Lab Rounds July 17th, 2008 Shawn Dowling. Case 56F. Presents with sudden onset of worse HA of her life. Peaked within 3 minutes. Residual neck/occipital.

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Presentation transcript:

Lab Rounds July 17th, 2008 Shawn Dowling

Case 56F. Presents with sudden onset of worse HA of her life. Peaked within 3 minutes. Residual neck/occipital pain. CT head normal. What test are you going do now?

Objectives Brief review of CSF Review pathophysiology of xanthochromia Distinguishing xanthochromia from bloody tap Ddx of xanthochromia

CSF Produced by choroid plexus in 3rd/4th ventricles Produced at a rate of 20ml/hr CSF volume typically ml/hr - 20% is w/i ventricles the rest is in the subarachnoid space, cranium and spinal cord

Normally CSF appears clear and colourless –As few as 200 WBC’s and 400 RBC’s/microL will cause CSF to appear turbid/cloudy –CSF will appear grossly bloody if >6,000 RBC’s/microL

Xanthochromia What three abnormalities can you see in CSF for SAH? –Xanthochromia –RBC’s - what else can this be from –Elevated opening pressure (2/3rds of patients and not in isolation - need to have one of the other two above)

Traumatic taps Puncture of venous plexuses located ventrally or dorsally to spinal sac or from vessels that accompany the cauda equina Incidence of traumatic taps is unknown, recent study suggests 10% Being able to distinguish a bloody tap from a SAH is critical –65% of untreated SAH will die or experience serious neuro disability - usually within first few days following initial rupture –Is there any problem with overcalling traumatic taps?

Chronology of SAH and LP Within first few hours after a SAH RBC’s will be present and disappear over days to weeks Xanthochromia is absent during the first few hours and once formed, remains present for weeks –Dependent on amount of pigment (RBC’s) and how it is measured (visual vs spectophotometry)

Xanthochromia Refers to yellow coloured CSF Blood in CSF undergoes rapid lysis to: –oxyhemoglobin (reddish/pink/orange) –bilirubin (yellow) –Methemoglobin (brown, occasionally present) RBC Lyse hgb oxyhgb bilirubin In vitro or in vivo In vivo only by Heme oxygenases In leptomeniges 2 hours6-12 hours

How can we distinguish SAH from traumatic tap? Xanthochromia Opening pressures - not reliable Three tube method –How many RBC’s are you allowed in the final tube before you call the tap traumatic rather than SAH? Crenated RBC’s, erythrophages, D-dimer - not reliable Clear tap (NO RBC’s) one space higher - suggests traumatic tap

What are the two methods of determining whether CSF is xanthochromic? 1.Visual (sensitive, more specific) 2.Spectrophotometric (sensitive, poor specificity) Visual is likely the best (and it’s all we have) Spectrophotometric would lead to increase # of CTA and likely more NSx interventions

How long do you have to wait before xantho is present?

DDx of Xanthochromia SAH Bilirubin (>170 umol/L) Rifampin Sample took too long to process** Previous traumatic tap –CANNOT OCCUR FROM THIS TRAUMATIC TAP UNLESS… Too many RBC’s (>100,000/mm3) - serum Too much protein (at least 150mg/dL) High carotenoid ingestion

False -ve xanthochromia for SAH Too early (<12 Hours) Too late: –12hrs - 2weeks100% –2 - 3 weeks91% –3 - 4 weeks71%

Summary Only reliable way to differentiate traumatic tap from SAH is presence or xanthochromia (or its’ absence if >12H after HA started)