A CONFUSED TEENAGER
History
Jake is a 13-year-old boy referred to the A&E department by his GP with a sudden change in behaviour. The previous day he complained of tiredness, but had been playing a lot of football with his friends and training at a club. He watched television during the evening and apparently slept well. The morning of the admission he had been quieter than usual but had gone to school. His mother was phoned to say that his behaviour was very out of character; he was refusing to obey commands and looked ‘spaced out’. At home Jake seemed unable to perform simple tasks such as changing his clothes, putting on his pyjamas rather than his shorts. He then became rather jumpy and nervous. He denies any headache and there have been no abnormal movements witnessed. He has had no diarrhoea or vomiting. Jake has no significant past medical history. His older brother has epilepsy, which is well controlled with lamotrigine. Jake struggles at school, needing extra help with literacy and maths. There were some minor behaviour problems in his junior school but nothing since.
Examination
Jake looks generally well. His height is on the 91st centile and his weight is on the 75th centile. He is afebrile. His pulse is 88 beats/min and his blood pressure is 110/75 mmHg. Examination of the cardiovascular, respiratory and abdominal systems is unremarkable. There is no meningism. When asked, he does not know the day of the week, which town the hospital is in, or his birthday. He cannot remember the name of his favourite football club. He becomes agitated and aggressive when being questioned and is very slow to answer. Both pupils appear dilated and have a slightly sluggish response to light. He is uncooperative with attempts at fundoscopy. There are no obvious focal neurological signs but he cannot understand the instructions for the tests of cerebellar function, e.g. finger–nose test. His gait is normal.
Questions
• What further history should you specifically obtain?
• What other investigations would you request and why?
Medicine
This previously healthy teenage boy has developed an acute confusional state. One of the most obvious causes is drug ingestion, either recreational or a deliberate overdose, possibly with his brother’s lamotrigine. It is important to ask the family specific questions. Has he been out of their sight? Are there any other drugs in the house? If necessary, send them home to check and make sure none are missing. Phone the school and his friends. All these steps could be life-saving. A urine screen for ‘drugs of abuse’ and toxicology, including lamotrigine, should be requested but the result will take some time. However, never jump to conclusions – there are numerous other possibilities. With an acute history, metabolic problems are unlikely although they must be excluded. Hyponatraemia could be due to inappropriate antidiuretic hormone secretion following an unreported head injury. Hypercalcaemia and renal failure are likely to have a more insidious onset and other symptoms, such as tiredness. Thyroid disease is a possibility. Thyrotoxicosis can present with an isolated behaviour disturbance such as school phobia. At this age, a previously undiagnosed inborn error of metabolism is unlikely but is certainly possible, especially in a child with learning difficulties. Measure blood sugar (bedside and laboratory), a venous pH, lactate and ammonia. Keep urine for amino and organic acid analysis. Ask the laboratory to keep any spare blood in case it is needed for future analysis. Most will do so for up to 6 months. Even in the absence of clinical signs, bacterial and viral infections are possible diagnoses. They are also treatable. Send a full blood count, C-reactive protein, blood cultures, a midstream urine and acute viral titres. If indicated, convalescent titres can be sent 10–14 days later. It is safest to start treatment with broad-spectrum antibiotics, e.g. cefotaxime, and aciclovir. A lumbar puncture is currently contraindicated because he is very confused and raised intracranial pressure cannot be excluded. It may be indicated once he has improved. An acute neurological event must also be excluded, including seizures and migraine. He merits an urgent CT and/or a MRI scan and an EEG. This boy’s EEG the following day showed generalized bursts of spike and slow-wave activity with a frontotemporal emphasis. He recovered within 24 hours but went on to have further similar episodes of confusion, culminating in a generalized seizure. The final diagnosis was complex partial epilepsy with secondary generalization. He responded very well to anticonvulsants.
KEY POINTS
• Do everything possible to identify any drug that a child might have taken inadvertently or deliberately. It might save their life.
• Never assume that an acute confusional state is due to drug ingestion at any age.
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