The pulmonary acid-aspiration syndrome was first reported 50 years ago (1) in a group of parturients undergoing general anaesthesia for vaginal delivery. The description given by the author was so accurate and so complete that it rapidly acquired the eponym 'Mendelson's syndrome'.

For the full picture to develop ("cyanosis and labored respiration ... with a pink froth exuding from the respiratory passages"), aspiration must occur in the presence of a 'triad' of features, namely:
1. A stomach that contains gastric secretions at a 'low' pH (less than 2.5) or one that contains particulate matter.
2. Vomiting or regurgitation.
3. Depression of the laryngeal reflexes.

An essential component of the syndrome is the development of a pulmonary 'burn' - usually produced by the inhalation of gastric acid at a 'low' pH. As such, Mendelson's syndrome is at one end of the spectrum of the pulmonary aspiration syndromes. Aspiration of non-particulate, gastric contents at a 'high' pH (&gt6.0) does not produce the same histological lesion as acid-aspiration (2) and is probably associated with a lower mortality rate. Aspiration of 'high' pH, particulate matter also produces a different histological picture from acid-aspiration, but may be associated with an equally poor outcome. This may account, in part, for the wide variation (3 to 70%) (1) in reported mortality rates from aspiration in association with anaesthesia.

Since the description of the syndrome, important therapeutic strategies intended to minimise the risks of aspiration, have been evolved by anaesthetists. This has led to a progressive reduction in the maternal death rate from aspiration syndromes such that, in the United Kingdom, the first Report on Confidential Enquiries into Maternal Deaths (1952) indicated that there were 32 deaths from aspiration and by 1988-90 this had fallen to zero.

The therapeutic strategies which have been adopted include:
1. Fasting of women in labour.
2. Measures which may increase gastric pH.
3. Measures which may reduce the volume of gastric secretions.
4. The use of regional rather than general anaesthesia.

And, if general anaesthesia is administered:
5. Pre-oxygenation and the application of cricoid pressure prior to intubation.
6. Protection of the airway by a cuffed endotracheal tube.

1. Fasting during labour.
There is a fundamental conflict between the needs of the parturient as perceived by the patient or her midwife and the needs of the parturient as perceived by the obstetric anaesthetist. As far as the latter is concerned, the safest strategy with regarding to a feeding policy is to insist on fasting during labour, to meet all maternal needs for hydration by the administration of intravenous fluids, and to limit oral intake to the sucking of ice. It has been clearly demonstrated that both the intake of food (3) and the drinking of dextrose-containing solutions (4) can significantly delay gastric emptying (Chapter 26).

2. Measures which may increase gastric pH (Chapter 80).
Two techniques intended to raise the gastric pH before the administration of an obstetric anaesthetic have gained widespread acceptance.
a. The administration of 30mls of 0.3Molar sodium citrate 15-20 minutes before anaesthesia for caesarean section (CS) has been shown to raise gastric pH above 2.5 in about 90% of patients (5). This antacid is preferable to the particulate antacids because the solution mixes more effectively with the gastric contents, and it has also been suggested that particulate antacids themselves are capable of producing a severe aspiration syndrome (6).
b. The administration of an H2 antagonist such as ranitidine is even more effective than sodium citrate at raising gastric pH. If used prior to elective CS, two oral doses of ranitidine (150mg) should be given, one the night before surgery and one on the morning of surgery. For emergency CS, ranitidine 50mg can be given intravenously. Sodium citrate should also be used. H2 antagonists may have the additional advantage of reducing gastric volume. The combined use of ranitidine and sodium citrate will raise gastric pH above 2.5 in the great majority of parturients (7).

3. Measures which may reduce the volume gastric secretions.
Metoclopramide has been used by some to promote gastric emptying during labour (8). However, the effectiveness of this technique is debatable (9). Attempts to empty the stomach by the use of a nasogastric tube or a pro-emetic drug are likewise relatively ineffective and are also unacceptable to most patients. The effect of the analgesic technique used in labour and its relationship to the volume of gastric contents measured at subsequent CS has also been studied. Holdsworth (10) found that the largest gastric aspirates were found in patients who had received pethidine analgesia and the smallest aspirates in patients who had received either epidural analgesia or no analgesia. Pethidine, rather than the 'emotional stress of labour', was thought to cause the relative gastric stasis.

4. The use of regional rather than general anaesthesia.
Provided that no sedation is administered and that regional anaesthesia is complication-free, the use of major regional blockade for CS virtually eliminates the risk of aspiration. Nevertheless, it is still imperative to administer aspiration prophylaxis to patients who are to undergo CS under regional anaesthesia.

5. The use of cricoid pressure.
If a general anaesthetic is administered, the use of cricoid pressure ('Sellick's Manoeuvre') at induction (11) (in association with pre-oxygenation) is mandatory. Properly applied pressure will withstand a 'head' of pressure of 100cms of water. There may be a small risk of oesophageal rupture if pressure is applied in the presence of active vomiting. Some authorities have advocated the release of the applied pressure if vomiting occurs but others disagree.

6. Protection of the airway by a cuffed endotracheal tube.
If a general anaesthetic is administered, protection of the airway by a cuffed endotracheal tube is also mandatory. However, it should be noted that modern high-volume, low-pressure cuffs, inflated to 25cms H2O, do not afford complete protection against aspiration.

References:
1. Mendelson CL The aspiration of stomach contents into the lungs during obstetric anesthesia. Am J Obstet Gynecol 52:191 1946

2. Schwartz DJ, Wynne JW, Gibbs CP et al The pulmonary consequences of aspiration of gastric contents at pH values greater than 2.5. Am Rev Respir Dis 121:119 1980

3. Lewis M, Crawford JS Can one risk fasting the obstetric patient for less than 4 hours? Br J Anaesth 59:312 1987

4. Hinder RA, Kelly KA Canine gastric emptying of solids and liquids. Am J Physiol 233:335 1977

5. Dewan DM, Floyd AM, Thistlewood JM et al Sodium citrate pretreatment in elective cesarean section patients. Anesth Analg 64:34 1985

6. Gibbs CP, Schwartz DJ, Wynne JW et al Antacid pulmonary aspiration in the dog. Anesthesiology 51:380 1979

7. Ormezzano X; Francois TP; Viaud JY; Bukowski JG; Bourgeonneau MC; Cottron D; Ganansia MF; Gregoire FM; Grinand MR; Wessel PE Aspiration pneumonitis prophylaxis in obstetric anaesthesia: comparison of effervescent cimetidine-sodium citrate mixture and sodium citrate Br J Anaesth 1990 Apr;64(4):503-6

8. Howard FA, Sharp DS Effect of metoclopramide on gastric emptying during labour. Br Med J 1:446 1973

9. Cohen SE, Jasson J, Talafre M-L Does metoclopramide decrease gastric volume in cesarean section patients? Anesthesiology 61:604 1984

10. Holdsworth JD Relationship between stomach contents and analgesia in labour. Br J Anaesth 50:1145 1978

11. Sellick BA Cricoid pressure to control regurgitation of stomach contents during induction of anesthesia. Lancet 2:404 1961