Birthing pools and infection control

of the Finnish type,’ SRNl is the second gene known to be involved in autosomal recessive nephrotic syndrome. These findings will lead to an increasing demand of prenatal diagnosis in near future. At the moment, however, genetic heterogeneity of SRN limits presymptomatic and prenatal diagnosis to large multiplex families. A Fuchshuber, F Janssen, O Gribouval, P Niaudet, A Kamoun, *C Antignac *INSERM U423, Hôpital Necker-Enfants Malades, 75743 Paris, France; Hôpital Universitaire des Enfants, Bruxelles, Belgium; and Hôpital Charles Nicolle, Tunis, Tunisia

1 Fuchschuber A, Jean G, Gribouval O,

et

al.

Mapping

a

gene

(SRN1)

1q25-q31 in idiopathic nephrotic syndrome confirms a distinct entity of autosomal recessive nephrosis. Hum Mol Genet 1995;

to chromosome

11: 2155-58.

2 Dib C, Fauré S, Fizames C, et al. A comprehensive genetic map of the human genome based on 5,264 microsatellites. Nature 1996; 380: 152-54. 3 Kestilä M, Männikkö M, Holmberg C, et al. Congenital nephrotic syndrome of the Finnish type maps to the long arm of chromosome 19. Am J Hum Genet 1994; 54: 757-64.

Iodine-induced thyrotoxicosis SiR-The difficulties

experienced by Bourdox and colleagues

may have resulted from the iodised salt without establishing an appropriate monitoring system to ensure against excessive iodisation, contrary to World Health Organization/United Nations Childrens’ Fund (UNICEF)/International Council for Control of Iodine Deficiency Disorders (ICCID) recommendations. The remarkable success of salt iodisation in effectively correcting iodine deficiency throughout the world represents an unprecedented public health achievement. Nearly 1600 million people were estimated in 1993 to be at risk of iodinedeficiency disorders (IDD).2 By 1996, universal salt iodisation had been adopted in almost all countries earlier identified as having such a public health problem. Undoubtedly, this has resulted in a striking reduction in the global population at risk of the unnecessary consequences of IDD-notably, brain damage, cretinism, mental retardation, and iodine-induced hyperthyroidism (IIH). IIH is transitory and disappears once iodine deficiency has been corrected.3 Every effort should be made to control the condition, including by identification and treatment of those individuals affected. The reported occurrence of IIH in Zimbabwe and Zaire reinforces the need, repeatedly expressed by WHO, UNICEF, and ICCIDD, for monitoring and evaluation. This view is supported by a resolution that the January, 1996, WHO Executive Board recommended should be endorsed by the World Health Assembly in Geneva in May, 1996. UNICEF, WHO, and ICCIDD have provided training, supplies, technical assistance, and laboratory equipment to many countries for the establishment of effective monitoring systems. In addition, guidelines are provided for monitoring

(Feb 24,

p

Clugston, Micheline Beaudry, François Delange

at

of

factory, importation, wholesale, retail, district,

and community levels.4 Finally, a detailed monitoring manual has been produced by the Programme Against Micronutrient Malnutrition (PAMM) and the Micronutrient Initiative, with joint support from the three organisations.5 These groups are assisting countries to establish appropriate systems for monitoring both salt iodisation levels and their

biological impact. Consideration

was given by scientists with wide field in arriving at the suggested levels for salt iodisation under varying conditions of humidity, temperature, and average daily intake-ie, 20-50 parts per

experience

*Graeme

Division of Food and Nutrition, World Health Organisation, Geneva 1211, Switzerland; Nutrition Programme Division, UNICEF, New York, USA; and International Council for Control Iodine Deficiency Disorders, Brussels, Belgium

552)’ in Kivu, Zaire,

introduction

procedures

million (ppm) iodine in salt consumed in households. The recommended levels are similar to those that have been safely and effectively used in North America for over 70 years. Virtually all kitchen and table salt used in Canada, and over 54% of all salt purchased in the USA, is fortified with between 45 and 76 ppm iodine. Over the past 30 years similar iodisation levels were introduced in several countries in Latin America with few, if any, untoward effects being reported. The international organisations are now engaged in a multicentre review of the situation in seven African countries. Results are expected in mid-1996; recommended iodisation levels will be reviewed in light of the scientific evidence. From the inception of the universal salt iodisation programme, WHO, UNICEF, and ICCIDD have always recognised that variations in iodine delivery are possible because of differences in salt quality, per capita consumption, and iodine losses. In fact, one of the main objectives of the programme is to ensure a steady supply of iodine from production to consumption by establishing a monitoring system that will keep this variation to a minimum.

1

2 3

4

5

Bourdox PP, Ermans AM, Mukalay wa Mukalay A, Filetti S, Vigneri R. Iodine-induced thyrotoxicosis in Kivu, Zaire. Lancet 1996; 347: 552-53. WHO/UNICEF/ICCIDD. Global prevalence of iodine deficiency disorders. MDIS Working Paper no 1. Geneva: WHO, 1993. World Health Organization. Iodine and health: eliminating iodine deficiency disorders safely through salt iodization: a statement by the World Health Organization (document WHO/NUT/94.4). Geneva: WHO, 1994. WHO/UNICEF/ICCIDD. Indicators for assessing iodine deficiency disorders and their control through salt iodisation (document WHO/NUT/94.6). Geneva: WHO, 1994. Sullivan KM, Houston R, Gorstein J, Cervinskas J, eds. Monitoring universal salt iodisation programmes. Atlanta, Georgia: PAMM, MI, ICCIDD, 1995.

Birthing pools

and infection control

birthing pool was purchased by this hospital’s department of obstetrics and gynaecology. We were asked, as members of the infection control team, to advise on its use. To develop our own protocols we asked our colleagues in midwifery to obtain guidelines from other hospitals already using this method of delivery. We were surprised to learn that such protocols seemed not to exist. After discussion with colleagues in the neonatal unit, who had expressed concern over the physiological effects of water births on the newborn baby, it was agreed that a formal research proposal be drawn up. This proposal was approved by the ethics committee. The birthing pool is now in use and the research programme is being completed. In any clinical situation, and especially in an experimental one, patients expect doctors to exercise all measures to maintain safety and doctors have a duty to do so. The data available on the microbiological and virological safety of this mode of delivery were unhelpful. In the face of this uncertainty we decided that pregnant women using the pool for delivery must be uninfected by the blood-borne viruses hepatitis B and C and HIV 1 and 2. This decision, particularly the requirement for HIV testing, was received with considerable hostility. Amniotic fluid, blood, and faeces makes contamination of the birthing pool surfaces with large quantities of maternal bacteria and viruses inevitable. Although one would expect SiR-In

1994

a

1051

thorough cleaning to remove that contamination, sterility cannot be guaranteed. This could be crucial if, for example, the next patient required an episotomy while in the pool. We argued that there was a duty of care to ensure that the pools users (and their babies) were exposed to the least risk possible of acquiring a blood-borne virus infection from a previous user. These concerns have recently found substance in the transmission of hepatitis B in an unexpected situation.’ We considered that a birthing pool is likely to be heavily contaminated with infectious material from the mother. In the case of an HIV-infected mother, the water might pose a risk to mother and infant if the infant is also HIV-infected. Where the infant is not infected, it seems illogical to allow the baby to be delivered in the potentially infectious water of a pool. We also wished to protect midwives and other attendants from blood-borne virus infection. It seemed that handling sharp instruments in the environment of the birthing pool would be hazardous and that the central dogma of infection control of blood-borne viruses (containment of blood loss) could not be achieved in

practice. Screening for blood-borne viruses, for purposes of infection control, is not without precedent. Maintenance haemodialysis and organ and tissue donation are prominent examples. Nevertheless we are being criticised for this policy in the professional and lay press and by midwives, patients and pressure groups. The matter is scheduled for discussion national Expert Advisory Group on AIDS. The time has come for an open debate.

by the

Geoffrey L Ridgway, *Richard S Tedder

unpleasant flashbacks

and anxiety symptoms but was otherwise well. The arginine vasopressin and sodium/osmolality levels that indicate vasopressin release was the primary pathogenetic mechanism rather than water intoxication, but it is likely that excess water ingestion, a common practice at raves, contributed to its severity.’ Four less severe cases of ecstasy-induced hyponatraemia have been reported in the UK.24 Arginine vasopressin was not measured in these cases. Otherwise we have found no evidence that drugs of the amphetamine class can cause inappropriate vasopressin secretion in previous reports. It is curious that no cases have been reported in other countries. The effect may be direct or mediated by some other mechanism. Experimental research on the effects of ecstasy is legally and ethically constrained by drug toxicity. Although this may be an unusual reaction, we emphasise the importance of urgent electrolyte estimation together with attention to fluid balance in persons presenting unwell with a history of ecstasy ingestion in order to detect either this or the more common hyperpyrexia syndrome.’ If in doubt, an urgent computed tomogram scan of the head should be done. Hyponatraemia after ecstasy use requires early recognition as the vasopressin level may remain high for some time after ingestion of the drug, leading to worsening hyponatraemia and possible death.

Mary Forsling of the Departments of Obstetrics and Gynaecology and Physiology, United Medical and Dental Schools, London, and Mike Penney of the Royal Gwent Hospital, Newport, Gwent for helpful discussion.

We thank

*Roger Holden, Maurice A Jackson Department of Medicine, New Cross Hospital, Wolverhampton WV10 0QP, UK

*Department of Clinical Microbiology, University College Hospital, London WC1E 6DB, UK

1

Tedder RS, Zuckerman MA, Goldstone AH, et al. Hepatitis B transmission from contaminated cryopreservation tank. Lancet 1995; 346: 137-40.

1

2 3

4

Robson WL, Leung AK. Side effects and complications of treatment with desmopressin for enuresis. J Natl Med Assoc 1994; 86: 775-78. Maxwell DI, Polkey MI, Henry JA. Hyponatraemia and catatonic stupor after taking ecstasy. BMJ 1993; 307: 1339. Satchell SC, Connaughton M. Inappropriate antidiuretic hormone secretion and extreme rises in serum creatine kinase following MDMA ingestion. Br J Hosp Med 1994; 51: 495. Kessel B. Hyponatraemia after ingestion of ecstasy. BMJ 1993; 308: 414.

hyponatraemic coma due to vasopressin over-secretion after "ecstasy" (3,4-MDMA) Near-fatal

SIR-A 20-year-old woman took an ecstasy tablet at a "rave" party. Previously she had used ecstasy without serious adverse effects. She experienced some unpleasant alterations of perception and was encouraged to drink a large quantity of water. She subsequently became stuporose and was incontinent of urine. She may have had a fit. She was taken to hospital. On examination 9 hours after ingestion of the tablet, she was talking unintelligibly and lying prostrate or in a Buddha-like posture with little response to pain or commands. Her pupils were dilated with a diminished light reflex. Pulse, temperature, and blood pressure were normal. Serum sodium concentration was 112 mmol/L (normal range 135-145 mmol/L). Serum osmolality was 238 mosmol/kg. Urine sodium was 112 mmol/L. Urine osmolality was 256 mosmol/kg. Plasma arginine vasopressin was 4-5 pmol/L, which is diagnostic of vasopressin excess in this context. Computed tomographic brain scan showed cerebral oedema. 3,4-methylenedioxymetamphetamine (ecstasy) was detected in urine. The patient was thought to be at imminent risk of coning. She was ventilated to decrease cerebral oedema and given mannitol and dexamethasone intravenously. 24 hours later, serum sodium was 120 mmol/L and she was extubated. By day 4, serum sodium had risen to 131 mmol/L and she had largely recovered. On the follow up 2 months later, she reported 1052

5

Henry JA, Jeffreys KJ, Dawling S. Toxicity and deaths from 3,4-MDMA. Lancet 1992; 340: 384-87.

Gas

cooking

SIR-Jarvis

and

respiratory health in

women

426),’ report that in of gas for cooking is increased risk of respiratory symptoms

and co-workers

(Feb 17,

young women, but not in men, the

p

use

associated with an and impaired lung function. We have also addressed this issue with data for 441 men and 506 women aged 20-44 years, from the Paris and Montpellier centres of the European Community Respiratory Health Survey (ECRHS). We also found no significant relation between gas cooking and respiratory symptoms in men, whereas in women gas with an increased risk of cooking was associated (p<0-05) awakening with shortness of breath), with having asthma, with taking asthma medication (odds ratios 2-1, 3-3, and 4-9 respectively, after adjustment for age, smoking, and town of residence). There was no association between gas cooking and allergy (atopy, IgE, nasal allergies), and the relations between gas cooking and symptoms were similar in atopic and non-atopic women. Jarvis and co-workers did not report any findings about usual cough or phlegm. In our study population, among women gas cooking was associated with increased frequency of usual morning phlegm (OR=1-9, p=004). The relation with usual morning cough was not significant (ORl-5.