Revision of national guidelines for cerebrospinal fluid analysis in suspected subarachnoid haemorrhage

Ann Clin Biochem 2008;45:236-237
doi:10.1258/acb.2008.007256
© 2008 Association for Clinical Biochemistry

 

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Guidelines


Anne M Cruickshank, on behalf of the UK NEQAS Specialist Advisory Group for External Quality Assurance of CSF Proteins and Biochemistry


Department of Biochemistry, Southern General Hospital, Glasgow G51 4TF, UK


Email: anne.cruickshank{at}sgh.scot.nhs.uk


National guidelines for analysis of cerebrospinal fluid (CSF) in suspected subarachnoid haemorrhage (SAH) were published by a UK National External Quality Assessment Scheme (NEQAS) Immunochemistry Working Group in 2003.1 These guidelines provided recommendations on sampling requirements, spectrophotometric analysis and interpretation of results. The same group, having evolved into the UK NEQAS Specialist Advisory Group for External Quality Assessment (EQA) of CSF Proteins and Biochemistry, published in 2007 the results of the audit it conducted into current UK laboratory practice for the biochemical investigation of CSF.2 As a result of the findings of this audit and in the light of experience in the use of the 2003 guidelines, amendments have been made to the original guidelines and the revised guidelines are published in this journal.3

The main aims of the revision are threefold: to ensure thatCSF is always analysed spectrophotometrically if sufficientsample is received; to downgrade the clinical significance ofdetecting small amounts of haemoglobin with no increase in bilirubin;and to emphasize the clinical significance of increased bilirubinwith a visible oxyhaemoglobin absorbance peak irrespective ofCSF protein or serum bilirubin concentrations.

The National Audit of CSF Testing identified 78 laboratories which offered spectrophotometric analysis of CSF either on site or elsewhere.2 Twenty-one of these 78 laboratories rejectedsamples delivered by pneumatic tube, 17 rejected heavily blood-stainedsamples and 14 rejected samples taken outwith sample timingguidelines. These sample rejection policies are indefensiblebecause useful information may be gained from spectrophotometryin all of these circumstances. CSF usually will be blood-stainedfollowing SAH – blood staining does not necessarily reflecta traumatic tap. The detection of increased bilirubin is significantirrespective of the mode of sample delivery or sample timing.Use of pneumatic tube would not be expected to cause false-negativebilirubin results. CSF is precious. Repeat sampling is invasiveand interpretation of any positive results highly problematic.Laboratories are duty bound to analyse any CSF sample if sufficientis received and to interpret the results in the light of allthe available information.

It is the combined experience of the group over several years that the probability of SAH in a patient whose correctly timed CSF sample contains only small amounts of oxyhaemoglobin is vanishingly small. We know of one patient with a posterior communicating artery aneurysm whose CSF sample had a borderline net bilirubin absorbance (0.0067 AU) with a net oxyhaemoglobin absorbance of 0.067 AU. We are aware of no other cases of SAH where the CSF sample had a net oxyhaemoglobin absorbance <0.1 AU and a net bilirubin absorbance 0.007 AU. The reporting comment recommendedin the original guidelines for such samples ‘oxyhaemoglobinon its own has a low predictive value for SAH but does not exclude’confuses and frustrates clinicians. We recommend that it bereplaced by the less ambiguous comment ‘no evidence tosupport SAH’.

In the original guidelines, the recommended interpretation effectivelydowngrades the likelihood of SAH when net bilirubin absorbance>0.007 AU but CSF protein concentration is >1 g/L. The1 g/L cut-off is an arbitrary figure selected in recognitionof the fact that high CSF protein concentrations (and thereforebilirubin absorbances) may reflect alternative pathology suchas meningitis. However, it is important that biochemists realizethat by its nature SAH usually results in a raised CSF proteinconcentration, sometimes >1 g/L. A blood-stained CSF samplewith increased oxyhaemoglobin and bilirubin absorbances andCSF protein concentration >1 g/L is entirely consistent withSAH. For example, of 18 cases of SAH with net bilirubin absorbance>0.007 AU identified in one laboratory last year, five hadCSF protein concentrations >1 g/L. The relevant comment inthe 2003 guidelines for these cases is ‘This finding maybe consistent with: SAH; an increased bilirubin accompanyingthe increased CSF protein; or other sources of CSF blood.’Clinicians do not understand this comment. Our priority shouldbe to alert them to the fact that there is a real possibilitythat a patient has had a SAH, not confuse matters by citingother potential causes of increased CSF bilirubin. The key findingis a net bilirubin absorbance >0.007 AU along with a visibleoxyhaemoglobin peak. We recommend that such findings be reportedas ‘consistent with SAH’, irrespective of CSF proteinconcentration. Conversely, the absence of a visible oxyhaemoglobinpeak suggests that an alternative diagnosis such as meningitisis more likely, and therefore a CSF protein concentration >1g/L should be factored into interpretation along with an increasedserum bilirubin concentration.

(Accepted January 1, 2008)



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References


  1. UK National External Quality Assessment Scheme for Immunochemistry Working Group. National guidelines for the analysis of cerebrospinal fluid for bilirubin in suspected subarachnoid haemorrhage. Ann Clin Biochem 2003;40:481–8[Abstract/Free Full Text]
  2. Holbrook I, Beetham R, Cruickshank A, et al National audit of cerebrospinal fluid testing. Ann Clin Biochem 2007;44:443–8[Abstract/Free Full Text]
  3. Cruickshank A, Auld P, Beetham R, et al Revised national guidelines for the analysis of cerebrospinal fluid for bilirubin in suspected subarachnoid haemorrhage. Ann Clin Biochem 2008;45:238–44[Abstract/Free Full Text]

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