Abstract

National guidelines for cerebrospinal fluid (CSF) xanthochromia testing have recently been updated. 1 Our Lincolnshire-wide pathology network decided to audit our practices against these guidelines, notably those standards relating to specimen requirements, transport and specimen handling/analysis.
A retrospective audit of 281 CSF xanthochromia requests received between 1 September 2008 and 31 October 2009 was undertaken and we also compared the results with clinical outcomes.
A number of points and audit failures have emerged.
In particular, our standard operating procedures must be improved in order to comply fully with current guidelines to ensure that:
Where possible, four CSF samples are taken and the sample used for analysis is logged (only 7 of 281 samples were confirmed to be sample 4 [2.5%]); Samples are always protected from light (compliance rate 84/281 [65%]); Use of pneumatic tube is prohibited and recorded in every case (this is not systematically recorded on all sites and therefore compliance is variable); A blood sample is simultaneously taken for bilirubin and total protein (compliance rate 241/281 [86%]); A computed tomography scan is always done prior to CSF sampling and reported as negative (confirmed compliance rate 266/281 [95%]); Samples are taken at least 12 hours post onset of symptoms (compliance rate 252/281 [90%]); Samples are transported to the laboratory in a timely manner (27/281 samples [10%] took > 3 hours to get to the lab, but note that some labs within the network are >30 miles apart); Samples are centrifuged with one hour and stored in the dark prior to testing (this is not systematically recorded but confirmed compliance rate 74/281 [26%]).
Five patients with an elevated net bilirubin absorbance (NBA) also had an elevated CSF protein concentration. Four of these patients had either viral or bacterial meningitis and one had Guillain–Barré syndrome. The guideline suggests that where NBA is >0.007 and the net oxyhaemoglobin absorbance (NOA) is ≤0.02, or NOA >0.02 but with no visible oxyhaemoglobin peak and the CSF protein is >1.0 g/L, the CSF analysis should be reported as ‘Increased CSF bilirubin. This finding may be consistent with: SAH; an increased bilirubin accompanying the increased CSF protein; or other source of CSF blood. Interpret with caution in relation to SAH especially if within the first week of event’ (SAH, subarachnoid haemorrhage).
1
Given our experiences we will, from now on, be very cautious when interpreting elevated NBA in cases where the CSF protein is elevated, particularly when meningitis is being considered in the differential diagnosis. In these cases it is vital to have close dialogue with medical colleagues to avoid potential misinterpretation or overemphasis of the importance of the xanthochromia results. Interestingly, this issue was also recently discussed on the UK Association for Clinical Biochemistry discussion list and the consensus was to always discuss results with clinical teams, especially when CSF xanthochromia requests are not vetted by laboratory staff. 2
Given these findings, we would encourage all laboratories that provide a xanthochromia service to review their practice against the new guidelines. We intend to undertake a follow-up audit in one year once we have addressed the above shortcomings.
DECLARATIONS
