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Clinical Evaluation of Haloperidol as an Adjuvant to Thiopentone and Ketamine Anesthesia in Dogs

Busakala Prakash Kumar R V Suresh Kumar Ch. Srilatha
Vol 7(9), 245-249
DOI- http://dx.doi.org/10.5455/ijlr.20170710032641

The clinical assessment of haloperidol as an adjuvant to thiopentone and ketamine anesthesia in dogs was studied. Induction of anesthesia with thiopentone was rapid (1.50±0.07 minutes) smooth and without any complications whereas induction with ketamine was a little slower (1.94±0.04 minutes).The mean duration of surgical anesthesia in thiopentone group (I) and ketamine group (II) were 41.0±0.94 and 28.0±4.09 minutes respectively. Complete recovery took place within 120.0 ±3.9 minutes in group I and at 46.0±0.24 minutes after the last incremental dose in group II. The mean rectal temperature were 101.66±0.53OF and 101.96±0.38OF in group I and II respectively and the values remained within the normal range Haloperidol was not only potentiated the anesthetic effects of thiopentone but helped to prolong the duration of anesthesia.


Keywords : Dogs Ketamine Haloperidol Thiopentone

Introduction

The use of combination of anesthetic drugs provides safe, comfortable and adequate surgical anesthesia with quick induction and smooth recovery. Hofmyer (1981) stated that haloperidol could be used successfully to sedate wild herbivores and it also suppresses cortically evoked tongue contractions as well as ketamine induced contractions (Marco, 1989). The present work was undertaken to study the clinical assessment of haloperidol as an adjuvant to thiopentone and ketamine anesthesia in dogs.

Materials and Methods

The present study was carried out on twelve clinically healthy dogs aged between 2-5 years presented for animal birth control operations. All the dogs were uniformly medicated with haloperidol @ of 0.87mg/kg body weight and divided equally in to two groups. In group I, 2.5 % solution of thiopentol sodium was used as an intravenous anesthetic induction agent while in group II, anaesthesia was induced by intravenous administration of ketamine hydrochloride @ 10mg/kg body weight. The anesthetic effects like induction, the surgical anesthesia and recovery were assessed. The rectal temperature, heat rate and respiratory rates were recorded at 0, 5, 15, 30, 45 and 90 minutes interval. The clinical signs and reflex activity at 0 and 5 minutes after haloperidol administration and 15, 30 and 45 minutes interval following general anesthetic administration were recorded. Ovariohysterectomy was performed in conventional manner to assess the surgical tolerance in all the animals. The data was subjected to student’s t test for two samples as described by Snedecor and Cochran (1980).

Results and Discussion

All the animals in both the groups attained sternal recumbency following haloperidol administration has also been observed by Sobti et al. (1990). Induction of anesthesia with thiopentone was rapid (1.50±0.07 minutes) smooth and without any complications whereas induction with ketamine was a little slower (1.94±0.04 minutes). In the present study haloperidol was administered @ 0.87mg/kg body weight intravenously in all dogs as recommended by Sobi et al. (1990). The mean duration of surgical anesthesia in group I and II were 41.0±0.94 and 28.0±4.09 minutes respectively (Table 1). In group I there was good abdominal muscle and jaw relaxation with flaccidity of limbs and tail. Induction with thiopentone sodium after 5 minutes of haloperidol administration was effectively abolished all the painful reflexes efficiently which was clearly evident by easy end tracheal intubation. Excellent muscle relaxation indicated that haloperidol could accentuate the anesthetic qualities of thiopentone further more. In group II the dogs remained with eyes open, responded to painful stimuli with poor muscle relaxation and urination. All the dogs required incremental doses of ketamine at 30 and 45 minutes of observation period. Muscle rigidity and stiffness was observed in 2 out of 6 animals. Lumb and Jones (1997) reported that usage of ketamine alone @ 10mg/kg body weight would give short duration and inadequate analgesia for surgery. Complete recovery took place within 120.0 ±3.9 minutes in group I and at 46.0±0.24 minutes after the last incremental dose in group II. In group I, the recovery was smooth without any excitement while in group II, recovery was accompanied by muscle rigidity and vocalization. Disappearance of reflexes 15 minutes after administration of haloperidol ketamine combination indicated delayed response of the animal to the anesthetic combination. This was probably due to haloperidol’s poor synergistic action with dissociative anesthetics (Hofmyer, 1981).

Table 1: Variation in Mean + SE values of induction time, duration of anaesthesia and recovery time following intravenous administration of haloperidol – thiopentone (Group I) and haloperidol – ketamine (Group II)

Group Induction time (in minutes) Duration of anaesthesia (in minutes) Recovery time (in minutes)
Group I 1.50 ± 0.07 41.0 ± 0.94 120.0 ± 3.0
Group II 1.94 ± 0.04 28.0 ± 4.09 46.0 ± 0.24

The mean rectal temperature was 101.66±0.53OF and 101.96±0.38OF in group I and II respectively and the values remained within the normal range during anesthesia. The mean preanesthetic heart rate values were 112.6±8.31 and 125.0±3.68 betas/minute in group I and II respectively. Following anesthetic injections the values decreased to 91.16±4.49 and 116±8.69 beats/minute in group I and II respectively. Later the values tended to rise upto 60 minutes and the changes were within normal range. The decrease in heart rate was significant (P≤0.05) at 10 minutes interval in group I and at 30 minutes in group II. The heart rate values showed significant decrease upto 15 minutes in haloperidol-thiopentone combination and upto 30 minutes in haloperidol-ketamine combination. The initial decrease in heart rate was more in haloperidol-thiopentone group, propably because of depressant effects of both haloperidol and thiopentone sodium. Kumar et al. (2001) opined that haloperidol could moderate cardio stimulatory effects of ketamine in dogs. In the present study the cardio stimulatory effects of ketamine could be minimized by haloperidol but not as effectively as it was with thiopentone. Singh and Dhablania (2000) reported an increase in heart rate during haloperidol – ketamine anesthesia, which was attributed due to the surgical stress. The pre administration mean respiratory rate/minute were 32.6±3.60 and 37.66±1.41 in group I and II respectively, which was dropped to 14.5±1.26 in group I and 14.68±1.84 in group II at 30 minutes. Though there was mild rise in the respiratory rate but the remained decrease was significant (P≤0.05) in both the groups. Haloperidol could influence both thiopentone sodium and ketamine hydrochloride to cause significant decrease in respiratory rate. This was due to reduction on the sensitivity of the respiratory center to carbon dioxide and reduced tissue oxygen uptake during anesthesia. These findings were in accordance with the observations of Singh and Dhablania (2000), Kumar et al. (2001). Ketamine hydrochloride produced apnuestic pattern of respiration in man, dogs and cats (Domino, 1965) and was directly related to total dose and rate of intravenous administration (Thurmon and Benson, 1987). Haloperidol could influence the apnuestic pattern of respiration induced by ketamine hydrochloride and hence there was significant decrease in respiratory rate (Table 2).

Table 2: Variation in Mean + SE values of different physiological parameters before during and after administration of haloperidol – thiopentone and haloperidol – ketamine combinations in dogs

Parameters Groups Minutes
0 5 15 30 45 60
Temperature (0F) Group I 101.66 + 0.53 100.66 + 0.55 98.86 + 0.31* 99.6 + 9.44* 99.53 + 0.24 99.9 + 0.39*
Group II 101.96 + 0.38 101.63 + 0.32 101.03 + 0.36 100.56 + 0.59 100.6 + 0.42* 100.6 + 0.34*
Respiratory rate (breathes / minute) Group I 32.6 + 3.60 21.3 + 4.44 15.6 + 0.84* 14.5 + 1.26* 17.6 + 1.59 18.8 + 1.17
Group II 37.66 + 1.41 16.16 + 0.47 15.58 + 1.12 14.68 + 1.84* 15.16 + 1.50 15.15 + 1.83*
Heart rate (beats / minute) Group I 112.6 + 8.31 91.6 + 4.49 96.33 + 9.94 104.5 + 9.94 112.16 + 5.52 112.33 + 8.75
Group II 125.5 + 3.68 116 + 8.69 124.5 + 3.98 112.16 + 4.61 114.66 + 7.63 117.00 + 4.44
SPO2 (Percentage) Group I 94.16 + 2.06 97.16 + 2.64 92.3 + 4.19 95.5 + 2.05 94.8 + 1.89 95.6 + 1.73
Group II 90.66 + 1.54 90.83 + 1.45 94.5 + 4.85 102.1 + 4.10 101 + 5.03 103.8 + 2.72

* values differ significantly (P<0.05), Group I : Haloperidol – Thiopentone, Group II : Haloperidol – ketamine

All the reflexes were lost in both the groups at 15 minutes, but reappearance of reflexes was very quick in group II. At 60 minutes post injection all the animals showed jaw, pedal and corneal reflexes. Surgical tolerance revealed that Haloperidol-thiopentone combination produced excellent muscle relaxation and it did not require any incremental dose. The recovery was smooth without any complications. Haloperidol-ketamine combination produced satisfactory muscle relaxation and required incremental doses of ketamine. Recovery was associated with muscle rigidity and moderate vocalization in haloperidol –ketamine anesthesia. Haloperidol not only potentiated the anesthetic effects of thiopentone but helped to prolong the duration of anesthesia. Since haloperidol’s influence on ketamine in terms of muscle relaxation and abolition of reflexes was less satisfactory from induction itself, the reappearance of reflexes was also quick. Similar results were also observed by Kumar et al. (2001). Hence the procedure necessitated incremental dose of ketamine at 30 and 45 minutes to continue the anesthetic effects. This indicates that haloperidol has lesser influence on ketamine when compared to barbiturates. Neuroleptic tranquilizers potentiate the anesthetic effects of barbiturates and produce smooth recovery. Similar results were experienced in the present study. But Neuroleptics has lesser influence on cateleptics which was evident by presence of muscle rigidity, vocalization and shivering at the time of recovery. This was probably due to dissociative anesthetic effects of ketamine could not overcome the extrapyramidal action produced muscle rigidity and vocalization (Ebedis and Rath, 1999).

References

  1. Domino EF. 1965. Pharmacologic effects of CJ-581, A new dissociative anaesthetic in man. Clinical pharmacology and therapeutics6: 277-91.
  2. Ebedis HYM and Rath JP. 1999. Chapter 85 Artiodactyles, Use of tranquilizer in wild herbivores, Zoo and wild animal medicine. Ed 4 Lea and Febriger, Philadelphia. pp. 578-583.
  3. Hofmyer JM. 1981. The use of haloperidol as a long acting neuroleptic in game capture operations. Journal of the South American Veterinarian Association. 52(4): 273-282.
  4. Kumar A, Sobti VK and Singh KI. 2001. Studies on haloperidol followed by ketamine anaesthesia in dogs. Indian Journal of Veterinary surgery22(1): 46-48.
  5. Lumb WV and Jones EW. 1997. Veterinary Anaesthesia 3rd edition. Lea and Febiger, Philadelphia. pp. 92-400.
  6. Marco LA. 1989. Clinical experimental pharmacology physiology 16(5):395-401. Cited in Goodman and gillman’s. The pharmacological basis of therapeutics, 9th edn (1988). pp. 399-402.
  7. Singh PJ and Dhablania DC. 2000. A Study on haloperidol thiopentone sodium combination for femoral grafting in dogs. Indian Veterinary Journal77: 870-871.
  8. Snedecor AW and Cochron WC. 1980. Statistical Methods . 7th edn, Iowa State University Press, Ames,Iowa, USA.
  9. Sobti VK, Singh KI, Bansal PS, Singh N and Rathor SS. 1990. Haloperidol as a premedicant for thiopental anaesthesia in dog. Journal of Veterinary Medicine, series-A37(3): 170-173.
  10. Thurmon JC and Benson GJ. 1987. Pharmacologic consideration in selection of anaesthetics for animals. Journal of American Veterinary Medical Association191: 245-51.
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