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accomplished intermittently for 20 min. Three hours later her mental state abruptly returned to normal. She had patchy recall of events during her acute confusional state. Repeat blood samples taken 5 h later, after a diuresis of 2.5 L, showed [Na+] 121 mmol/L, serum osmolality 261 mOsmol/ kg and normal blood gases. After 24 h and a diuresis of a further 6.5 L, [Na+] had returned to 135 mmol/L at which point fluid restriction was stopped. Retrospective estimation of her oral fluid intake suggested that she had consumed in excess of 10 L of water and sports drink during her labour, which had lasted approximately 10 h. She suffered no long-term neurological consequences. Hyponatraemia in our patient resulted from an excess oral intake of water. The transient syndrome of inappropriate antidiuretic hormone secretion in pregnancy presented by Wilson and Shutt1 differs from events in our patient in that she excreted large volumes of dilute urine (an appropriate response to an excess water intake) whereas their patient excreted a small volume of concentrated urine (due to the inappropriate ADH secretion). Our patient had not received intravenous fluids until immediately before delivery, nor had she received exogenous oxytocics to augment labour. An extrarenal cause for her water intoxication was supported by a low (<5 mmol/L) urinary sodium concentration and a history of excess fluid intake; unfortunately the tonicity of the sports drink was not recorded. Only one prospective examination of use of sports drinks in labour exists. It reported serum ketone and glucose concentrations, and residual gastric fluid volumes, but did not examine the difference in serum sodium between groups consuming sports drinks and plain water.2 Our patient's hyperventilation remains unexplained, but may be associated with a psychogenic cause for polydipsia. Several case reports of hyponatraemia in the peripartum period exist.37 Although thought to be rare, it can lead to convulsions and is potentially fatal.8 Women in labour are commonly encouraged to drink. Pregnant women retain fluid at term, usually in excess of 6 L, because osmotic thresholds that normally control thirst and vasopressin release are reset,9 leading to a fall in plasma osmolality. An excessive intake of water without solute in labour will further lower serum osmolality and may cause serum sodium concentrations to fall below 120 mmol/L, which is considered the critical level at which symptoms may occur.10 Fluid balance charts are not routinely kept for women in labour on the FBU and polydipsia might have gone unrecognised but for the development of neuropsychiatric symptoms that prompted further investigations. This leads us to question whether water intoxication may be more common than is generally supposed. If that is the case, how much water is safe? Andrew Green Registrar in Anaesthesia Philip Popham Senior Principal Anaesthetist, Department of Anaesthesia, Royal Women's Hospital, Carlton, Australia

R E F E R E N C E S

1. Wilson H, Shutt L. Syndrome of inappropriate ADH secretion in a woman with pre-eclampsia. Int J Obstet Anesth 2007; 16: 3602. 2. Kubli M, Scrutton M J, Seed P T, O'Sullivan G. An evaluation of isotonic sport drinks during labor. Anesth Analg 2002; 94: 4048. 3. Goodner D M, Arnas G M, Andros G J, Waterhouse R B. Psychogenic polydipsia causing acute water intoxication in pregnancy at term. A case report. Obstet Gynecol 1971; 37: 8736. 4. Graham K, Palmer J. Severe hyponatraemia as a result of primary polydipsia in labour. Aust N Z J Obstet Gynaecol 2004; 44: 5867. 5. Johansson S, Lindow S, Kapadia H, Norman M. Perinatal water intoxication due to excessive oral intake during labour. Acta Paediatr 2002; 91: 8114. 6. Lurie S, Feinstein M, Mamet Y. Symptomatic hyponatremia following cesarean section. J Matern Fetal Neonatal Med 2002; 11: 1389. 7. Paech M J. Convulsions in a healthy parturient due to intrapartum water intoxication. Int J Obstet Anesth 1998; 7: 5961. 8. Siragy H M. Hyponatremia, fluid-electrolyte disorders, and the syndrome of inappropriate antidiuretic hormone secretion: diagnosis and treatment options. Endocr Pract 2006; 12: 44657. 9. Lindheimer M D, Davison J M. Osmoregulation, the secretion of arginine vasopressin and its metabolism during pregnancy. Eur J Endocrinol 1995; 132: 13343. 10. Swales J. Management of hyponatraemia. Br J Anaesth 1991; 67: 146153.

2007 Published by Elsevier Ltd. doi:10.1016/j.ijoa.2007.09.002

Epistaxis in pregnancy not to be sniffed at!

We would like to present a rare, but potentially life-threatening cause of haemorrhage in pregnancy. A 37-year-old woman at 26 weeks of gestation (G2, P1) was admitted to her local hospital with spontaneous epistaxis. She was treated with nasal packing and intravenous fluids, but continued to bleed over the next 48 h and was referred to our hospital for definitive surgical management. At preoperative assessment she complained of lethargy, but reconciled this with her inability to sleep the previous night due to discomfort from the nasal packs. She had a tachycardia of 110 beats/min, her blood pressure was 110/60 mmHg and capillary refill time was <2 s. Her laboratory-measured haemoglobin (Hb) concentration was 7.1 g/dL, having been 10.6 g/dL 48 h earlier. She was seen by the obstetric team. The fetal heart trace was reassuring. Steroids were not given because there was no indication for delivery. She received ranitidine, sodium citrate and 2 L of intravenous fluids and was transferred immediately to the operating theatre. She was placed supine with left lateral tilt and anaesthesia induced using a rapid sequence technique. Unfortunately, removal of the nasal packs produced brisk arterial bleeding from what turned out to be the sphenopalatine and anterior ethmoidal arteries, prompting a further Hb estimation. The initial reading, measured using a HemoCue near-patient testing device (Hemoscope

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Ltd, Derbyshire UK), was 1.1 g/dL (manufacturer's reference range of 0-25.6 g/dL1). She received a rapid transfusion of a unit of allogeneic red cell concentrate (RCC) after which blood analysis was repeated. Formal laboratory and HemoCue measurements at that time were identical at 5.5 g/dL and the coagulation screen was normal. She remained cardiovascularly stable and received a total of four units of RCC intraoperatively after which her Hb concentration was 9.5 g/dL. The arterial bleed did not respond to initial electrocautery and was eventually controlled by ligation of the offending vessels. She was discharged home on the fourth postoperative day, having been regularly reviewed by the obstetric team. There were no further complications and she gave birth to a healthy baby girl by vaginal delivery eight weeks later. Although we suspected that the patient had bled significantly more than her cardiovascular parameters suggested, we did not expect such a low intraoperative Hb concentration. Our first opportunity to check the Hb was in the operating theatre using the HemoCue device. This device was available in the ENT theatre only because we were conducting a validation study on its accuracy. We accept that, if the first HemoCue reading of 1.1 g/dL were accurate, the level would not be expected to rise to 5.5 g/dL after one unit of RCC, or to 9.5 g/dL after a further four units. The initial reading may, therefore, reflect a combination of sampling error and acute haemodilution after fluid resuscitation. Nevertheless, the decision to use the near patient testing device alerted us to the fact that this patient had developed a life-threatening anaemia. Fortunately, the HemoCue device guided our transfusion practice and we believe it averted a potentially disastrous outcome for mother and baby. Epistaxis in pregnancy is common but the vast majority of cases do not require medical attention. Severe epistaxis leading to maternal and fetal compromise is rare; a literature search revealed only three published reports of life-threatening epistaxis in the past forty years.24 The extent of our patient's blood loss was difficult to quantify due to effective cardiovascular compensation of pregnancy. In accordance with the Confidential Enquiry into Maternal Deaths, we run regular obstetric fire drills in our labour suite, obstetric ward and accident and emergency department to ensure multidisciplinary teams are able to respond appropriately to obstetric emergencies, including major haemorrhage.5 In response to the lessons learnt in this case, we are planning to extend the drills to general wards, which have only occasional responsibility for pregnant women. In addition, we have introduced an ongoing staff training programme to increase awareness and competent use of the HemoCue device for rapid estimation of Hb concentrations in emergency situations. J.J. Hardy, C.M. Connolly, C.J. Weir Department of Anaesthesia, Ninewells Hospital and Medical School, Dundee, UK E-mail: jjhardy@doctors.org.uk

R E F E R E N C E S

1. http://www.hemocue.com/index.php?page=2054. Accessed 31/05/2007 2. Cooley S M, Geary M, O'Connell M P, Keane D P. Hypovolaemic shock secondary to epistaxis in pregnancy. J Obstet Gynaecol 2002; 22: 22930. 3. Green L K, Green R S, Harris R E. Life-threatening epistaxis associated with pregnancy. Am J Obstet Gynecol 1974; 120: 11134. 4. Braithwaite J M, Economides D L. Severe recurrent epistaxis causing antepartum fetal distress. Int J Gynaecol Obstet 1995; 50: 1978. 5. Why Mothers Die 2000-2002. The Sixth Report on Confidential Enquiries into Maternal Deaths in the United Kingdom. London: RCOG Press; 2004.

2007 Published by Elsevier Ltd. doi:10.1016/j.ijoa.2007.09.003

Post caesarean delivery pain management: do not dismiss pethidine

I agree with the main thrust of the editorial by Peter Pan on the importance of a multimodal approach to post-caesarean analgesia.1 He correctly asserts that the neuraxial approach provides superior pain control compared with systemic administration of opioids. Different opioids are discussed along with the advantages of the epidural and intrathecal routes. Intrathecal morphine is described in some detail although no mention is made of the high incidence of adverse effects such as nausea, vomiting and pruritus, which are dose related. Diamorphine is also favourably described although it is only available for clinical use in the UK and Hong Kong. Epidural pethidine (meperidine) is given only brief mention. It is stated that it possesses some local anaesthetic properties, which cause undesirable motor blockade and reduced mobilisation. No evidence is given to support this suggestion. While pethidine has local anaesthetic properties, it does not produce motor block in doses used clinically. Norpethidine toxicity has not been reported in patients receiving epidural pethidine, which is probably related to low dose requirements and relatively brief use. The use of epidural pethidine was first described in 1979 by Cousins et al. for relief of chronic and postoperative pain in patients with cancer.2 Brownridge subsequently reported epidural boluses of pethidine for analgesia in obstetrics.3 Epidural pethidine was reviewed by Ngan Kee in 1998 and its use in obstetric anaesthesia was highlighted.4 It has been used extensively in Australasia for some time by bolus, infusion and PCEA for postoperative analgesia following caesarean section. It compares favourably to epidural and spinal morphine in providing good quality analgesia but with fewer side effects such as respiratory depression, pruritus and nausea and vomiting.5,6 Pethidine appears to have been ignored by the epidural route for some time, especially in the US and UK. I note a previous review of epidural opioid choices over a decade ago made no mention of pethidine,7 prompting a similar letter in response.8