|Year : 1976 | Volume
| Issue : 2 | Page : 5-8
Ketamine and Intraocular pressure
VB Dave, JM Chokshi, AK Bandopadhyaya
Grant Medical College and J.J. Group of Hospitals, Mumbai, India
V B Dave
Grant Medical College and J.J. Group of Hospitals, Mumbai
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Dave V B, Chokshi J M, Bandopadhyaya A K. Ketamine and Intraocular pressure. Indian J Ophthalmol 1976;24:5-8
|How to cite this URL:|
Dave V B, Chokshi J M, Bandopadhyaya A K. Ketamine and Intraocular pressure. Indian J Ophthalmol [serial online] 1976 [cited 2021 Apr 19];24:5-8. Available from: https://www.ijo.in/text.asp?1976/24/2/5/31509
Going through the vast literature on Ketamine, one comes across only a few studies and some conflicting reports of its actions on intraocular pressure and acceptability for intraocular surgery.
The present study was carried out to observe the effect of Ketamine anaesthesia on intraocular pressure in individuals with normal eyes, undergoing surgical procedures requiring short duration of anaesthesia.
| Material and Method|| |
A total of 60 patients of both sexes undergoing different surgical procedures were studied. Only those patients who were found normal on clinical and systemic examination were included. Before surgery, after a thorough pre-operative check up and record of body weight, the intraocular pressure was recorded under local surface anaesthesia.
All the patients were properly premedicated 1-I2 hours before the operation. Seven children received Trimeprazine (Vallergan) syrup orally and injection Atropine 0.3 mg. intramuscularly. Remaining patients were given injection Atropine 0.6 mg. and injection Calmpose (Diazepam) 7.5 to 10 mg. separately intramuscularly.
Ketamine was administered in doses of 2 mg./ kg. body weight intravenously to those 10 years of age and above and in doses of 8 mg./kg. body weight intramuscularly to those below the age of 10 years.
During the procedure the effects of Ketamine on pulse rate, respiration and blood pressure were also recorded. Intraocular pressure was meticulously recorded by the same person and with the same Schiotz tonometer before Ketamine and after 5, 10 and 15 minutes after anaesthetic effect of Ketamine.
| Results|| |
In the present series the cases selected were those who required a short duration of anaesthesia [Table - 1]. In the 60 patients, there were 27 males and 33 females [Table - 2] and the age ranged from 7 days to 49 years [Table - 3].
The effects of Ketamine on pulse rate, [Table - 4], respiration [Table - 5] and blood pressure [Table - 6] were found to be stimulatory. In no case bradycardia, respiratory depression or fall in blood pressure was noticed.
Out of the 60 patients 36 patients (60%) have shown a rise in intraocular pressure [Table - 7]. There was no change in the remaining patients. No fall of pressure was noticed in any patient. This rise was noticed more at 5 and 10 minutes of Ketamine anaesthesia and generally remained sustained at 15 minutes [Table - 8]. It is worth noting that all the 9 patients over the age of 40 years have shown a rise of intraocular pressure.
The average rise noticed was moderate [Table - 9] and in no case did the intraocular pressure rise above the acceptable limits. There was a rise of 2 m.m. Hg. in 11 (30.55%), 2 to 4 m.m. Hg. in 16 (44.44%) and 4 to 6 m.m. Hg. in 9 (25%) patients. Further the rise of intraocular pressure could not be distinctly correlated with the rise in the pulse rate, respiration and blood pressure.
| Discussion|| |
The studies on intraocular pressure changes after Ketamine in general show a moderate and transient rise. Among the early workers Falls et a1 were the first to raise some doubt regarding its use in intraocular procedures. Corssen and Hoy in a series of 46 patients within the age of 6 months and 77 years found that unlike the conventional anaesthetic agents, Ketamine caused a slight rise of intraocular pressure. Further there was no co-relation between this change, the patient's age or changes in systemic blood pressure.
They have advocated its use in ophthalmic diagnostic and minor surgical procedures. Lengrehr et al in their first report on 500 cases found that the intraocular pressure elevation remained within the limits of 2 to 8 cm. of water and was not of special significance. They did not observe any initiation of critical condition in their two patients of glaucoma.
In our series we have found a rise of intraocular pressure ranging from 2 m.m. to 6 m.m. Hg. in 36 (60%) out of the 60 patients. No fall of intraocular pressure was noticed in any patient. This compares with the findings of Corssen and Hoy and Lengrehr et al. The rise was maximum at 5 and 10 minutes and was generally sustained at 15 minutes after Ketamine anaesthesia. It is worth noting that in the patients above the age of 40 years, a very small number (9), statistically, have shown a rise of pressure but in all the cases the rise of pressure was within the acceptable limits. Corssen and Hoy found no correlation between the patient's age and the rise of intraocular pressure. But like the other findings of the same authors, this rise cannot be correlated by us also with the rise in pulse rate, respiration and blood pressure.
Dillon also reported slight rise in intraocular pressure with rise of pulse rate and blood pressure and that this rise was transient and probably of no significance. He does not recommend Ketamine to a patient with an open globe but sees no contra-indication for extraction of cataract if this agent is indicated.
Yoshikowa and Murai found in 15 patients a rise of intraocular pressure 5 minutes after Ketamine anaesthesia and the highest value recorded at 15 minutes. We found the highest rise at 5 and 10 minutes. While the pressure was generally sustained at 15 minutes, the patients in the age-group of 20-30 years showed highest rise at 15 minutes. The above authors proposed that the rise of pressure was due to change in the balance of tones of extraocular muscles.
We have used Diazepam in small doses for the premedication in most of our patients. Diazepam produces relaxation of muscles. If the rise of pressure is due to the change in the balance of tones of extraocular muscles, larger dose of Diazepam may possibly reduce the incidence and extent of rise of intraocular pressure. The same effect may probably be seen after retro-bulbar block along with Ketamine.
Adams found in 15 children that the rise of intraocular pressure was more with Ketamine than with nitrous oxide, oxygen and halothane anaesthesia and that the pressure did not rise beyond acceptable limits. Gudi et al in 16 patients for ophthalmic surgery reported no significant change in intraocular pressure.
Chandorkar et al, who in their preliminary study found a significant rise in intraocular pressure, now in their experiments on rabbits have found a rapid and consistent fall in intraocular pressure from 2 to 8 m.m. Hg. on varying doses of 2, 4 and 8 mg./kg. of Ketamine. They presume that Ketamine induced catecholamine release might be causing vaso constriction of ocular vessels, thus reducing the formation of aqueous humour. This is surprising whether such a reduction in formation of aqueous humour does occur and whether in an UN interfered anterior chamber such a rapid fall can occur in one minute and so. Takeshita et al have shown that with 3 mg./kg. Ketamine given intravenously cerebral blood flow increased and cerebral vascular resistance decreased. The cerebral perfusion pressure and PaCO 2 increased after Ketamine and was mainly due to cerebral vasodilatation. Even if there is vaso constriction of the ocular vessels, liberated catecholamines also produce and increase in the blood pressure and cardiac output, thus increasing the overall blood flow.
They further propose that an increased dose of Ketamine might have a depressant action on corticothalamic pathways influencing the postulated diencephalic regulatory centres of intraocular pressure, producing greater decrease in intraocular pressure by absolute absence of myocontractile stimuli on extrinsic muscles of the eyes. It is extremely difficult to state regarding the sites of central actions of Ketamine but it is well known that Ketamine is an excellent analgesic but a poor relaxant of the muscles.
| Summary|| |
Intraocular pressure was recorded preoperatively and at the intervals of 5, 10 and 15 minutes after Ketamine anaesthesia in 60 patients with normal eyes. 36 patients (60%) showed a rise of pressure ranging between 2-6 m.m. Hg. No fall in intraocular pressure was noticed in any patient
The rise was found at 5 and 10 minutes after onset of Ketamine anaesthesia and was generally sustained at 15 minutes. The rise could not be correlated with rise in pulse rate, respiration or blood pressure. In the normal eyes the extent of rise was without acceptable limits and not dangerous enough to jeopardise the intraocular procedures.
| References|| |
Adams, A. K. 1973, Anaesthesia, 28,
Bovill, J. G., Dundee, J. W., Coppel D. H. and Moore, J., 1971, Lancet, 1,
Chandorkar, A. G., Jain, P. K. and Albal M. V., 1975, Ind. J. Ophth. 23,
Corssen, G. and Domino, E. F., 1966, Anaesth. Analg., 45, 2.
Corssen, G. and Hoy, J. E., 1967, J. Paed. Ophth.
Dillon, J. B., 1971, Proc. Roy, Soc. Med., 64,
Duke-Elder, 1968, System of Ophthalmology,
4,299, Henry Kimpton, London.
Falls, H. F., Hoy, J. E. and Corssen, G., 1966, Amer. J. Ophth., 61,
Gibbs J. M., 1972, Brit. J. Anaesth., 44,
Gudi, A. R., Jagavkar, S. Y. and Sathe. S. M., 1974, Ind, J. Anaesth., 22,
Hunter, A. R., 1972, Recent Adv. Anaesth. and Analg.,
11th Edn., 5, Churchill Livingstone, Edinburgh and Lond.
Lengrehr, D., Alai, P., Andjelkovic, J., and Kluge L., 1967, Der Anaesthesist, 16,
Takeshita, H., Okuda, Y., and Sari, A., 1972, Anaesthesiology, 36,
Takki, S., Nikki, P., Jaattela, A. and Tamisto, T., 1972, Brit. J. Anaesth., 44,
Yoshikawa, K., and Murai, Y., 1971, Anaesth. Analgesia, 50,199.
[Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5], [Table - 6], [Table - 7], [Table - 8], [Table - 9]