CHILDPROOF CONTAINERS

1132 The

girl was

admitted

to

another

SALICYLATE INTOXICATION CAUSED BY TEETHING OINTMENT

hospital on June 18, 1979,

because of vomiting and respiratory difficulty. Upper airway infection was suspected. The child was given oxygen and ’Soludacortine’. In the evening, flaring of the nostrils was observed and fine moist rales were heard, predominantly in the right

lung base. Ampicillin was prescribed. The chest X-ray revealed pulmonary vascular congestion. During the night, her temperature rose to 38-2°C, polypnoea increased, and rales were heard at both lung bases. The child was transferred to the pxdiatric intensive-care unit at our hospital. On admission she was fully conscious, slightly dehydrated, and apyrexial. There was no cyanosis but there was tachypnoea (56/min) with prolongation of the expiratory phase of respiration. Arterial blood-pressure was 10 mm Hg, the pulse-rate 150/min, ECG normal except for sinus tachycardia. Diuresis was satisfactory. The diagnosis was bronchopneumonia or non-cardiogenic pulmonary oedema. The child was given oxygen, fluid restriction, and antibiotics. Arterial blood gas analysis revealed: pH 7.09, Pa02 110 mm Hg, PCOz 15 mm Hg, bicarbonate 4 mmol/1. Serum electrolytes (mmol/1) were: Na+ 138, K+ 3-9, Cl- 115. Prothrombintime 12.2 s (control 16.4), thrombin-time 16.2 s (control 19.2). Urine contained ketone bodies. The association of respiratory distress and severe metabolic acidosis suggested salicylate poisoning, and this diagnosis was confirmed by a strongly positive ferric-chloride test for salicylate in the urine and by a blood salicylate of 48 mg/dl. Sodium bicarbonate was added to the treatment, with frusemide intravenously. We could not find out the type of salicylate, its amount, or the time of ingestion but aspirin tablets were available in the child’s home. On the same day (June 19) the patient became more exhausted and less conscious, with widespread shadows in both lungs but no heart enlargement. She required intubation and positive-pressure ventilation, and over the next 16 h she seemed to improve. The serum bicarbonate returned to normal and the serum salicylate fell to 25-2mg/dl. However, 24 h after admission (June 20, 2 A.M.) severe hypoxaemia (Pa02 31 mm Hg) and hypercapnia (60 mm Hg) developed. A chest X-ray revealed almost confluent patchy infiltrates in both lungs. Severe fluid restriction was instituted and albumin was infused. The bronchospasm was intense. Pulmonary opacification was total. The child died after three cardiac arrests. All cultures of tracheal aspirates, blood, and urine showed no pathogens. Post mortem lung studies showed alveolar oedema with hyaline membranes and intracapillary fibrinous thrombi. Over an eight-year period sixteen children have been admitted for acute salicylate poisoning to this hospital. The serum salicylate on admission ranged from 22 to 100 mg/dl or from 33 to 141 mg/dl when extrapolated to time zero. All but one survived on conservative treatment. The only fatal case was this 26-month-old girl who ingested an unknown number of aspirin tablets. The clinical findings and the chest X-ray revealed severe, progressive pulmonary oedema. The child had no history of heart-disease, ECG on admission was normal, and there was no evidence of congestive cardiac failure. Overhydration cannot have been a precipitating factor because fluid restriction was started early and laboratory data, weight, and fluid balance records ruled out fluid overload. Besides the usual metabolic disturbances associated with salicylate poisoning in young children, there was evidence of blood hypercoagu-

SIR,-A 21-month-old boy was admitted on July 29, 1979. On the day before his admission he had been reluctant to take his foods: he became very drowsy that evening and was semiconscious by the morning of admission. He was apyrexial and dehydrated; respiration 50/min and pulse 150/min; chest and cardiovascular system were otherwise normal, and there was no CNS abnormality. White cell count 34 000/ml (neutrophils 64%, lymphocytes 34%, monocytes 2%); haemoglobin 12.2 g/dl; platelet count 400 000/_l; serum sodium 138, potassium 4.3, chloride 108, bicarbonate 10 mmol/1 and urea 9.5 mmol/1 (57 mg/dl). Cerebrospinal fluid showed no white cells, no organisms, and was sterile on culture. Blood sugar 4 mmol/1 (72 mg/dl). Urine negative for sugar and protein, strongly positive for ketones but negative to ’Phenistix’. Serum salicylate 380 mg/1. He was treated with intravenous fluids and forced alkaline diuresis and recovered within 48 h. After establishing the diagnosis we questioned the mother more closely. The patient was the first child of a 46-year-old woman. The parents claimed that there was no aspirin or other analgesic in the house, but the mother did mention that her son had had "trouble with his teeth" for 48 h before the onset of symptoms. She had rubbed ’Bonjela’ teething ointment on his gums several times a day and had used up three tubes in this time. She had bought the tubes over the counter but had not read the instructions which came with the ointment.

Bonjela is presented in 10 g tubes containing 8-7% choline salicylate; each tube therefore contains 870 mg of choline salicylate (equivalent to 600 mg aspirin). This child had therefore ingested over 2-5’ g of aspirin in 48 h. The box contains instructions "to keep all medicines away from children" and "not to exceed the stated application". Dosage of one application 3 hourly allows for about one third of a tube (200 mg aspirin) to be used in 24 h. Although the detailed instructions within the box explain that there is aspirin in the ointment, this is not made clear on the box or where it will be best seen and noted. Department of Pædiatrics, Newcastle General Hospital, Newcastle upon Tyne NE4 6BE

and

severe

hypoxxmia

with

hypercapnia. Lung

tissue

obtained after death showed changes suggestive of "shock lung". In this case, the oedema could have been caused by salicylate : salicylates increase fluid and protein permeability in the pulmonary vascular bed. The hypercoagulability could have been an additional precipitating factor. We thank Prof. H. L. Vis for his supervision. Pædiatric Intensive Care Unit,

Department of Pædiatrics, Hôpital Universitaire Saint-Pierre, B-1000 Bruxelles, Belgium

A. KAHN D. BLUM

the outside of the tube,

ARTHUR S. PAYNTER FRASER W. ALEXANDER

CHILDPROOF CONTAINERS

-

lability

on

SiR,—Dr Sibert and his colleagues describe the efficacy of childproof containers for medicines (Sept. 8, p. 522). Unfortunately, the British Standards Institution recommends that childproof containers must not be tested on children who have ever themselves been accidentally poisoned. This might exclude children most likely to succeed in opening the containers,

so

I have done tests

on

children admitted after acciden-

tally ingestion of medicines. followed BSI DD30 (1973) recommendations. The child the container, in the parents’ presence, for 5 min; he or she was shown (with parental consent) how to open it once, and was given a further 5 min to try again. 30 children were tested; three childproof containers (’Pop Lok’, ’Clic Loc’, and ’Snap safe’) as well as the ’Securitainer’ were used. Eight different blister packs were also tried. The children were offered the containers in a random order and the same containers were used each time to assess their robustness. Most of the children were aged 3-5 years, though the age range was 18 months to 8 years. 3 children tested had given medicine to younger siblings after opening the containers. The

was

tests

given

The securitainers proved as easy to open as a conventional screw-top bottle; almost all of the children opened them without being shown. Some 20 children managed to open the blister-packs and extract a tablet, usually within 20 s. Children under 2 years were not successful. The inclusion of perforations slowed some children down but only by 10 or 15 s. Foil-wrapped tablets

1133 seemed even easier to open. 6 children had been admitted to the ward having taken potentially dangerous quantities of medicine wrapped in blister packs. The pop lok was successfully opened by 12 children over the age of 3. It became progressively less childproof as the study proceeded, cracking easily (only the plastic version container was tested) under the strain of strong children’s teeth and had to be replaced after 22 tests. Four mothers failed to close it safely. The snap safe is manufactured in various sizes. Large diameter containers (>30 mm) proved too much for all but 5 children tested; all were over the age of 4 and used their teeth to prise the lid off. The small lid could be removed by 19 children, either by random turning until the lid came off or by biting it off. The clic loc proved childproof in all the children tested, even when they were shown how to open it. Despite teeth marks around the cap it functioned well throughout the test.

When thirty-six pharmaceutical companies supplying medicines to be consumed by the public were questioned about their packaging policy, only four replied that they routinely packaged their drugs in childproof containers. Twenty-three packaged some in blister packs and nine used no form of deterrent at all. My findings suggest that all containers passing the BSI DD30 are not equally childproof, and that Sibert’s results may not be reproducible elsewhere where another type of container might be more popular. Unit packaging seems to be a poor means of preventing child poisoning though obviously it is better than an ordinary screw-top bottle. I apologise for the lack of numerical data; some of my figures were accidentally incinerated. I thank the pharmaceutical companies for their samples and helpful advice. Royal Hospital for Glasgow G3 8SJ

Sick

YEAR OF THE CHILD: LOOK AT KERALA

SIR,-One important index of the health of the community and of the child is the infant mortality rate (IMR). This is less than 20 per 1000 live births in most Western countries but rates in eighty-one developing countries in 1970 ranged from 19 to 200 per 1000.’ In 64% of the countries the rates exceeded 100, and in about 30% the rates exceeded 140. Such high rates were recorded in Western countries over a century ago. Some developing countries (Fiji, Hongkong, Jamaica, Puerto Rico, Taiwan, Trinidad and Tobago, Singapore) do now have IMRs at Western levels, but in much of the developing world this goal must seem formidable. Some hope comes from the State of Kerala in South-Western India. The table shows mean values for IMRs computed from results published for India’s seventeen States.2 India’s IMR is very high (130), but inter-State rates in the rural areas range from 56 in Kerala to 165 in Uttar Pradesh, and in the urban areas they range from 40 in Kerala to 131 in Gujarat. The IMR in the rural areas is 50% higher than that in the urban areas but in the two States bordering the Himalayas (Himachal Pradesh, Jammu and Kashmir) the rural rate is double the urban rate. MEAN INFANT MORTALITY RATES

RURAL AND URBAN AREAS OF

(PER 1000 17

LIVE BIRTHS FOR

STATES IN INDIA

1970)

Children,

T. V. STANLEY

DECLINE IN HYPERNATRÆMIA

SIR,-Professor Arneil and Dr Chin (Oct. 20, p. 840) report dramatic reduction in mortality and morbidity from hypernatrxmia in young Glasgow infants and attribute this to the switch from high-solute milks following the DHSS report Present-Day Practice in Infant Feeding. They state that reports of the effects of the widespread use of lower-solute milks on the prevalence of hypernatroemic illness are largely lacking, yet as long ago as 1977 a decline in hypernatraemia was reported at the Queen Elizabeth Hospital for Children’ and in 1978 this observation was extended.2 Such a decline was also reported from Leicester in 1977,3 and this year most convincingly of all by Sunderland and Emery,’ who described the apparent disappearance of hypernatrxmic dehydration as a cause of infant death from Sheffield. Thus there is no lack of reports from south of the border of this dramatic and exciting observation. It is clear that warnings4°5 concerning the dangers of overconcentrating feeds coupled with promotion of breast feeding, as well as the widespread use of low-solute milks since 1975, have reduced the incidence of hypernatraemia, especially in infants with gastroenteritis, throughout Britain and so further reduced mortality of infantile gastroenteritis. a

Academic Department of Child Health, Queen Elizabeth Hospital for Children, London E2 8PS

Kerala, with a population of over 20 million, has thus achieved a good health status, an achievement that is doubly commendable because this State has the highest population density In India (549 persons per km2; inter-State range 62-549). Kerala has a very high literacy rate (60%), far above that.of other States in India (range 19—60%); second highest Tami Nadu 40%). Many other factors contribute to the lowering of IMRs. Funding is important to combat malnutrition and deprivation but by itself this does not seem to be the answer. In oil-rich Iran, with a per caput gross national productof $US1500, infant mortality is 140 per 1000; in Sri Lanka ($235) it is 50. Again the role of education appears vital; the literacyrate in Sri Lanka is 80%. The attainment of the Alma-Ata goal of health for all by the year 2000 demands battles on many fronts. The answers to some of the vital questions may lie in Kerala, and epidemiological investigations should be mounted to find out why Kerala is so very different in health status from the rest of India. Department of Medical Statistics, Welsh National School of Medicine, Cardiff CF4 4XN

MEASLES MORTALITY IN RWANDA

J. A. WALKER-SMITH P. D. MANUEL

to December, 1978, measles was the of admission to the paediatric department of the Centre Hospitalier de Kigali (C.H.K.) in Rwanda. Measles accounted for 30-40% of total admissions and the case fatality rate was about 20% (table I).

SIR,-From July, 1975,

most

1. Whaley P, Walker-Smith JA. Hypernatræmia and gastroenteritis. Lancet 1977;i: 51-52. 2. Manuel PD, Walker-Smith JA. Infant feeding practice. Br Med J 1978; ii: 705. 3. Davies DP, Ansari BM, Mandal BK. Hypernatræmia and gastroenteritis. Lancet 1977; i: 252. 4. Sunderland R, Emery JL. Apparent disappearance of hypernatræmic dehydration from infant deaths in Sheffield. Br Med J 1979; ii: 575-77. 5. Oates RK. Infant feeding practices. Br Med J 1973; ii: 762-64.

T. KHOSLA

frequent

cause

1. Nortman DL, Hofstatter E. Population and family planning programs, 9th ed. New York: Population Council, 1978. 2. Health Statistics of India. New Delhi: Ministry of Health and Family Plan-

ning, 1976.