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The girl was admitted to another hospital on June 18, 1979,because of vomiting and respiratory difficulty. Upper airwayinfection was suspected. The child was given oxygen and ’Solu-dacortine’. In the evening, flaring of the nostrils was observedand fine moist rales were heard, predominantly in the rightlung base. Ampicillin was prescribed. The chest X-ray revealedpulmonary vascular congestion. During the night, her tem-perature rose to 38-2°C, polypnoea increased, and rales wereheard 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 butthere was tachypnoea (56/min) with prolongation of the ex-piratory phase of respiration. Arterial blood-pressure was 10mm Hg, the pulse-rate 150/min, ECG normal except for sinustachycardia. Diuresis was satisfactory. The diagnosis wasbronchopneumonia or non-cardiogenic pulmonary oedema.The child was given oxygen, fluid restriction, and antibiotics.Arterial blood gas analysis revealed: pH 7.09, Pa02 110 mmHg, PCOz 15 mm Hg, bicarbonate 4 mmol/1. Serum electro-lytes (mmol/1) were: Na+ 138, K+ 3-9, Cl- 115. Prothrombin-time 12.2 s (control 16.4), thrombin-time 16.2 s (control19.2). Urine contained ketone bodies. The association of res-piratory distress and severe metabolic acidosis suggested salicy-late poisoning, and this diagnosis was confirmed by a stronglypositive ferric-chloride test for salicylate in the urine and by ablood salicylate of 48 mg/dl. Sodium bicarbonate was added tothe 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 thechild’s home.On the same day (June 19) the patient became more

exhausted and less conscious, with widespread shadows in bothlungs but no heart enlargement. She required intubation andpositive-pressure ventilation, and over the next 16 h sheseemed to improve. The serum bicarbonate returned to normaland the serum salicylate fell to 25-2 mg/dl. However, 24 hafter admission (June 20, 2 A.M.) severe hypoxaemia (Pa02 31mm Hg) and hypercapnia (60 mm Hg) developed. A chestX-ray revealed almost confluent patchy infiltrates in both

lungs. Severe fluid restriction was instituted and albumin wasinfused. The bronchospasm was intense. Pulmonary opacifica-tion was total. The child died after three cardiac arrests.

All cultures of tracheal aspirates, blood, and urine showedno pathogens. Post mortem lung studies showed alveolaroedema with hyaline membranes and intracapillary fibrinousthrombi.

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Over an eight-year period sixteen children have been admit-ted for acute salicylate poisoning to this hospital. The serumsalicylate on admission ranged from 22 to 100 mg/dl or from33 to 141 mg/dl when extrapolated to time zero. All but onesurvived on conservative treatment. The only fatal case wasthis 26-month-old girl who ingested an unknown number ofaspirin tablets. The clinical findings and the chest X-rayrevealed severe, progressive pulmonary oedema. The child hadno history of heart-disease, ECG on admission was normal,and there was no evidence of congestive cardiac failure. Over-hydration cannot have been a precipitating factor becausefluid restriction was started early and laboratory data, weight,and fluid balance records ruled out fluid overload. Besides theusual metabolic disturbances associated with salicylate poison-ing in young children, there was evidence of blood hypercoagu-lability and severe hypoxxmia with hypercapnia. Lung tissueobtained after death showed changes suggestive of "shocklung". In this case, the oedema could have been caused by sali-cylate : salicylates increase fluid and protein permeability in thepulmonary vascular bed. The hypercoagulability could havebeen 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. KAHND. BLUM

SALICYLATE INTOXICATION CAUSED BYTEETHING OINTMENT

SIR,-A 21-month-old boy was admitted on July 29, 1979.On the day before his admission he had been reluctant to takehis foods: he became very drowsy that evening and was semi-conscious by the morning of admission. He was apyrexial anddehydrated; respiration 50/min and pulse 150/min; chest andcardiovascular system were otherwise normal, and there wasno CNS abnormality. White cell count 34 000/ml (neutrophils64%, lymphocytes 34%, monocytes 2%); haemoglobin 12.2

g/dl; platelet count 400 000/_l; serum sodium 138, potassium4.3, chloride 108, bicarbonate 10 mmol/1 and urea 9.5 mmol/1(57 mg/dl). Cerebrospinal fluid showed no white cells, noorganisms, and was sterile on culture. Blood sugar 4 mmol/1(72 mg/dl). Urine negative for sugar and protein, strongly posi-tive for ketones but negative to ’Phenistix’. Serum salicylate380 mg/1. He was treated with intravenous fluids and forcedalkaline diuresis and recovered within 48 h.

After establishing the diagnosis we questioned the mothermore closely. The patient was the first child of a 46-year-oldwoman. The parents claimed that there was no aspirin orother analgesic in the house, but the mother did mention thather son had had "trouble with his teeth" for 48 h before theonset of symptoms. She had rubbed ’Bonjela’ teething oint-ment on his gums several times a day and had used up threetubes in this time. She had bought the tubes over the counterbut had not read the instructions which came with the oint-ment.

Bonjela is presented in 10 g tubes containing 8-7% cholinesalicylate; each tube therefore contains 870 mg of choline sali-cylate (equivalent to 600 mg aspirin). This child had thereforeingested over 2-5’ g of aspirin in 48 h. The box contains in-structions "to keep all medicines away from children" and"not to exceed the stated application". Dosage of one appli-cation 3 hourly allows for about one third of a tube (200 mgaspirin) to be used in 24 h. Although the detailed instructionswithin the box explain that there is aspirin in the ointment,this is not made clear on the box or on the outside of the tube,where it will be best seen and noted.

Department of Pædiatrics,Newcastle General Hospital,Newcastle upon Tyne NE4 6BE

ARTHUR S. PAYNTERFRASER W. ALEXANDER

CHILDPROOF CONTAINERS

SiR,—Dr Sibert and his colleagues describe the efficacy ofchildproof containers for medicines (Sept. 8, p. 522). Unfor-tunately, the British Standards Institution recommends thatchildproof containers must not be tested on children who haveever themselves been accidentally poisoned. This mightexclude children most likely to succeed in opening the con-tainers, so I have done tests on children admitted after acciden-tally ingestion of medicines.The tests followed BSI DD30 (1973) recommendations. The child

was given the container, in the parents’ presence, for 5 min; he or shewas shown (with parental consent) how to open it once, and was givena 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 offeredthe containers in a random order and the same containers were usedeach time to assess their robustness. Most of the children were aged3-5 years, though the age range was 18 months to 8 years. 3 childrentested had given medicine to younger siblings after opening the con-tainers.The securitainers proved as easy to open as a conventional

screw-top bottle; almost all of the children opened them with-out being shown.

Some 20 children managed to open the blister-packs andextract a tablet, usually within 20 s. Children under 2 yearswere not successful. The inclusion of perforations slowed somechildren down but only by 10 or 15 s. Foil-wrapped tablets