|Year : 1967 | Volume
| Issue : 6 | Page : 203-212
Physiological considerations from ocular changes in hypothermia during cardiac surgery
IS Jain, DC Agarwal, Kapalmit Singh, IA Chitambar
Postgraduate Institute of Medical Education and Research Chandigarh, India
|Date of Web Publication||22-Jan-2008|
I S Jain
Postgraduate Institute of Medical Education and Research Chandigarh
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Jain I S, Agarwal D C, Singh K, Chitambar I A. Physiological considerations from ocular changes in hypothermia during cardiac surgery. Indian J Ophthalmol 1967;15:203-12
It is because of hypothermia that open heart surgery has been made possible. With hypothermia one is able to occlude circulation for a good length of time without causing any permanent damage to the central nervous system. The main methods to achieve this end are:
1. Surface cooling, and
2. Extra corporeal circulation.
In the first method the body temperature is lowered from 37° C to 30°C or a bit lower. At this temperature because oxygen requirements are reduced, it is possible to occlude the circulation for 6 to 7 minutes.
In the extra corporeal technique, the heart and lungs are by-passed completely by a pump oxygenator. The additional advantage of cooling the blood directly is also achieved. Whereas in the former method a long time is required to cool the body and also to warm it subsequently, in the latter method both these can be quickly achieved. DREW and ANDERSON (1959) used deep hypothermia, where temperature of body fell to 15°C. The method was modified by SIMPSON, GIBSON and BLOOMFIED (1960) who achieved a profound hypothermia for open heart surgery. LAMB (1961) was the first to study the ocular responses to such low temperature of the body achieved by this method of SIMPSON et al. At different places, the methods employed for cardiac surgery are likely to vary because of the limitation of availability of a particular type of appliance. Because of these differences, the observations are likely to vary accordingly. It was with this view in mind that we have tried to make our own observations and compare them with those of Lamb.
| Material and Methods|| |
The study was conducted on 12 cases operated for various cardiac defects in the Institute of Postgraduate Medical Education and Research, Chandigarh. Three cases were operated under surface hypothermia only, while 9 were operated under extra-corporeal circulation with cooling. In the latter technique following steps were followed:
i) Premedication with Pethidine and Phenergan
ii) Induction of anxsthesia with Pentothal sodium and relaxant.
iii) Anaesthesia with ether, nitrous oxide and oxygen.
During anaesthesia, the cannulations were done in the external jugular vein and radial and femoral arteries. The chest was opened, venous and arterial cannulae were placed and the patient was made ready for circulatory bypass.
iv) By-pass-cooling: When the circuit was complete, the mechanical pump was turned on which circulated the blood through oxygenator and cooling device.
In LAMB's series, following cooling, the circulation was occluded for some time, but in our study this occlusion was not resorted to.
v) By-pass rewarming: When surgery was complete, rewarming of the blood was started.
During both these procedures when cooling was started intraocular tension, pupil size and fundus changes were noted down at regular intervals.
| Observations|| |
In surface cooling there were 3 cases as shown in [Table - 1].
The table clearly indicates that by lowering of temperature on surface cooling, the intraocular tension remains almost unchanged; if at all there is a small fall.
As can be seen from graphs I and II, the pupil shows a definite dilatation on cooling the body. In graph I of the first case, the pupil began to dilate as the temperature dropped to 35.5° C and the change became more abrupt when the temperature fell from 33.8° to 33.0°C. After this maximum dilatation, the pupil began to lose its dilatation on further lowering of the temperature, the drop being more abrupt at first. On removing the hypothermia the pupil continued to contract and not go through a reverse phase, as the previous levels began to be reached from 30° back to 34°C.
In graph II of the second case a similar change was observed in pupil size, the dilatation curve first gradual, then abrupt began to flatten out to 32.5°C to reach the maximum dilatation (7mm) between 31° and 30.6°C. With further cooling the pupil began to contract (or lose dilatation). At 30°C when the aortic clamp was applied the pupil became further dilated to 8mm after which the pattern of the drop followed that in graph I.
It may thus be noted that dilatation of the pupil which accompanied hypothermia was not achieved proportionately with it. There was a maximum which was achieved between 32.4°C and 32.0°C in one case and at 30.6°C in the other two cases, after which the pupil began to contract, or lose dilatation. Aorticclamping caused a reflex dilatation of the pupil which was independent of hypothermia.
In all the cases there was no change in the fundus. In one case where aortic clamp was applied, there was immediate pallor of the disc and the colour returned to normal, as soon as the clamp was relieved.
In this group there were 9 cases, as analysed in [Table - 2] and in these cases, by-pass cooling technique was employed.
There were five males and four females with ages ranging from 3 to 35 years. The changes in pupil size and intraocular tension are shown in four illustrative cases in graphs III, IV, V and VI.
i) It is observed from these that pupillary dilatation set in 5-10 minutes after the cooling started.
ii) The maximum pupillary dilatation observed was 7 mm.
iii) As is seen in graphs V and VI, when aortic clamping was needed and applied then pupil dilated to 8.0 mm, while in graph IV, it can be seen that when cardiac arrest occurred, the pupil dilatated to 8.0 mm.
iv) On rewarming after 10-15 minutes the pupil size got smaller and then remained constant.
Intraocular tension showed a fall during anaesthesia in all cases but no further drop occurred during cooling. In one case there was a fall by 1.5 mm. whereas in another there was a rise by 1.5 after the initial fall. [Table - 2]. However during cardiac arrest as seen in graphs IV and VI it became unrecorded.
There were no changes in the fundus picture in any of these cases. However, in the cases where cardiac arrest occurred, there was generalised fungus pallor, with absence of pulsation and fullness of veins. The picture returned to normal on restoration of circulation.
| Dicussion|| |
Intraocular tension in surface cooling as well as in by-pass cooling showed a fall. In the first group there was a negligible fall of 0.5 to 1.0 mm in two cases, while in one case it remained unchanged. In group II of bypass cooling there was an average fall of 2.5 mm Hg. during anaesthesia and later during cooling it remained at the same level, except in one case where during the cooling procedure tension fell by 1.5 mm Hg. and in one it rose by 1.5 mm. LAMB also noted a fall of about 2 mm Hg. during anesthesia, and also noticed a fall during occlusion. In our series because no circulatory arrest was attained, no fall was observed. However, in two cases where aortic clamp was applied, and in the other two cases where cardiac arrest occurred, it became unrecordable but soon returned to the original level. In one case only, we observed a slight fall in tension during cooling and in one a rise, while in LAMB'S series the tension during cooling was fairly constant showing only a slight fall.
On rewarming no change was noticed in the tension, however in one case where it had fallen from 16 to 14.5 mm. Hg. it returned to 16 mm. when rewarming started in 15 minutes time. By and large it indicates that cooling has no effect on the intraocular aqueous circulation and cilliary body function remains normal as long as circulation is maintained.
Generalising from these studies, it can be stated that on surface cooling the pupil becomes dilated, but the dilation does not keep pace with the progressive body cooling. It is gradual at first, becoming abrupt as cooling progresses till a maximum dilatation of 7 mm is reached at an average temperature of about 31°C. With further cooling the pupil ceases to dilate and begins to contract. In extra-corporeal cooling, because of the very rapid cooling and rewarming the pupils show more precise correlation with the temperatures. If during this contraction stage any vascular catastrophe is introduced, like clamping of the aorta or cardiac arrest, a reflex dilatation of the pupil occurs which is greater (8 mm) than the maximum obtained during cooling. It is interesting to observe that in case 9 where there was cardiac arrest before cooling started the pupil became abruptly dilated from 5 to 8 mm and then a fall to 5 mm on recovery. Then cooling was started on recovery and the pupil dilatation continued.
Comparing Graphs I and III of the two different forms of cooling which are not vitiated by any vascular catastrophe we find that although there is a basic resemblance in the patterns, there appears to be a slight difference.
Whereas in Graph III the rise and fall are abrupt and uniform because of rapid cooling and rewarming, the curve in Graph I, because of its slow rise and fall becomes available for more effective study. In Graph I there is first a slow rise then an abrupt one reaching a maximum of 7 mm between 33° and 32°C, then it drops to 6 mm at 31°C and remains steady till 29° C, after which it tends to fall. Just after 28°C is reached, rewarming begins and there follows a continuous drop, slow at the beginning, gaining in speed as normalcy is reached.
In the hypothalamus there are thermo-regulators which control body temperatures and which operate through the sympathetic and parasympathetic tones. In the neighbouring thalamus (mid-brain) there are pupil regulating centres which operate similarly through the two autonomic nervous systems. Impulses directed to the thermo-regulators may therefore easily affect the pupillary centres or overflow into them.
As would be natural the sympathetic, being the alarm system resists the unnatural and sudden chilling and the resistance increases progressively as the chilling progresses. The resistance becomes more pronounced as a temperature of about 35°C is reached. The limit of resistance is reached at about 31°C after which the sympathetic tone is overcome by the slower para-sympathetic. The pupil ceases to dilate, the para-sympathetic counter resistance asserts itself and after a slight drop a balance is reached. The pupil dilatation is maintained at about 7 mm till rewarming begins.
On rewarming, since the process is towards normalization there is no attempt on the part of the sympathetic to offer resistance. On the contrary it gives up its resistance which is again reflected in the pupil which continues to contract or lose dilatation. In Graph IV, however, a momentary reflex dilatation on commencing rewarming can be observed.
That the sympathetic is not knocked out of action but only offers resistance can be gathered from the fact, that another kind of reflex, a vascular catastrophe like shock is still capable of producing a pupil dilatation. We have two instances of those in our series of observations. One was when an aortic clamp was applied during the phase when the pupil was contracting, when the pupil showed a brisk dilatation even greater than the maximum obtained at 31°C and another when there was cardiac arrest during the same phase, when again the pupil dilated similarly. Case 9 was an instance of pupil dilatation due to cardiac arrest before cooling was started where again the pupil dilatation was upto 8 mm.
One can conclude therefore that surface hypothermia first stimulates and later inhibits the sympathetic control of the thermo-regulators in the hypothalamus but the sympathetic is still ready to go into action to face a catastrophe of another kind. In vascular shock when the blood-pressure drops, the sympathetic reacts by trying to compensate the drop in pressure. However, the demands on the body structure being minimum in a hypothermia state, the vascular balance is soon achieved as can be seen reflected in return of the pupil size to that present on preapplication of clamp or after cardiac arrest.
The negligible effect on the intraocular pressure in hypothermia suggests an absence of any sympathetic control mechanism to the secretory part of the ciliary body and the ciliary vessels just as the cerebral and coronary vessels are supposed to have no sympathetic control mechanism in order to keep all vital circulation moving at an even pace under all conditions of stress. This may appear strange because the ciliary vessels are known to become congested under emotional stress and cause increased I.O.P. However in hypothermia there is no stimulation of an emotional nature, but the capillaries all over the body must contract in order to resist reduction in body temperature. The cilliary capillaries must contract along with the other capillaries and consequently the effect on the I.O.P. will be its reduction if at all. Our observations show that on an average there was no drop in IOP further than that obtained during general anesthesia preceding the hypothermia although the pupil dilated with hypothermia, thus maintaining the IOP at a vital level.
However when circulation through the ciliary body is excluded by aortic clamping or by cardiac arrest, the tension drops to zero although the pupil dilates maximally indicating a high degree of sympathetic alarm reaction. Arguing on these lines it seems very probable that there is very little or no sympthetic control for the ciliary vessels bringing them under the same category of vital vessels as the cerebral and the coronary.
The same applies for retinal vessels for no changes in the retinal vessels were noticed during hypothermia but during cardiac arrest there was blanching of the fundus vessels.
Some retinal damage has been encountered by LAMB (1961) during total occlusion and as a result this technique has been changed to low flow by-pass system. We have not encountered any change in fundus produced by cooling per se, however in some cases where cardiac arrest occurred, the immediate fundus changes were the same as reported by LAMB (1961).
| Summary|| |
Observations on pupil size, intraocular pressure and fundus of the eyes of 12 cases in which hypothermia was produced are recorded. Pupils became dilatated to a maximum of 7 mm at which level or at a little lower the dilatation was maintained. Further dilatation to 8 mm was reached during vascular catastrophies like aortic clamping or cardiac arrest. The intraocular tension remained constant during hypothermia after the usual drop during induction of anesthesia. Retinal circulation also showed no change during hypothermia.
These observations are used to argue that although there is a sympathetic alarm mechanism in the case of the pupils, this mechanism is not present in the case of ciliary and retinal circulations which latter have to be maintained under all conditions of stress.
| References|| |
DREW C. E. and ANDERSON I. M (1959) Lancet 1, 748.
LAMB, A., Ocular changes occurring during cardiac survey under profound hypothermia and occlusion: Brit. Jour. Ophthal. (11)61) 45. 490.
SIMPSON. .J. A.. GIBSON, P. and BLOOMFIFLD, D. A. (1960), Med. J. Australia 1. 647.
[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6]
[Table - 1], [Table - 2]