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Beware CSF pressure measured under general anaesthesia
  1. A Gallagher1,
  2. M Pike2,
  3. S Berg2
  1. 1Worcestershire Royal Hospital, Charles Hastings Way, Worcester WR5 1DD, UK
  2. 2John Radcliffe Hospital, Headley Way, Oxford, UK
  1. Correspondence to:
    Dr A Gallagher
    Worcestershire Royal Hospital, Charles Hastings Way, Worcester WR5 1DD, UK; andrew.gallagherworcsacute.wmids.nhs.uk

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Wraige et al describe three children suffering from idiopathic intracranial hypertension (IIH) in the absence of papilloedema.1 MRI findings in two cases along with an initial symptomatic improvement following lumbar puncture support the diagnosis. In the third case MRI scan was normal and the child’s headaches did not respond to lumbar puncture or acetazolamide. In all three cases CSF pressure was measured under general anaesthesia with control of position and of carbon dioxide concentration, presumably by end-tidal CO2 monitoring. The anaesthetic technique is not reported.

The message that children with IIH may not have papilloedema is a valuable one. However, we would like to add a note of caution regarding the measurement of CSF pressure under general anaesthesia. We have found unexpectedly raised CSF pressure when performing lumbar punctures under sevoflurane anaesthesia, administered to facilitate MRI scanning, in children with a variety of neurological disorders.

All inhalational anaesthetic agents have a cerebral vasodilating action and will increase cerebral blood volume and hence intracranial pressure (ICP). In addition the spontaneously breathing child will sustain an appreciable rise in ICP from the respiratory depressant action of these drugs and consequent hypercarbia. This increase can be prevented by controlled ventilation. Volatile agents may also reduce cerebral perfusion pressure by their hypotensive effect which is due to a combination of systemic vasodilatation and direct myocardial depression; in higher doses cerebral autoregulation may be abolished altogether.2,3

Obstruction to venous return also increases ICP. The flexed position of the anaesthetised child during lumbar puncture may be more marked than when performed without anaesthesia. Coughing and straining at induction of anaesthesia and obstruction to respiration from bronchospasm or the introduction of positive end expiratory pressure (PEEP) will all cause a rise in ICP which may remain a factor at the time of lumbar puncture. Finally, end-tidal CO2 is always lower than arterial CO2 and it is not always possible or desirable to check a blood gas prior to lumbar puncture.

It seems likely that the use of general anaesthesia to facilitate lumbar puncture will increase as deep sedation on paediatric wards becomes less acceptable and increasingly de-skilled paediatricians perform fewer lumbar punctures. We are concerned that children having lumbar puncture under general anaesthesia could be erroneously diagnosed as having intracranial hypertension. Until a standard anaesthetic technique is developed which can be shown to have a minimal effect on intracranial pressure, we believe that measurements of CSF opening pressure under general anaesthesia should be interpreted with caution. If doubt exists, and certainly if surgical treatment is contemplated, insertion of an intracerebral transducer allows definitive measurement of ICP over a period of hours or days.

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