lode of extraneous debris, to a cell processing device which will minimize embolic activity.

It is perhaps equally important to be able to deal with a patient that has had an embolic event or some neurologic ischemia. The routine open-heart procedure has multiple reasons to stimulate concerns about emboli that might result from manipulation of the aorta, the other great vessels, and even, the heart itself. Periods of low flow and non-pulsatile flow are also quite common. The careful use of temperature control may be of far greater importance than has been generally acknowledged.

Considering the review just offered we should be able to more carefully design our perfusion practice. Hypothermia would seem to offer a great deal of neurologic protection. Hyperthermia, on the other hand, is a very dangerous maneuver with a normal circulation and the situation will be made even worse when it is used after embolic events or periods of ischemia. The more severe the hyperthermia, the higher the risk of having a poor outcome. Systemic rewarming of the open-heart patient without a normal pulsatile flow constitutes another elevation in risk. Slow rewarming over an extended period may be in the best interests of the open-heart patient with staged increases in the blood temperature so that the most profound period of hyperthermia will accompany the resumption of pulsatility. The desire to have a fully rewarmed patient for the post-operative period may be based on an improper risk management plan and perhaps a new lower target temperature should be adopted. Certainly, the treatment of fever in the post-operative period should be aggressively pursued. Methods should be designed to better measure the inter-cranial temperature and to control the amount of brain hyperthermia that is allowed. The employment of non-invasive cold air blowers for the cranium would seem to be a wise consideration. The elimination of unnecessary emboli from IV solutions and from the intra-cardiac suction devices will greatly aid the perfusion of the brain during and after extracorporeal circulation and reduce the degree of neurological change observed with these patients.

REFERENCES

1. Ehrenhaft JL, Claman MA, Layton JM, et al. Cerebral complications of open-heart surgery: further observations. J Thorac Surg 1961;42:514-26.

2. Helmsworth JA, Gall EA, Perrin EV, et al. Occurrence of emboli during perfusion with an oxygenator pump. Surg 1963;53:177-85.

3. Kornfeld DS, Zimberg S, and Malm JR. Psychiatric complications of open heart surgery. N Engl J Med 1965;273:287-92.

4. Gilman S. Cerebral disorders after open-heart operations. N Engl J Med 1965;272:489-98.

5. McKhann GM, Goldsborough MA, Borowicz LM, et al. Predictors of stroke risk in coronary artery patients. Ann Thorac Surg 1997;63:516-21.

6. Newman MF, Croughwell ND, Blumenthal JA, et al. Predictors of cognitive decline after cardiac operation. Ann Thorac Surg 1995;59:1326-30.

7. Tardiff BE, Newman MF, Saunders AM, et al. Preliminary report of a genetic basis for cognitive decline after cardiac operations. Ann Thorac Surg 1997;64:715-20.

8. Cook DJ, Oliver WC, Orszulak TA, et al. Cardiopulmonary bypass temperature, hematocrit, and cerebral oxygen delivery in humans. Ann Thorac Surg 1995;60:1671-7.

9. Mora CT, Henson MB, Weintraub WS, et al. The effect of temperature management during cardiopulmonary bypass on neurolgic and neuropsychologic outcomes in patients undergoing coronary revascularization. J Thorac Cardiovasc Surg 1996;112:514-22.

10. Martin TD, Craver JM, Gott JP, et al. Prospective, randomized trial of retrograde warm blood cardioplegia: Myocardial benefit and neurologic threat. Ann Thorac Surg 1994;57:298-304.

11. Reith J, Jorgensen HS, Pedersen PM, et al. Body temperature in acute stroke: relation to stroke severity, infarct size, mortality, and outcome. Lancet 1996;347(8999):422-5.

12. Azzimondi G, Bassein L, Nonino F, et al. Fever in acute stroke worsens prognosis. A prospective study. Stroke 1995;26(11):2040-3.

13. Castillo J, Davalos A, Marrugat J, and Noya M. Timing for fever-related brain damage in acute ischemic stroke. Stroke 1998;29:2455-60.

14. Schwab S, Schwartz S, Spranger M, et al. Moderate hypothermia in the treatment of patients with severe middle cerebral artery infarction. Stroke 1998;29:2641-6.

15. Cook DJ, Oliver WC, Orszulak TA, and Daly RC. A prospective, randomized comparison of cerebral venous oxygen saturation during normothermic and hypothermic cardiopulmonary bypass. J Thorac Cardiovasc Surg 1994;107:1020-8.

16. Cook DJ, Orszulak TA, Daly RC, and Buda DA. Brief Communications: Cerebral hyperthermia during cardiopulmonary bypass in adults. J Thorac Cardiovasc Surg 1996;111:268-9.

17. Croughwll ND, Frasco P, Blumenthal JA, et al. Warming during cardiopulmonary bypass is associated with jugular bulb desaturation. Ann Thorac Surg 1992;53:827- 32.

18. Wass CT, Lanier WL, Hofer RE, et al. Temperature changes of > or = 1 degree C alter functional neurologic outcome and histopathology in a canine model of complete cerebral ischemia. Anesthesiology 1995;83(2):325-35.

19. Wass CT and Lanier WL. Hypothermia-associated protection from ischemic brain injury: implications for proper patient management. Int Anesthesiol Clin 1996;34:95-111.

20. Wass CT, Waggoner JR, Cable DG, et al. Selective convective brain cooling during normothermic cardiopulmonary bypass in dogs. J Thorac Cardiovasc Surg 1998;115:1350-7.

21. Wass CT, Waggoner JR, Cable DG, et al. Selective convective brain cooling during normothermic cardiopulmonary bypass in dogs. Ann Thorac Surg 1998;66:2008-14.

22. Nichols RD. Filtration of IV fluids in the bypass circuit. Perf Quart 1985;1:2-5.

23. Nichols RD. Intracorporeal protection. Perf Quart 1990;6:1-3.

24. Brooker RF, Brown WR, Moody DM, et al. Cardiotomy suction: a major source of brain lipid emboli during cardiopulmonary bypass. Ann Thorac Surg 1998;65:1651- 5.110