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Post anaesthetic reflux oesophagitis in dogs and cats
-
J vet. Anaesth Vol. 22 (1995)
Editorial
Post anaesthetic reflux oesophagitis in dogs and cats Reflux of gastric contents into the oesophagus may result in oesophagitis. In fact, gastro-oesophageal reflux (GOR) is the most common cause of oesophagitis in dogs and cats. In particular, GOR, occurring during anaesthesia, is one of the most common causes of reflux oesophagitis (Zawie 1987, Tams 1989).In humans, reflux oesophagitis is a common disease, accounting for as many as 23% of new referrals for endoscopy (Stocker and Williams 1991). In contrast, it seems that it is only rarely diagnosed in small animal patients. Reviewing the reported cases, Galatos and Raptopoulos (1995b)found 24 and 15 cases of post-operative oesophagitis and stricture formation in dogs and cats respectively. In all the cases reflux that had occurred during anaesthesia was considered to be the triggering factor. The pathogenesis of reflux oesophagitis is multifactorial, although it is usually associated with lower oesophageal sphincter (LOS) incompetence. It is the difference between the LOS pressure (LOSP) and the intragastric pressure, termed the barrier pressure (BrP), which determines whether significant reflux will occur. While with a permanently decreased LOSP, reflux can easily be explained, in patients with GOR disease who have a normal LOSP, transient LOS relaxations have been shown to be the main mechanism of GOR (Dodds, Dent, Hogan, Helm, Hauser, Patel and Egide, 1982). Transient LOS relaxations are abolished by anaesthesia (Cox, Martin, Dent and Westmore, 1988). However, other factors prevailing during anaesthesia and/ or surgery may promote the movement of gastric contents into the oesophagus. The incidence of GOR during anaesthesia has been studied by continuous lower oesophageal pH measurement in a series of 510 dogs (Galatos and Raptopoulos 1995a,b). The overall incidence of reflux (pH<4.0 or pH>7.5) was 16,9% (86/510), but regurgitation and flow of gastric contents from the mouth occurred in only 3 dogs (0.6%).GOR usually occurred shortly after induction of anaesthesia; almost half of the cases occurred within 15 min and about two thirds of them within 20 min following induction. Moreover, prolongation of anaesthesia and surgery was not associated with an increased incidence of GOR. The refluxate was usually acid (pH<4.0),but in 9.3% of the reflux episodes (8/86) it was alkaline (pH>7.5). The mean duration of the reflux episodes was about 47 min (range: 5-115 min). Reflux with an oesophageal pH of less than 2.5 occurred on 46 occasions (9%),which represent 59% (46/78) of the acid reflux cases, and had a mean duration of about 42 min (range 15-75 min). It is known that most of the pre-anaesthetic and anaesthetic agents decrease, to a lesser or greater degree, LOSP (Cotton and Smith 1984, Strombeck and Harrold 1985, Hashim and Waterman 1991, 1993, Waterman and Hashim 1992).With regard to premedication, in the above series, it was found that following premedication with
diazepam, pethidine or propionylpromazine, GOR occurred less frequently than when dogs had not been premedicated or premedicated with atropine combined with either xylazine or propionylpromazine. Apart from decreased LOSP, an increased intra-gastric pressure can result in a decrease of BrP and, thus, in an increased incidence of GOR. A significantly higher incidence of GOR was observed in dogs undergoing intraabdominal operations compared with a similarly treated group of dogs subjected to non-abdominal operations. In fact, post-anaesthetic oesophageal stricture formation has been reported more frequently in animals undergoing intra-abdominal operations. It is believed that intraabdominal manipulations resulting in transient increases of intra-adbominal and intra-gastric pressures are the cause of the high incidence of GOR on such occasions. Of the 13 reflux episodes observed in animals which underwent intra-abdominal operations, 9 occurred after intraabdominal manipulations had commenced (Galatos and Raptopoulos 1995b). Body position during anaesthesia is another factor that may affect GOR. In animals with incompetent LOS, a head-down position in association with an increased volume of gastric contents may easily result in COR. Moreover, on such occasions, body position may also partially determine the volume of the refluxate, as well as the area of the oesophagus in which it will accumulate; thus, a head-down position may predispose to pooling of refluxed fluid in more cranial segments of the oesophagus than the horizontal position (Galatos et al., 1994). However, there was no correlation between oesophageal pH and tilt of the body during surgery both in dogs (Galatos and Raptopoulos 199513) and humans (Heijke, Smith and Key, 1991, IIling, Duncan and Yip, 1992). Waterman ct al. (1995) found that LOSP and BrP are better maintained in right lateral recumbency compared to dorsal recumbency in dogs. However, they concluded that the incidence of reflux in both positions could have been similar, and in any case probably minimal, since the difference in LOSP or BrP between the two positions were only just significant and the mean of both pressures was higher than 10 mmHg. It should be noted that the site of recumbency (right or left lateral, sternal and dorsal) had no significant influence on the incidence of GOR during anaesthesia in dogs (Galatos and Raptopoulos 199513). There is a trend for the incidence of GOR to increase with age, so that geriatric patients may be at increased risk, especially since increased age was also associated with increased gastric acidity (Galatos and Raptopoulos 1995b). Puppies and kittens may also be at increased risk of developing GOR since LOS is incompetent at birth, and at 6 weeks of age LOSP is only one-half that of adults (Strombeck and Guilford 1991). Gender does not appear to affect the incidence of GOR in dogs (Galatos and Raptopoulos 1995b).However, post6
1. vet. Anaesth. Vol. 22 (1995) -
gastric acidity following narcotic or oral premedication in adult human patients. The increased acidity of gastric contents reduces LOSP, which may lead to an increased incidence of GOR. In turn, strongly acidic refluxate may result in more severe oesophageal tissue injury and if aspirated into the lungs, the consequences can be devastating. This has led to the use of antacids, H2-receptor antagonists or proton pump inhibitors pre-operatively. Winkelstein (1935) was the first to suggest that free hydrochloric acid and pepsin may damage oesophageal mucosa, resulting in ”peptic oesophagitis” in humans. Acid and pepsin are still considered the major factors in the pathogenesis of reflux oesophagitis, while reflux of duodenal contents does not play an important role (Timmer, Breumelhof, Nadorp and Smout, 1993). However, duodenal secretions are present in the normal and post-operative stomach, and bile salts and pancreatic enzymes have been shown capable of producing oesophageal mucosal damage in the laboratory. Moreover, there is evidence that when acid and duodenal secretions mix there may be a toxic synergism leading to changes which produce the clinical picture of reflux oesophagitis, with or without symptoms (Stoker and Williams 1991).In this respect, it is interesting to note that, in dogs, in about 9% of the reflux episodes, lower oesophageal pH was alkaline (>7.5), indicating reflux of duodenal contents (Galatos and Raptopoulos 1995a,b). It has been suggested that oesophagitis results from exposure of the oesophageal mucosa to gastric contents of pH below 2.5 for as little as 20 min (Wilson 1977). In conscious animals, once gastric contents have refluxed into the oesophagus, the defense mechanisms against the development of inflammation consist of oesophageal clearance, salivation and oesophageal epithelial resistance. The pre-epithelial, epithelial and post-epithelial factors contributing to the oesophageal defense against acid injury (Timmer et al., 1993) and the way they are affected by anaesthesia, have not been studied in veterinary medicine. Secretion of saliva is usually depressed during anaesthesia, especially if anticholinergicsare used. Moreover, suppression of oesophageal motility, abolition of swallowing and a horizontal or head-down position of the body during anaesthesia do not favour oesophageal luminal clearance or neutralization of the refluxate. Indeed, lower oesophageal pH remained below 4.0 or 2.5 for a mean of about 47 min or 42 min, respectively (Galatos and Raptopoulos 1995a,b). With 9% of anaesthetised dogs experiencing an oesophageal pH of less than 2.5 for 42 min, post-anaesthetic reflux oesophagitis and stricture formation would be expected to occur more frequently than is reported. It may therefore be that the normal canine oesophageal mucosa can tolerate gastric contents of pH below 2.5 for longer than 20 min. Moreover, factors other than the mere presence of refluxate in the oesophagus, may have to exist for oesophageal damage to develop. Timmer et al. (1993) concluded that GOR disease is not merely due to excessive acid secretion, but rather to the presence of acid at inappropriate sites for abnormally long periods. The possibility remains that asymptomatic, mild oesophagitis develops, which passes unnoticed.
anaesthetic oesophagitis and stricture has been reported more frequently in female rather than male dogs and cats. The majority of these animals had been subjected to ovariohysterectomy. Apart from the fact that the latter is a rather frequently performed procedure involving intraabdominal manipulations, if the operation is performed during the luteal phase of the ovarian cycle, increased progesterone levels may be responsible for a high incidence of reflux, since they are known to reduce LOSP (Tams 1989). Post-anaesthetic oesophagitis and stricture formation have been recorded in a variety of breeds and sizes in dogs. Galatos and Raptopoulos (1995a,b) failed to correlate the incidence of GOR with the breed or bodyweight of the animals. Illing et al. (1992) also found no association between GOR during anaesthesia and body conformation, in humans. Patients with an increased volume of gastric contents are generally believed to be at increased risk of developing GOR and, traditionally, pre-operative fasting is used to decrease that volume. However, an increase in the duration of pre-operative fasting does not appear to guarantee a decrease in the volume of gastric contents (Miller, Wishart and Nimmo, 1983, Manchikanti, Colliver, Marrero and Roush, 1985).Moreover, Hardy, Lepage and Bonneville-Chouinard(1990) found that the occurrence of GOR on induction of anaesthesia does not correlate with the volume of gastric contents in humans. It is now suggested that human patients should be allowed to take clear fluids until 3 hours before anaesthesia (Strunin 1993). In dogs, no reflux occurred in animals fed 2-4 hours before the induction of anaesthesia, while prolonged pre-operative fasting was associated with decreased gastric pH and an increased incidence of GOR (Galatos and Raptopoulos 1995a).It is clear that prolonged withholding of food and, especially, water cannot be justified, since, it is normally unpleasant for patients, especially in hot weather and when antisialogogue premedication has been given and it also predisposes to dehydration. Clearly further detailed studies are required in order to be able to define the optimal duration of pre-operative fasting. The effect of drugs used in anaesthesia on gastric pH is not well understood. Administration of an anticholinergic agent alone decreases gastric acid secretion although the concentration of acid is not necessarily lowered, possibly because the secretion of bicarbonate, as well as of hydrogen ions, is blocked (Brown 1990).In dogs, Roush, Keene, Eicker and Bjorling (1990) found that pre-anaesthetic administration of atropine or glycopyrrolate had no effect on gastric pH. In the present authors’ study, premedication with atropine combined with propionylpromazine or xylazine was associated with significantly increased gastric pH compared with no premedication or premedication with pethidine or diazepam. However, the combination of atropine with propionylpromazine was associated with significantly lower gastric pH than the administration of propionylpromazine alone (Galatosand Raptopoulos 1995a). Diazepam and general anaesthesia with halothane have been found to increase gastric pH (Schurizek, Kraglund, Andreasen, Jensen and Juhl, 1988; Schurizek,Willacy, Kraglund, Andreasen and Juhl, 1989). Furthermore, Manchikanti et al. (1987) found no change in 7
1. vet. Anaesth. Vol. 22 (1995)
In conclusion, post-anaestheticreflux oesophagitis only rarely occurs, even though gastro-oesophageal, mainly acid, reflux is not uncommon during anaesthesia in dogs. Conditions that are associated with increased incidence of GOR include: prolonged pre-operative fasting, preanaesthetic administration of atropine, performance of intra-abdominal surgery and there may also be a link with extremes of age. The circumstances under which reflux may lead to the production of oesophagitis and stricture post-operatively, have yet to be elucidated.
and barrier pressure in anaesthetised cats. Veterinary Record, 133,158160. Heijke SAM, Smith G & Key A (1991). The effect of the Trendelenburg position on lower oesophageal sphincter tone. Anaesthesia, 46, 185187. Illing L, Duncan PG & Yip R (1992). Gastroesophageal reflux during anaesthesia. Canadian Journal of Anaesthesia, 39,466-470. Manchikanti L, Canella MG, Hohlbein LJ & Colliver JA (1987). Assessment of effect of various modes of premedication on acid aspiration risk factors in outpatient surgery. Anesthesia Analgesia, 66, 81-84. Manchikanti L, CoIliver JA, Marrero TC & Roush JR (1985). Assessment of age-related acid aspiration risk. Anesthesia Analgesia, 64, 11-17,
D. Raptopoulos and A.D. Galatos Aristotle University of Thessaloniki Faculty of Veterinary Medicine Department of Clinical Sciences St. Voutyra 11 54627 Thessaloniki Greece
Miller M, Wishart HY & Nimmo WS (1983). Gastric contents at induction of anaesthesia. Is a 4-hour fast necessary? British Journal of Anaesthesia, 55,1185-1188. Roush JK, Keene BW, Eicker SW & Bjorling DE (1990).Effects of atropine and glycopyrrolate on esophageal, gastric, and tracheal pH in anesthetized dogs. Veterinary Surgery, 19,88-92.
REFERENCES
Schurizek BA, Kraglund K, Andreasen F, Jensen LV & Juhl B (1988). Gastrointestinal motility and gastric pH and emptying following ingestion of diazepam. British Journal of Anaesthesia, 61,712-719.
Brown JH (1990). Atropine, scopolamine, and related antimuscarinic drugs. In: Goodman Gilman A, RaIl TW, Nies A S B Taylor P (eds) Goodman and Gilman’s The Pharmacological Basis of Therapeutics, 8th ed. New York Pergamon Press, pp 150-165.
Schurizek BA, Willacy LHO, Kraglund K, Andreasen F & juhl B (1989). Effects of general anaesthesia with halothane on antroduodenal motility, pH and gastric emptying rate in man. British Journal of Anaesthesia, 62, 129-137.
CottonBR& Smith G (1984).The lower oesophageal sphincter and anaesthesia. British Journal of Anaesthesia, 56, 37-46.
Stoker DL &Williams JG (1991). Alkaline reflux. Gut, 32,1090-1092, Strombeck DR & Guilford WG (1991). Small Animal Gastroenterology, 2nd ed. London: Wolfe Publishing Ltd, pp 129-139.
Cox MR, Martin CJ, Dent J & Westmore M (1988). Effect of general
anaesthesia on transient lower oesophageal sphincter relaxations in the dog. Australian and New Zealand Journal of Surgery, 58, 825830.
Strombeck DR & Harrold D (1985). Effects of atropine, acepromazine, meperidine and xylazine on gastro-esophageal sphincter pressure in the dog. American Journal of Veterinary Research, 46,963-965.
Dodds WJ, Dent J, Hogan WJ, Helm IF, Hauser R, Pate1 GK & Egide MS (1982). Mechanisms of gastroesophageal reflux in patients with reflux esophagitis. New England Journal of Medicine, 307,1547-1552.
Strunin L (1993).How long should patients fast before surgery? Time for new guidelines. Editorial. British Journal of Anaesthesia, 70, 1-3.
Galatos AD, Rallis T & Raptopoulos D (1994). Post anaesthetic oesophageal stricture formation in three cats. Journal of Small Animal Practice, 35, 638-642.
Tams TR (1989). Reflux esophagitis. In Kirk RW (ed) Current Veterinary Therapy X Small Animal Practice. Philadelphia: WB Saunders Co, pp 906-910.
Galatos AD & Raptopoulos D (1995a). Gastro-oesophageal reflux during anaesthesia in the dog: The effect of pre-operative fasting and premedication. Veteriiiary Record, 137, 479-483.
Timmer R, Breumelhof R, Nadorp JHSM & Smout AJPM (1993). Recent advances in the pathophysiology of gastro-oesophageal reflux disease. European Journal of Gastroenterology 0 Hepatology, 5,485-491. Waterman AE & Hashim MA (1992). Effects of thiopentone and propofol on lower oesophageal sphincter and barrier pressure in the dog. Journal of Small Animal Practice, 33, 530-533.
Galatos AD & Raptopoulos D (1995b).Gastro-oesophageal reflux during anaesthesiain the dog: Theeffect of age, positioningand type of surgical procedure. Veterinary Record, 137,515-516.
Waterman AE, Hashim MA & I’earson H (1995).Effect of body position on oesophageal and gastric pressures in the anaesthetised dog. Journal of Small Animal Practice, 36,196-200.
Hardy JF, Lepage Y & Bonneville-Chouinard N (1990). Occurrence of gastroesophageal reflux on induction of anaesthesia does not correlate with the volume of gastric contents. Canadian Journal of Anaesthesia, 37,502-508.
Wilson GI‘ (1977). Ulcerative esophagitis and esophageal stricture. Journal of the American Animal Hospital Association, 13, 180-185.
Hashim MA & Waterman AE (1991). Effects of thiopentone, propofol, alphaxalone-alphadolone, ketamine and xylazine-ketamine on lower oesophageal sphincter pressure and barrier pressure in cats. Veferinay Record, 129,137-139.
Winkelstein A (1935). Inflammation of the lower third of the oesophagus. Journal ofthe American Medical Association, 104,906-909.Cited by Stoker and Williams 1991.
Hashim MA & Waterman AE (1993). Effects of acepromazine, pethidine and atropine premedication on lower oesophageal sphincter pressure
Zawie DA (1987). Medical diseases of the esophagus. Compendium oil Continuing Education, 9,1146-1152.
8
J vet. Anaesth Vol. 22 (1995)
Editorial
Post anaesthetic reflux oesophagitis in dogs and cats Reflux of gastric contents into the oesophagus may result in oesophagitis. In fact, gastro-oesophageal reflux (GOR) is the most common cause of oesophagitis in dogs and cats. In particular, GOR, occurring during anaesthesia, is one of the most common causes of reflux oesophagitis (Zawie 1987, Tams 1989).In humans, reflux oesophagitis is a common disease, accounting for as many as 23% of new referrals for endoscopy (Stocker and Williams 1991). In contrast, it seems that it is only rarely diagnosed in small animal patients. Reviewing the reported cases, Galatos and Raptopoulos (1995b)found 24 and 15 cases of post-operative oesophagitis and stricture formation in dogs and cats respectively. In all the cases reflux that had occurred during anaesthesia was considered to be the triggering factor. The pathogenesis of reflux oesophagitis is multifactorial, although it is usually associated with lower oesophageal sphincter (LOS) incompetence. It is the difference between the LOS pressure (LOSP) and the intragastric pressure, termed the barrier pressure (BrP), which determines whether significant reflux will occur. While with a permanently decreased LOSP, reflux can easily be explained, in patients with GOR disease who have a normal LOSP, transient LOS relaxations have been shown to be the main mechanism of GOR (Dodds, Dent, Hogan, Helm, Hauser, Patel and Egide, 1982). Transient LOS relaxations are abolished by anaesthesia (Cox, Martin, Dent and Westmore, 1988). However, other factors prevailing during anaesthesia and/ or surgery may promote the movement of gastric contents into the oesophagus. The incidence of GOR during anaesthesia has been studied by continuous lower oesophageal pH measurement in a series of 510 dogs (Galatos and Raptopoulos 1995a,b). The overall incidence of reflux (pH<4.0 or pH>7.5) was 16,9% (86/510), but regurgitation and flow of gastric contents from the mouth occurred in only 3 dogs (0.6%).GOR usually occurred shortly after induction of anaesthesia; almost half of the cases occurred within 15 min and about two thirds of them within 20 min following induction. Moreover, prolongation of anaesthesia and surgery was not associated with an increased incidence of GOR. The refluxate was usually acid (pH<4.0),but in 9.3% of the reflux episodes (8/86) it was alkaline (pH>7.5). The mean duration of the reflux episodes was about 47 min (range: 5-115 min). Reflux with an oesophageal pH of less than 2.5 occurred on 46 occasions (9%),which represent 59% (46/78) of the acid reflux cases, and had a mean duration of about 42 min (range 15-75 min). It is known that most of the pre-anaesthetic and anaesthetic agents decrease, to a lesser or greater degree, LOSP (Cotton and Smith 1984, Strombeck and Harrold 1985, Hashim and Waterman 1991, 1993, Waterman and Hashim 1992).With regard to premedication, in the above series, it was found that following premedication with
diazepam, pethidine or propionylpromazine, GOR occurred less frequently than when dogs had not been premedicated or premedicated with atropine combined with either xylazine or propionylpromazine. Apart from decreased LOSP, an increased intra-gastric pressure can result in a decrease of BrP and, thus, in an increased incidence of GOR. A significantly higher incidence of GOR was observed in dogs undergoing intraabdominal operations compared with a similarly treated group of dogs subjected to non-abdominal operations. In fact, post-anaesthetic oesophageal stricture formation has been reported more frequently in animals undergoing intra-abdominal operations. It is believed that intraabdominal manipulations resulting in transient increases of intra-adbominal and intra-gastric pressures are the cause of the high incidence of GOR on such occasions. Of the 13 reflux episodes observed in animals which underwent intra-abdominal operations, 9 occurred after intraabdominal manipulations had commenced (Galatos and Raptopoulos 1995b). Body position during anaesthesia is another factor that may affect GOR. In animals with incompetent LOS, a head-down position in association with an increased volume of gastric contents may easily result in COR. Moreover, on such occasions, body position may also partially determine the volume of the refluxate, as well as the area of the oesophagus in which it will accumulate; thus, a head-down position may predispose to pooling of refluxed fluid in more cranial segments of the oesophagus than the horizontal position (Galatos et al., 1994). However, there was no correlation between oesophageal pH and tilt of the body during surgery both in dogs (Galatos and Raptopoulos 199513) and humans (Heijke, Smith and Key, 1991, IIling, Duncan and Yip, 1992). Waterman ct al. (1995) found that LOSP and BrP are better maintained in right lateral recumbency compared to dorsal recumbency in dogs. However, they concluded that the incidence of reflux in both positions could have been similar, and in any case probably minimal, since the difference in LOSP or BrP between the two positions were only just significant and the mean of both pressures was higher than 10 mmHg. It should be noted that the site of recumbency (right or left lateral, sternal and dorsal) had no significant influence on the incidence of GOR during anaesthesia in dogs (Galatos and Raptopoulos 199513). There is a trend for the incidence of GOR to increase with age, so that geriatric patients may be at increased risk, especially since increased age was also associated with increased gastric acidity (Galatos and Raptopoulos 1995b). Puppies and kittens may also be at increased risk of developing GOR since LOS is incompetent at birth, and at 6 weeks of age LOSP is only one-half that of adults (Strombeck and Guilford 1991). Gender does not appear to affect the incidence of GOR in dogs (Galatos and Raptopoulos 1995b).However, post6
1. vet. Anaesth. Vol. 22 (1995) -
gastric acidity following narcotic or oral premedication in adult human patients. The increased acidity of gastric contents reduces LOSP, which may lead to an increased incidence of GOR. In turn, strongly acidic refluxate may result in more severe oesophageal tissue injury and if aspirated into the lungs, the consequences can be devastating. This has led to the use of antacids, H2-receptor antagonists or proton pump inhibitors pre-operatively. Winkelstein (1935) was the first to suggest that free hydrochloric acid and pepsin may damage oesophageal mucosa, resulting in ”peptic oesophagitis” in humans. Acid and pepsin are still considered the major factors in the pathogenesis of reflux oesophagitis, while reflux of duodenal contents does not play an important role (Timmer, Breumelhof, Nadorp and Smout, 1993). However, duodenal secretions are present in the normal and post-operative stomach, and bile salts and pancreatic enzymes have been shown capable of producing oesophageal mucosal damage in the laboratory. Moreover, there is evidence that when acid and duodenal secretions mix there may be a toxic synergism leading to changes which produce the clinical picture of reflux oesophagitis, with or without symptoms (Stoker and Williams 1991).In this respect, it is interesting to note that, in dogs, in about 9% of the reflux episodes, lower oesophageal pH was alkaline (>7.5), indicating reflux of duodenal contents (Galatos and Raptopoulos 1995a,b). It has been suggested that oesophagitis results from exposure of the oesophageal mucosa to gastric contents of pH below 2.5 for as little as 20 min (Wilson 1977). In conscious animals, once gastric contents have refluxed into the oesophagus, the defense mechanisms against the development of inflammation consist of oesophageal clearance, salivation and oesophageal epithelial resistance. The pre-epithelial, epithelial and post-epithelial factors contributing to the oesophageal defense against acid injury (Timmer et al., 1993) and the way they are affected by anaesthesia, have not been studied in veterinary medicine. Secretion of saliva is usually depressed during anaesthesia, especially if anticholinergicsare used. Moreover, suppression of oesophageal motility, abolition of swallowing and a horizontal or head-down position of the body during anaesthesia do not favour oesophageal luminal clearance or neutralization of the refluxate. Indeed, lower oesophageal pH remained below 4.0 or 2.5 for a mean of about 47 min or 42 min, respectively (Galatos and Raptopoulos 1995a,b). With 9% of anaesthetised dogs experiencing an oesophageal pH of less than 2.5 for 42 min, post-anaesthetic reflux oesophagitis and stricture formation would be expected to occur more frequently than is reported. It may therefore be that the normal canine oesophageal mucosa can tolerate gastric contents of pH below 2.5 for longer than 20 min. Moreover, factors other than the mere presence of refluxate in the oesophagus, may have to exist for oesophageal damage to develop. Timmer et al. (1993) concluded that GOR disease is not merely due to excessive acid secretion, but rather to the presence of acid at inappropriate sites for abnormally long periods. The possibility remains that asymptomatic, mild oesophagitis develops, which passes unnoticed.
anaesthetic oesophagitis and stricture has been reported more frequently in female rather than male dogs and cats. The majority of these animals had been subjected to ovariohysterectomy. Apart from the fact that the latter is a rather frequently performed procedure involving intraabdominal manipulations, if the operation is performed during the luteal phase of the ovarian cycle, increased progesterone levels may be responsible for a high incidence of reflux, since they are known to reduce LOSP (Tams 1989). Post-anaesthetic oesophagitis and stricture formation have been recorded in a variety of breeds and sizes in dogs. Galatos and Raptopoulos (1995a,b) failed to correlate the incidence of GOR with the breed or bodyweight of the animals. Illing et al. (1992) also found no association between GOR during anaesthesia and body conformation, in humans. Patients with an increased volume of gastric contents are generally believed to be at increased risk of developing GOR and, traditionally, pre-operative fasting is used to decrease that volume. However, an increase in the duration of pre-operative fasting does not appear to guarantee a decrease in the volume of gastric contents (Miller, Wishart and Nimmo, 1983, Manchikanti, Colliver, Marrero and Roush, 1985).Moreover, Hardy, Lepage and Bonneville-Chouinard(1990) found that the occurrence of GOR on induction of anaesthesia does not correlate with the volume of gastric contents in humans. It is now suggested that human patients should be allowed to take clear fluids until 3 hours before anaesthesia (Strunin 1993). In dogs, no reflux occurred in animals fed 2-4 hours before the induction of anaesthesia, while prolonged pre-operative fasting was associated with decreased gastric pH and an increased incidence of GOR (Galatos and Raptopoulos 1995a).It is clear that prolonged withholding of food and, especially, water cannot be justified, since, it is normally unpleasant for patients, especially in hot weather and when antisialogogue premedication has been given and it also predisposes to dehydration. Clearly further detailed studies are required in order to be able to define the optimal duration of pre-operative fasting. The effect of drugs used in anaesthesia on gastric pH is not well understood. Administration of an anticholinergic agent alone decreases gastric acid secretion although the concentration of acid is not necessarily lowered, possibly because the secretion of bicarbonate, as well as of hydrogen ions, is blocked (Brown 1990).In dogs, Roush, Keene, Eicker and Bjorling (1990) found that pre-anaesthetic administration of atropine or glycopyrrolate had no effect on gastric pH. In the present authors’ study, premedication with atropine combined with propionylpromazine or xylazine was associated with significantly increased gastric pH compared with no premedication or premedication with pethidine or diazepam. However, the combination of atropine with propionylpromazine was associated with significantly lower gastric pH than the administration of propionylpromazine alone (Galatosand Raptopoulos 1995a). Diazepam and general anaesthesia with halothane have been found to increase gastric pH (Schurizek, Kraglund, Andreasen, Jensen and Juhl, 1988; Schurizek,Willacy, Kraglund, Andreasen and Juhl, 1989). Furthermore, Manchikanti et al. (1987) found no change in 7
1. vet. Anaesth. Vol. 22 (1995)
In conclusion, post-anaestheticreflux oesophagitis only rarely occurs, even though gastro-oesophageal, mainly acid, reflux is not uncommon during anaesthesia in dogs. Conditions that are associated with increased incidence of GOR include: prolonged pre-operative fasting, preanaesthetic administration of atropine, performance of intra-abdominal surgery and there may also be a link with extremes of age. The circumstances under which reflux may lead to the production of oesophagitis and stricture post-operatively, have yet to be elucidated.
and barrier pressure in anaesthetised cats. Veterinary Record, 133,158160. Heijke SAM, Smith G & Key A (1991). The effect of the Trendelenburg position on lower oesophageal sphincter tone. Anaesthesia, 46, 185187. Illing L, Duncan PG & Yip R (1992). Gastroesophageal reflux during anaesthesia. Canadian Journal of Anaesthesia, 39,466-470. Manchikanti L, Canella MG, Hohlbein LJ & Colliver JA (1987). Assessment of effect of various modes of premedication on acid aspiration risk factors in outpatient surgery. Anesthesia Analgesia, 66, 81-84. Manchikanti L, CoIliver JA, Marrero TC & Roush JR (1985). Assessment of age-related acid aspiration risk. Anesthesia Analgesia, 64, 11-17,
D. Raptopoulos and A.D. Galatos Aristotle University of Thessaloniki Faculty of Veterinary Medicine Department of Clinical Sciences St. Voutyra 11 54627 Thessaloniki Greece
Miller M, Wishart HY & Nimmo WS (1983). Gastric contents at induction of anaesthesia. Is a 4-hour fast necessary? British Journal of Anaesthesia, 55,1185-1188. Roush JK, Keene BW, Eicker SW & Bjorling DE (1990).Effects of atropine and glycopyrrolate on esophageal, gastric, and tracheal pH in anesthetized dogs. Veterinary Surgery, 19,88-92.
REFERENCES
Schurizek BA, Kraglund K, Andreasen F, Jensen LV & Juhl B (1988). Gastrointestinal motility and gastric pH and emptying following ingestion of diazepam. British Journal of Anaesthesia, 61,712-719.
Brown JH (1990). Atropine, scopolamine, and related antimuscarinic drugs. In: Goodman Gilman A, RaIl TW, Nies A S B Taylor P (eds) Goodman and Gilman’s The Pharmacological Basis of Therapeutics, 8th ed. New York Pergamon Press, pp 150-165.
Schurizek BA, Willacy LHO, Kraglund K, Andreasen F & juhl B (1989). Effects of general anaesthesia with halothane on antroduodenal motility, pH and gastric emptying rate in man. British Journal of Anaesthesia, 62, 129-137.
CottonBR& Smith G (1984).The lower oesophageal sphincter and anaesthesia. British Journal of Anaesthesia, 56, 37-46.
Stoker DL &Williams JG (1991). Alkaline reflux. Gut, 32,1090-1092, Strombeck DR & Guilford WG (1991). Small Animal Gastroenterology, 2nd ed. London: Wolfe Publishing Ltd, pp 129-139.
Cox MR, Martin CJ, Dent J & Westmore M (1988). Effect of general
anaesthesia on transient lower oesophageal sphincter relaxations in the dog. Australian and New Zealand Journal of Surgery, 58, 825830.
Strombeck DR & Harrold D (1985). Effects of atropine, acepromazine, meperidine and xylazine on gastro-esophageal sphincter pressure in the dog. American Journal of Veterinary Research, 46,963-965.
Dodds WJ, Dent J, Hogan WJ, Helm IF, Hauser R, Pate1 GK & Egide MS (1982). Mechanisms of gastroesophageal reflux in patients with reflux esophagitis. New England Journal of Medicine, 307,1547-1552.
Strunin L (1993).How long should patients fast before surgery? Time for new guidelines. Editorial. British Journal of Anaesthesia, 70, 1-3.
Galatos AD, Rallis T & Raptopoulos D (1994). Post anaesthetic oesophageal stricture formation in three cats. Journal of Small Animal Practice, 35, 638-642.
Tams TR (1989). Reflux esophagitis. In Kirk RW (ed) Current Veterinary Therapy X Small Animal Practice. Philadelphia: WB Saunders Co, pp 906-910.
Galatos AD & Raptopoulos D (1995a). Gastro-oesophageal reflux during anaesthesia in the dog: The effect of pre-operative fasting and premedication. Veteriiiary Record, 137, 479-483.
Timmer R, Breumelhof R, Nadorp JHSM & Smout AJPM (1993). Recent advances in the pathophysiology of gastro-oesophageal reflux disease. European Journal of Gastroenterology 0 Hepatology, 5,485-491. Waterman AE & Hashim MA (1992). Effects of thiopentone and propofol on lower oesophageal sphincter and barrier pressure in the dog. Journal of Small Animal Practice, 33, 530-533.
Galatos AD & Raptopoulos D (1995b).Gastro-oesophageal reflux during anaesthesiain the dog: Theeffect of age, positioningand type of surgical procedure. Veterinary Record, 137,515-516.
Waterman AE, Hashim MA & I’earson H (1995).Effect of body position on oesophageal and gastric pressures in the anaesthetised dog. Journal of Small Animal Practice, 36,196-200.
Hardy JF, Lepage Y & Bonneville-Chouinard N (1990). Occurrence of gastroesophageal reflux on induction of anaesthesia does not correlate with the volume of gastric contents. Canadian Journal of Anaesthesia, 37,502-508.
Wilson GI‘ (1977). Ulcerative esophagitis and esophageal stricture. Journal of the American Animal Hospital Association, 13, 180-185.
Hashim MA & Waterman AE (1991). Effects of thiopentone, propofol, alphaxalone-alphadolone, ketamine and xylazine-ketamine on lower oesophageal sphincter pressure and barrier pressure in cats. Veferinay Record, 129,137-139.
Winkelstein A (1935). Inflammation of the lower third of the oesophagus. Journal ofthe American Medical Association, 104,906-909.Cited by Stoker and Williams 1991.
Hashim MA & Waterman AE (1993). Effects of acepromazine, pethidine and atropine premedication on lower oesophageal sphincter pressure
Zawie DA (1987). Medical diseases of the esophagus. Compendium oil Continuing Education, 9,1146-1152.
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