Dear Editor,

Richard Bowker and the Paediatric Accident and Emergency Research Group are to be congratulated on their excellent guideline [1]. It appears comprehensive enough to detect all possible diagnoses while being concise enough to be workable. It does appear vulnerable in the area of poisoning, however.

Carbon monoxide remains the most common cause of fatal poisoning in the UK [2], and should be considered in children presenting to the Emergency Department with a decreased conscious level. Symptoms progress from lethargy, headache and vomiting, to convulsions, coma and cardiovascular collapse [3]. Moreover for every case that comes to the attention of a clinician several may be missed, either because the patient or their carer does not report their vague symptoms or because the physician does not consider the diagnosis [4]. Although not completely sensitive or specific, a carboxyhaemoglobin (COHb) level may provide useful information in the search for a cause of reduced conscious level. COHb may be measured accurately on a venous sample [5] using an automated blood gas analyser.

I therefore recommend the following alteration to the algorithm: In Part III (Identify all problems) “Cause unknown” box, change “consider drug ingestion” to “consider poisoning (including drug ingestion and carbon monoxide exposure)”.

References:

1. Bowker RP, Stephenson TJ, Baumer JH. Evidence-based guideline for the management of decreased conscious level. Arch Dis Child Educ Pract 2006;91:ep115-ep122

2. Parfitt A, Henry JA. Troublesome toxins. Emerg Med J 2002; 19:192-193

3. Skinner D, Swain A, Peyton R, Robertson C (Eds). Cambridge textbook of accident and emergency medicine. Cambridge University Press, Cambridge, UK (1997) page 216

4. Wright J. Chronic and occult carbon monoxide poisoning: we don’t know what we’re missing. Emerg Med J 2002;19:386-390

5. Touger M, Gallagher EJ, Tyrell J. Relationship between venous and arterial carboxyhemoglobin levels in patients with suspected carbon monoxide poisoning. Annals Emergency Med 1995; 25: 481–3

Dear Editor,

In the UK we are presently in the middle of a significant heatwave with July 2006 declared the UK's hottest month on record (1). Both the Department of Health and NHS direct have been quick to disseminate health advice (2) particularly to parents and healthcare workers responsible for the care of children, about the dangers of heat exposure and dehydration. This advice has emphasised the need for adequate fluid intake, particularly that of water. Notably parents have been encouraged to ‘give babies plenty of cooled boiled water throughout the day’ (3) Although we believe this to be sound advice to parents in the majority of situations, we believe it is important for clinicians to be aware of the risks of water intoxication, especially in infants. Water intoxication in children has previously been well described (4) and as being on the increase, if not reaching epidemic proportions in the United States (5). It can cause significant morbidity and mortality from hyponatraemia, brain swelling and seizures. Primarily associated with inappropriate dilution of formula feeds, bottled water has previously been described as a significant cause (6,7). Children are at particular risk as it is thought that as well as renal function being immature, infants have a powerful thirst drive which may impede their ability to curb intake. Bhalla et al reported 4 cases in the UK of hyponatreamic seizures that were secondary to excessive solute ingestion in 1999 (8). As a paediatric intensive care retrieval service we have recently dealt with a previously normal hyponatraemic child presenting with abnormal neurology and seizures. A one-year-old child presented in status epilepticus following a 2 day history of vomiting during which time hypotonic fluids where administered. The child required iv lorazepam and one dose of rectal paraldehyde to terminate the seizure and was intubated, ventilated and transferred to a regional paediatric intensive care unit. Serum sodium on attendance was 116 mmol/L. The child was subsequently fluid restricted for 48 hours. Although we have insufficient evidence at present to implicate water intoxication in their pathogenesis we feel it is an issue that has not been addressed in the current DOH literature. This situation also emphasises the importance of parental education to the potential risks of this conditon.

Dr R M Kayani Retrieval Fellow Dr P Ramnarayan Consultant Paediatric Intensivist Children’s Acute Transport Service, Great Ormond Street Hospital, London

References:

1. Meteorological Office Press Release http://www.meto.gov.uk/corporate/ pressoffice/2006/pr20060801.html

2. ‘ Heatwave’ -A guide to looking after yourself and others during hot weather. Department of Health http://www.dh.gov.uk/assetRoot/ 04/13/53/04/04135304.pdf

3. Department of Health Website - http://www.nhsdirect.nhs.uk/articles/ article.aspx?ArticleId=1955

4. Dugan S, Holliday MA. Water intoxication in two infants following the voluntary ingestion of excessive fluids. Pediatrics 1967;39:418-20.

5. Keating JP,Schears GJ, Dodge PR. Oral water intoxication in infants. An American epidemic. Am J Dis Child. 1991 Sep;145(9):985-90.

6. Bruce RC , Kliegman RM Hyponatremic seizures secondary to oral water intoxication in infancy: association with commercial bottled drinking water. Pediatrics. 1997 Dec;100(6):E4. Review

7. From the Centers for Disease Control and Prevention-Hyponatremic Seizures Among Infants Fed With Commercial Bottled Drinking Water-- Wisconsin, 1993. JAMA 272(13),October 1994, pp 996-997

8. P Bhalla, F E Eaton, J B S Coulter, F L Amegavie, J A Sills and L J Abernethy

Lesson of the week: Hyponatraemic seizures and excessive intake of hypotonic fluids in young children 1999;319;1554-1557 BMJ

Dear Editor,

The recognition of endocrine-related hypernatraemia would be enhanced if account were taken, not only of biochemically overt hypernatraemia(1), but also of the possibility that this biochemical derangement might be masked by co-existing inability to excrete salt-free water. The clinical counterpart of this phenomenon is encapsulated in the statement "the symptoms of cranial diabetes insipidus may be masked by concomitant ACTH deficiency...(since) glucocorticoids are necessary for the kidneys to excrete salt-free water"(2). This scenario has no adverse iatrogenic sequelae if the recognition and treatment of cranial diabetes insipidus antedates replacement therapy for co-existing ACTH deficiency. The danger arises where glucocorticoid replacement therapy is instituted in the face of unsuspected cranial diabetes insipidus because this might be accompanied by a rapid rise in plasma sodium which, in one instance, was a rise from pre-treatment hyponatraemia to post treatment hypernatraemia, with consequent myelinosis(3). Even the use of ACTH for dynamic testing of the hypothalamo/pituitary/adrenal axis may have an unmasking effect, this time by precipitating profound polyuria as was the case in a patient with suspected anterior pituitary failure in whom co-existing cranial diabetes insipidus had not been identified(4). Where the investigators deliberately set out to identify both anterior and posterior pituitary failure in 12 patients with suspected panhypopituitarism. 4 patients in whom unequivocal carnial diabetes insipidus(charcterised by a negligible increase in plasma vasopressin following hypertonic saline infusion) co-existed with ACTH deficiency nevertheless had normal plasma sodium levels(range 140-143 mmol/l)(5). Patients in whom this constellation of parameters is associated with blunted diuresis are the ones most likely to be missed if, as in one study, the co-existence of hypernatraemia and polyuria is relied upon as one of the screening tests for cranial diabetes insipidus(6).

References:

(1) Haycock GB Hypernatraemia:diagnosis and treatment Arch Dis Child 2006:91:ep8-ep13

(2) Bayliss PH and Cheetham T Diabetes insipidus Arch Dis Child 1998:79:84-89

(3)Lasheen I., Doi SAR., Al-Shoumer KAS Glucocorticoid replacement in panyhpopituitarism complicated by myelinosis Medical principles and Practice 2005:14:115-117

(4) Schwartz AR and Leddy AL Recognition of diabetes insipidus in postpartum hypopituitarism Obstetrics and Gynecology 1982:59:394-8

(5) Iwasaki Y., Oiso Y., Yamauchi K., et al Neurohypophyseal function in postpartum hypopituitarism: impaired plasma vasopressin respnse to osmotic stimuli Journal of Clinical Endocrinology and Metabolism 1989:68:560-5

(6) Agha A., Rogers B., Mylotte D., et al Neuroendocrine dysfunction in the acute phase of traumatic brain injury Clinical Endocrinology 2004:60:584-91

Dear Editor,

Williams [1] highlights the key points in the management of inhaled foreign bodies (FB). One of the important points is to request inspiratory and expiratory chest radiographs if FB aspiration is suspected. Because young children are unable to co-operate, paired inspiratory and expiratory films are not always possible. The lateral decubitus film is a useful and convenient method to determine the presence of air trapping [2] as we show in the following case. When the child is placed on his side, the splinting of the dependent hemithorax results in restriction of movement of the thoracic cage on that side and under aeration of the lung while the hemithorax on the opposite side is unrestricted and the lung is well aerated.

A 22 months old, previously healthy, child presented with a 10 days history of cough, and fever. He had not improved after a week’s antibiotic course. A history of foreign body aspiration was not forthcoming. He had low-grade pyrexia, saturation of 91% on air, tachypnoea, mild recessions, reduced air entry on the left hemithorax and no added sounds. A chest x ray (fig 1) showed loss of the right heart border with generalised air space shadowing through out the lung, no midline shift and relatively hyperlucent left lung. On senior review and further direct questioning, possibility of choking on a peanut was elicited. As he was unable to cooperate for an expiratory film, a left lateral decubitus film (fig 2) was performed. This showed over expansion of the left (air trapping in the involved lung making it more hyperlucent despite being in the dependent position) but normally aerated right hemithorax. On a rigid bronchoscopy a peanut was removed piecemeal from the left main bronchus.

Figure 1.

Figure 2.

References:

1.Williams H. Inhaled foreign bodies. Arch Dis Child. Ed. Pract. 2005; 90: ep31-ep33.

2.The lateral decubitus film: an aid in determining Air-trapping in children. Capitanio MA, Kirkpatrick JA. Radiology; 1972:103; 460-462).