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SALICYLATE INTOXICATION CAUSED BY TEETHING OINTMENT
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
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