Obstetric anaesthesia matters

Obstetric anaesthesia and analgesia is always full of interest and challenge. As medically sicker patients becoming pregnant newer challenges have arisen. Some of these are discussed in the following article.

Pre-operative assessment
Early identification and planning of obstetric care by multidisciplinary teams was emphasised in the last CEMACH report¹. To this end all maternity units should now have obstetric anaesthetic antenatal clinics dealing with relevant anaesthetic problems, and obstetric or medical illnesses that need anaesthetic input. The problems of the obese patient from both a regional and a general anaesthetic point of view need special consideration. Anaesthetists are suggested to review patients who are morbidly obese (BMI > 35). Apart from predicting problems these clinics allow planning for more complicated parturient management. All elective caesarean section patients should now be seen in pre-assessment clinics by anaesthetists.

Classification of caesarean section
The degree of urgency of caesarean section has long been a source of tribulation between obstetricians and anaesthetists. Communication about the need of immediacy of caesarean section by obstetricians has often been subjective with a variety of results. The terms ‘crash section,’ emergency, semi-emergency, semi-elective and elective were used but meant different things to different members of the team. A ’30 minute’ rule was used for emergency surgery but this is also subjective in terms of the potential emergency nature of the surgery. NICE guidelines and the Royal Colleges of both Obstetricians and Anaesthetists now recommend that classification² be carried out on every case according to the following schedule:

Category 1: immediate threat to the life of the mother or fetus

Category 2: maternal or fetal compromise which is not immediately life threatening

Category 3: needing early delivery but no maternal or fetal compromise

Category 4: at a time to suit the woman and maternity team.

Equipment and staffing
Epidural equipment is standardised in the main with 16 or 18 gauge needles being in common practice. Newer refinements may occur soon with smaller and stronger epidural needles being manufactured. Newer advances in catheter material may allow for smaller atraumatic catheters to be manufactured. Safer loss of resistance devices which allow for two handed advancement of the needle and thus a potentially lower dural puncture rate have also been developed and the Epidrum® is one such example. This device has a small one ml priming pump attached to it which collapses once the epidural space is located.

Newer equipment that is often deemed necessary in the delivery suite include a thromboelastograph for instantaneous clotting profiles, haemoglobin measurement from oximetry, oesophageal Doppler cardiac output monitoring, a Level 1 tranfusor device to assist in major haemorrhage and major patient transfer equipment for the transfer of the critically ill patient to the Intensive Care Unit.

Maternity High Dependency Units of a Level 2 standard are now becoming an integral part of maternity units. Staffing of these areas is traditionally done by midwives. There are now several units with trained High Dependency Unit nurses assisting in the care of the ill parturient. Medical care can be delivered by these experienced staff and maternity care by midwives. More midwives are now trained in managing and understanding the sick mother.

Nerve injuries after neuraxial anaesthesia
Anaesthetists are often aware of obstetric palsies as regional anaesthesia is often blamed for them. However, the most common palsies are intrinsic and have a reported incidence of 0.6 to 92 per 10,000 deliveries. Stretch or compression injury to the lumbosacral plexus or lower extremity peripheral nerves in childhood is blamed for them but compression of the nerve vascular supply mechanism is another possibility. Nullparity, a prolonged second stage of labour, cephalo-pelvic disproportion, non-vertex presentation and forceps deliveries are associated with palsies. The most common is a lateral femoral neuropathy known as meralgia paresthetica. The nerve arises from the lateral border of the psoas muscle medial to the anterior superior iliac spine and then passes under or through the inguinal ligament and is vulnerable to compression. It is sensory to the lateral thigh and is also easily injured in caesarean section. Other nerves likely to be injured in childbirth include the femoral, obturator, sciatic and the common peroneal nerves³.

Anaesthetic related nerve damage does exist but is rare. Estimates in obstetric anaesthesia range from 1.2 – 0.3 per 100,000 procedures. Damage caused can include spinal haematoma, epidural abscess, traumatic spinal cord injury (from the needle), intracranial subdural haematoma, abducens nerve palsy and the development of Horner’s syndrome. Direct spinal cord trauma is most worrying as it can lead to permanent spinal cord injury and is most likely to arise from spinal or combined spinal epidural anaesthesia.

Recommendations for minimising this complication include choosing a lumbar puncture site below L3, halting needle advancement if the patient perceives pain or paraesthesia and injecting anaesthetic solutions only if all pain and paraesthesia has disappeared⁴.

Magnesium
Magnesium is a critical physiological cation and its deficiency in pregnant women may contribute to the development of pre-eclampsia, impaired neonatal development and to metabolic problems extending into adult life. Neurologically the inhibition of calcium channels and antagonism of the NMDA receptor raises the potential of neuronal protection and magnesium administration to prematurely labouring mothers may reduce the incidence of neonatal cerebral palsy. In the management of eclampsia magnesium has been shown to terminate convulsions and prevent further convulsions. It is also the agent of choice for the prevention of convulsions but the argument as to which pre-eclamptic mother should receive magnesium is unresolved. Magnesium therapy has potential complications in its own right and it is usually received for patients with severe disease⁵.

Effects of labour analgesia on the foetus
Labour pain and stress are associated with a progressive foetal acidosis. In terms of analgesia nitrous oxide relieves labour pain more effectively than pethidine and it is worth noting that if Entonox is found to be ineffective it is useless to offer pethidine. Pethidine is not recommended but is available for labour analgesia. It causes neonatal respiratory depression which is most severe if pethidine is given 3-5 hours prior to delivery but the depression is only slight if pethidine is given within an hour of delivery. Epidural analgesia in labour, whilst it has some short-term maternal side effects, when compared to systemic analgesia is shown to be consistently beneficial in terms of not only Apgar score but also of acid-base status and is less likely to impair breast feeding. Epidural analgesia is associated with maternal pyrexia but this does not appear to be of any consequence to the neonate because if it were there would be an increased incidence of fetal acidosis after epidural analgesia in labour whereas in reality the reverse is true⁶.

Coagulation in pregnancy
Pregnancy is associated with physiological changes that include an increase in the majority of clotting factors and a decrease in natural anticoagulants and a reduction in fibrinolytic activity. The mother becomes hypercoagulable and risks thromboembolism. The changes reverse to normal about 4 weeks post-partum. Pregnancy can induce changes in platelet numbers and function which can complicate the provision of regional analgesia and anaesthesia. Most practitioners will perform regional anaesthesia if the platelet count is above 80 x 109/l if the trend of platelet function is stable⁷. The use of low dose heparin is becoming more common and often decisions about the provision of regional anaesthesia are difficult. Normally the following rules are utilised:

• Regional anaesthesia should be avoided for 12 hours after a prophylactic dose of LMWH (6 hours after a dose of unfractionated heparin)
• Regional anaesthesia should be avoided for 24 hours after a therapeutic dose of LMWH
• LMWH can be given 2 hours after the placement of a regional block or removal of an epidural catheter. However, many units choose 6 hours to minimise the risk of post-operative haemorrhage.
• Risk/benefit analysis needs to be under taken in most cases.

Pharmacogenetics
Pharmacogenetics is the study of the variability in drug response due to genetic variability. The first observation of this influence was made in the 1950s when the genetic influence of the metabolism of suxamethonium was noted. It has been highlighted recently because of the variability of vasopressor requirement during spinal anaesthesia for caesarean section seems to have a genetically affected response distribution. This response is clearly affected by the ‚²AR genotype and it has been noted that women who are Gly¹⁶ homozygous and those who are heterozygous or homozygous for the Glu27 variant require significantly less vasopressors (ephedrine) for the treatment of hypotension during spinal anaesthesia. These 2 haploids appear to ‘protect’ women from requiring higher doses of vasopressors and these haploids are more likely to occur in Caucasian patients. These differences in the population may explain why a simple recipe approach to treating hypotension after regional anaesthesia is unsuccessful. Genetic differences may also explain why some ethnic groups respond better or are more resistant to blood pressure control in pre-eclampsia⁸.

Analgesic drugs, especially, codeine are also of significance in this sphere. Codeine is metabolised the cytochrome P450 enzymes. The gene coding for this enzyme is polymorphic and there are more than 75 different CYP2D6 alleles which results in a hugely variable enzyme activity which can range from 1 to 200%. The action of codeine varies from each individual. Poor metabolisers do not achieve analgesia whilst they encounter the side effects such as nausea and vomiting. Conversely codeine intoxication can be anticipated with ultra-rapid CYP2D6 metabolism. There is anxiety about codeine being used in breast feeding mothers. A recent FDA warning followed the death of a breast fed 13 day old neonate was issued because the neonate was thought to have died from a morphine overdose as the mother was taking codeine and was a CYP2D6 metaboliser⁹.

Haemorrhage
World-wide, haemorrhage is the biggest cause of maternal death. It is variably defined and loss is always difficult to assess. In England and Wales the Health Care Commission defined ‘significant’ haemorrhage as > 1000 ml and ‘major’ loss as > 2500 ml. The Scottish Confidential Audit of Severe Maternal Morbidity (SCASMM) considered major haemorrhage as a loss of > 2500 ml or a transfusion of 5 or more units or treatment for coagulopathy. It is stating the obvious but obstetric haemorrhage is notoriously difficult to estimate and is normally under-estimated. Recent thinking in the treatment of major haemorrhage of relevance to anaesthetists is to increase the ratio of clotting factors to packed cells to a ratio of 1:2 or even 1:1 to prevent the onset of coagulopathy. Attempts should be made to avoid further precipitant factors which increase disseminated intravascular coagulation such as shock, acidosis and hypothermia. Adjuncts to treatment with surgery and drugs include the use of cell salvage. A cell saver cuts down on donor blood usage and is cost effective but it must be emphasised that salvaged blood has no coagulation factors. Concerns about amniotic fluid embolism and rhesus immunisation problems have been unfounded. Interventional radiology services are now nationally recommended to be available for the use in the management of placenta accrete and praevia and the use of such facilities has proven to be life saving¹⁰.

References

1. Lewis G. The confidential enquiry into maternal and child health (CEMACH). Saving mothers’ lives: reviewing maternal deaths to make motherhood safer – 2003-5. The 7th report on confidential enquiries into maternal deaths in the United Kingdom. London. CEMACH. London: HMSO, 2007.
2. Lucas DN, Yentis SM, Kinsella SM, Holdcroft A, May AE, Wee M, Robinson PN. Urgency of caesarean section: a new classification. Journal of the royal society of Medicine 2000; 93: 346-50.
3. Wong CA. Neurologic deficits and labor analgesia. Regional Anaesthesia and Pain Medicine 2004; 29: 341-51.
4. Reynolds F. Neurologic complications of pregnancy and regional anesthesia. In: Chesnut DH, Polley LS, Tsen LC, Wong CA (editors). Obstetric Anesthesia: Principles and Practice. 4th edition, pp701-26. Philadephia: Elsevier Mosby, 2009.
5. Euser AG, Cipolla MJ. Magnesium sulfate for the treatment of eclampsia. Stroke 2009; 40: 1169-75.
6. Wilson MJA, MacArthur C, Shennan A. The effect of epidural analgesia on breast feeding: analysis of a randomized controlled trial. International Journal of Obstetric Anaesthesia 2009; 18: S7.
7. Burrows RF. Platelet disorders in pregnancy. Current Opinion in Obstetrics and Gynaecology 2001; 13: 115-9.
8. Smiley RM, Blouin JL, Negron M, Landau R. ‚2-adrenoceptor genotype affects vasopressor requirements during spinal anesthesia for caesarean delivery. Anesthesiology 2006; 104: 644-50.
9. Koren G, Cairns J, Chitayat D, Gaedigk A, Leeder SJ. Pharmacogenetics of morphine poisoning in a breastfed neonate of a codeine-prescribed mother. Lancet 2006; 368: 704.
10. Shrivastava V, Nageotte M, Major C. Case-control comparison of caesarean hysterectomy with and without prophylactic placement of intravascular balloon catheters for placenta accrete. American Journal of Obstetrics and Gynecology 2007; 197; 402e1- 402e5.

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