Effect of pre-operative starvation on intra-operative arterial oxygen tension in horses

Effect of pre-operative starvation on intra-operative arterial oxygen tension in horses

J. vet. Atiaesth. Vol. 23(2) (1996) Effect of pre-operative starvation on intra-operative arterial oxygen tension in horses P. DobromylskyJ*, P. M. T...

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J. vet. Atiaesth. Vol. 23(2) (1996)

Effect of pre-operative starvation on intra-operative arterial oxygen tension in horses P. DobromylskyJ*, P. M. Taylor?, J. C. Brearley, C. B. Johnson? and S . P. L. Luna** Aiiirnrrl Henlth Ti-ust, PO 80%5, Neic riitrrhc~t.Siiffolk, CB8 8JH, UK

SUMMARY

TABLE 1: Patient details, median (25-75 percentiles)

This study assessed the effect of pre-operative starvation on i n t ram pera t i ve art e r i a I oxygen ten s i o n ( Pa02 ) by examination of anaesthetic records from starved and nonstarved horses undergoing general :tnaesthesia. Pa02 data from 69 horses were included, 33 of which were starved preoperatively and 36 were not. Thirty minutes after induction of anaesthesia the mean Pa02 i n the non-starved group was higher than in the starved group (non-starved 40 [ 2 6 4 9 l kPa vs starved 30 [ 15-46! kPa. median and 25-75 percentile) but at 60 and 90 min the values for P a 0 2 for the non-starvcd group were lower than those for the starved group (60 min: starved 31 [ 15-49] kPa vs non-starved 27 [ 1 1-38] kPa; 90 min: starved 31 [ 12441 kPa vs non-starved 22 112-381 kPa) None of the differences between these values was statistically significant. Pre-operative starvation did not significantly increase intra-operativc PaO, under the conditions of this study.

Age (years) Weight (kg) M:F D:L Concentrate to anaesthesia (h) Hay to anaesthesia (h)

Starved

Non-starved

3 (2-8) 494 (406-540) 21:12 253 16.6 (16.3-19.8) 10.6 (10.3-13.8)

5 (1-6) 506 (443-571) 31:5 29:7 3.8 (3.1-6.5) 0.8

M:F, numbers of males and females within group D:L, numbers in dorsal or lateral recumbency within group

the patient (Moens c ~ trrl. 1995). inspired oxygen fraction (Young r t (11. 1992) and the anaesthetic technique used (Taylor ef trl. 1992). The cause appears to be related to a mismatch of pulmonary perfusion to ventilation (Hornof PI trl. 1986) due to airway closure and atclectasis (Nyman P / ( I / . 1990) and may be related to the fall in functional residual capacity (FRC) which has been shown to occur at induction of anaesthesia (McDonnell and Hall 1974). As starvation is known to increase FRC in horses (McDonnell and Hall 1974), the present study examined whether the clinical practice of pre-operative starvation had a detectable influence on P a 0 2 during subsequent anaesthesia.

INTRODUCTION Severe hypoxaemiii is a well recognised finding during general anaesthesia i n horses (Hall e / trl 1968; Trim and Wan 1990) which cannot always be corrected by provision o f an inspired oxygen fraction (FIO,) in excess of9S% (Hall e t rrl. 1968), intermittent positive pressure ventilation (IPPV) (Hall et crl. 1968; Beadle et rrl. 1975) or positive and expiratory pressure (PEEP: Hall and Trim 1975). Treatment using IPPV combined with PEEP is effective but at the cost of a marked reduction in cardiac output (Wilson and Sonia 1990). Selective ventilation of depcndent lung tissue is also effective (Nynian r t NI. 1987) but this has yet to be developed into a clinically useful form. Intravenous infusion of the p2 ag on i st c I e n bu t e ro I, w h i I e effect i ve , produces marked generalised sympathetic nervous system stimulation (Gleed and Dobson 1990). Factors which influence the severity of the hypoxaeinia are considered to include position during anaesthesia (Gleed and Dobson I988), anatomical shape of

M A T E R I A LASN D

METHODS

Data were collected from horses undergoing elective surgery that were the subjects of an investigation into the effect of pre-operative starvation on the development of post operative colic. Patient details, position during surgery and duration of pie-operative starvation are summarked i n Table I . Blood gas data were available for 69 individuals which form the basis of this investigation. All horses involved were free of clinically detectable cardiorespiratory abnormalities and were scheduled for elective body surface or orthopaedic surgery. They were allocated to be starved or not starved alternately according to case order. Starved horses were fed no concentrates after 17.00 h and no hay after 23.00 h on the day before anaesthesia. Nonstarved horses were fed concentrates at 08.00 h on the morning of anaesthesia and had free access to hay until 40 inin before induction of anaesthesia. Normal concentrate ration for each individual horse was calculated by the yard 7.5

J. vet. Anaesth. Vol. 23(2) (1996)

TABLE 2: Number of horses in each group and median (25-75 percentile) PaO, values

Time (min)

Group

Number of horses

PaO, (kPa)

15-45

NS S

24 23

40 (26-49) 30 (15-46)

45-75

NS S

28 25

27 (11-38) 31 (15-49)

75-1 05

NS S

15 13

22 (12-38) 31 (12-44)

Anaesthesia was divided into 30 rnin epochs (15-45 min, 45-75 min and 75-105 min). The PaO, data from all horses within each group during these epochs were pooled to give an average value. Arterial oxygen tensions in the 2 groups during each epoch were compared using Mann-Whitney U test. Results are expressed as median (25-75 percentile). P<0.05 was considered significant.

RESULTS The number of samples from starved and non-starved horses and the mean PaO2 during each epoch are shown in Table 2. The PaO, values of the starved horses were not significantly different from those of the non-starved horses during any epoch. Five horses in the starved group and 4 in the nonstarved group were found to have one or more PaO, values below 8.0 kPa. The PaO, data from these hqrses are shown in Table 3. No horse suffered any post operative problem which could be attributed to its feeding protocol.

There are no significant differences between groups NS=not starved, S=starved

TABLE 3: Feeding status and individual PaO, data of horses with PaO, < 8.0 kPa

Feed status S S S S S NS NS NS NS

PaOa(kPa)

PaO, (kPa)

PaO, (kPa)

15-45 mins

45-75 mins

75-105 mins

7.3 6.4 6.8

5.3 6.4

7.2 7.7 5.1 6.0

DISCUSSION 6.1 6.5

Starvation of horses before general anaesthesia is a widely accepted clinical practice (Hall and Clarke 1991) which increases the FRC (McDonnell et al. 1979; McDonnell and Hall 1974). This should decrease the airway closure and atelectasis which occurs when FRC falls below closing volume (Nunn 1987) and so reduce intra-operative hypoxaemia. However, many other factors can influence the PaOz during anaesthesia, and many of these factors, such as the position of the patient during anaesthesia, anatomical shape of the patient and metabolic oxygen consumption are beyond the control of the anaesthetist. Controllable factors, such as the FIO, and anaesthetic technique, were standardised within clinically practical limits of the present study whereas inotrope infusion and IPPV were titrated to clinically appropriate values of blood pressure and end tidal CO, respectively. If starvation is to be of benefit before anaesthesia, an improvement in PaO2 should accrue from a feeding protocol appropriate to practical management, hence the modest duration of food deprivation in the starved group of horses in the present study. Against any benefit must be balanced possible adverse effects of starvation. Horses are grazing animals adapted to frequent eating and may experience hunger if deprived of food for prolonged periods. Apart from the possibility that this is unpleasant for the animal, it can also result in metabolic acidosis with hyperlipidaemia (Naylor et al. 1980) and may pre-dispose to post operative gastrointestinal dysfunction if over-eating occurs once access to food is allowed (Blood and Radostits 1989). In the present study, under clinical conditions, there was no detectable increase in Pa02 associated with the starvation protocol described.

5.7 5.6 6.9

NS=not starved, S=starved

staff according to common equine husbandry practice. The following anaesthetic protocol was employed for all horses: Pre-medication was with acepromazine (30 pgkg bwt) and penicillin G (30,000 iukg bwt) by iv injection 3 0 4 5 min prior to induction of general anaesthesia with detomidine (20 pgkg bwt iv) and ketamine (2 mgkg bwt iv). After endotracheal intubation anaesthesia was maintained with halothane in oxygen delivered via a rebreathng system (J D Medical Ltd, Arizona, USA). A superficial artery was cannulated to allow direct arterial pressure monitoring (Roche Kontron system) and arterial blood sampling for blood gas analysis (Ciba Coming 168). End tidal carbon dioxide, inspired oxygen (Datex Normocap, Vickers Medical) and end tidal halothane (Kontron piezo-electric anaesthetic agent monitor) concentrations were monitored. Hypercarbia (arterial carbon dioxide tension >9.3kPa) was treated by IPPV using a time cycled pressure limited ventilator (Bird 7, J D Medical Ltd) and hypotension (mean arterial pressure <70 mmHg) was treated by iv infusion of dobutamine (up to 1.4 pgkg bwt/min). Hartmann’s solution (approximately 10 ml/kg bwt/h) was administered by iv infusion to all horses during anaesthesia. Arterial blood samples were taken anaerobically and blood gas analysis was performed within 5 rnin of collection. The first sample was taken as soon as practical after induction of anaesthesia and transportation to theatre. Subsequent samples were taken at 30 rnin intervals.

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