It is well known that the risk of morbidity and mortality from aspiration pneumonitis is high in the obstetric patient. The risk has theoretically increased over the last decades due to the ageing maternal population, multiple births associated with IVF and an increasing caesarean section rate (1). However there has been a significant decline in the anaesthetic contribution to perinatal deaths over the last two decades (2) which has been partially attributed to the increased use of regional anaesthesia and a better appreciation of airway protection in the parturient (3). Nevertheless, the use of regional techniques does not eliminate the risk of aspiration. There is still the possibility of aspiration with loss of airway protection in such circumstances as fitting, local anaesthetic toxicity (Chapter 89), high or total spinal anaesthesia (Chapter 11), severe hypotension and associated pathology such as aortocaval compression (Chapter 28), anaphylaxis (Chapter 69) or amniotic- or thrombo-embolism.
PROPHYLAXIS
a) Fasting regimens:
Fasting during labour has become controversial (4, 5). Interventions that put a mother at risk of aspiration are to a certain extent unplanned. Only 87% of parturients coming to caesarean section can be predicted; the remaining 13% are completely unforseen.
The outcome, in the rare event of aspiration of stomach contents, is dependent on the type of matter aspirated (ie particulate vs non particulate) and the pH and volume aspirated. As a consequence, it is reasonable to fast parturients at high risk of anaesthetic intervention in labour. Should we also fast "low risk" labouring parturients (for the sake of those who will go on to an unpredicted intervention) or should we fast only those at high risk (Chapter 26)? To date, this issue remains unresolved.
b) Pharmacological:
Non particulate antacid prophylaxis (eg. 30 ml 0.3 Molar Sodium citrate) aimed at raising gastric pH prior to epidural insertion or other anaesthetic intervention, or, indeed, in some institutions, throughout labour, is practised in the belief that if aspiration does occur then its severity will be reduced by raising pH of the aspirate. Whilst this is certainly true theoretically, the practicalities are that antacids are unreliable because their effect is variable both in duration (which may be as low as 1-2 hours) and in efficacy.
The additional administration of H2 antagonists (eg cimetidine or ranitidine) either orally or parenterally to the antacid provides longer prophylaxis.
Neither antacid nor H2 antagonist therapy reduces the gastric volume, so drugs such as metoclopramide can be added.
c) Protection of the airway:
Avoid general anaesthesia or depression of the airway reflexes (eg. by sedative drugs) in patients not afforded airway protection by a cuffed endotracheal tube.
MANAGEMENT OF ASPIRATION IN THE AWAKE PATIENT (6)
If the parturient has aspirated as a result of an alteration in the conscious state, the airway should be immediately protected with a cuffed endotracheal tube.
There is a clinical spectrum of presentation of aspiration ranging from immediate asphyxiation due to large airway obstruction or reflex airway closure through to more delayed ARDS. The resultant reduction in surfactant activity and interstitial and alveolar oedema leads to a large Alveolar-arterial gradient, venous admixture and hypoxaemia. Chest X-ray may show no early changes. Serial arterial blood gas analysis may help define the severity of the injury.
Treatment in the awake patient is aimed at maintaining tissue oxygen delivery by administering supplemental oxygen by mask, or, in more severe cases, intubation and modes of ventilation which are aimed at optimising oxygenation by recruiting non-ventilated alveoli (eg PEEP, CPAP). Unnecessarily high airway pressures should be avoided because reductions in cardiac output will compromise tissue oxygen delivery. Maintenance of optimal vascular filling is also important because severe aspiration pneumonitis may cause major fluid shifts in much the same way as can major burns. Consideration should be given in these severe cases to the use of a pulmonary artery catheter.
As dispersion of gastric acid is rapid, manoeuvres such as bronchial lavage with bicarbonate are not indicated. Airway suction as an initial manoeuvre may prevent further soiling. Bronchoscopy has a limited role in the management of particulate aspiration or severe atelectasis.
The use of steroids is controversial (with some authorities suggesting that the inflammatory response is modified). Steroids do not alter the course of the disease and may have a deleterious effect on healing and increase the risk of secondary infection. The use of antibiotics is only indicated if infection supervenes.
References:
1. Annual Report for the Year 1993 Consultative Council on Obstetric and Paediatric Mortality and Morbidity in Victoria
2. Report on Confidential Enquires into Maternal Deaths in the United Kingdom (1988-1990) London HMSO 1994
3. Benhamou D. Complications of Obstetric Anaesthesia. Current Opinion in Anaesthesiology 1995 8: 3; 216-219
4. Ludka L, Roberts. CC Eating and Drinking in Labour Journal of Nurse Midwifery 38:4;July-August 1993
5. Elkinton KW At The Waters Edge Where Obstetrics and Anaesthesia Meet. Obstetric and Gynaecology 1991: 67; 54-57
6. Gibbs CP Aspiration risk in parturients. In: Common Problems in Obstetric Anaesthesia, Datta S (Ed), 2nd Edition, Mosby, Boston, 1995 pp 15-38