Cerebrospinal fluid spectrophotometry
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Spectrophotometry of cerebrospinal fluid sis used in the diagnosis of sudden strokes especially when suspecting subarachnoid hemorrhage. It is especially important for those cerebral hemorrhages that are difficult to prove by imaging methods. It is especially valuable in the early stages of the disease. Provides information on the age of bleeding and prolonged or repeated bleeding. Spectrophotometric examination of cerebrospinal fluid in the visible part of the spectrum allows characterization on the basis of different absorption maxima oxyhemoglobin (at 415 nm ), methemoglobin (at 405 nm) and bilirubin (at 420–460 nm).
At the beginning of cerebral hemorrhage, there is mainly oxyhemoglobin in the cerebrospinal fluid, later spectrophotometry shows the summing curve of oxyhemoglobin, or methemoglobin and bilirubin. Degree of degradation ofhemoglobin to bilirubin is highly variable individually. Isolated bilirubin xanthochromy appears at the earliest in 5 days.
Methods of determination
Cerebrospinal fluid spectrophotometry is performed on a registration spectrophotometer in the wavelength range 370-600 nm. For spectrophotometric examination, it is recommended to centrifuge the cerebrospinal fluid within 1 hour of collection.
Evaluation
Physiological findings
The spectrophotometric curve of cerebrospinal fluid under physiological conditions is flat or slightly elevated in the direction from 600 nm to 370 nm. In the visible region of the spectrum, the absorbances are less than 0.02.
Pathological findings
Demonstration of oxyhemoglobin
- Erythrocytes, which have penetrated the ventricles or subarachnoid space, begin to undergo hemolysis in about 2 hours, and the released hemoglobin conditions the formation of absorption maxima characteristic of oxyhemoglobin. The presence of oxyhemoglobin is manifested by an "absorption maximum at 415 nm" and "two smaller peaks at 540 and 575 nm." Its detection in cerebrospinal fluid is a sign of fresh bleeding into the brain. It reaches its maximum in 4-5 days and disappears after 7-10 days (Figs. 5, 6). The same curve can be obtained for an artificial blood admixture if the cerebrospinal fluid was not centrifuged in time after collection.
Methaemoglobin detection
- The presence of methaemoglobin is a sign of older hemoglobin changes. The maximum at 415 nm shifts towards shorter wavelengths with a maximum at 406 nm. We find it as part of the summation curves, where the absorbances of the individual pigments overlap. However, it can be demonstrated by adding KCN to the sample. When methemoglobin is present, cyanomethemoglobin is formed with an absorption maximum in the region of 419 nm; if it does not occur, there will be no change. Detection of methaemoglobin in a mixture with oxyhemoglobin confirms that the blood in the fluid is caused by cerebral hemorrhage and not by artificial contamination during lumbar puncture.
Identification of bilirubin
- The presence of bilirubin in the cerebrospinal fluid indicates an older bleeding into the cerebrospinal fluid. After hemolysis of erythrocytes, it is formed by the conversion of hemoglobin unconjugated bilirubin with absorption maximum at 460 nm, so-called long bilirubin. It appears in the cerebrospinal fluid about 10-12 hours after bleeding, the maximum is recorded on day 3 and lasts 3-4 weeks. A typical spectrophotometric record confirming subarachnoid hemorrhage captures the oxyhemoglobin curve with a major peak at 415 & nm, on the descending side of which another broad peak belonging to bilirubin is visible. As erythrocyte hemolysis continues, the ratio of oxyhemoglobin to bilirubin decreases. Bilirubin can be conjugated to free fatty acids and amino acids later in CSF. Conjugated bilirubin has the absorption maximum shifted to the area of 420 nm, so-called short bilirubin. The spectrum of bilirubin alone can be observed no earlier than day 5 after subarachnoid hemorrhage.
- Cerebrospinal fluid can also be detected in serum bilirubin. It can penetrate the cerebrospinal fluid physiologically in the neonate through an immature blood-brain barrier, in adults with a damaged blood-brain barrier or in severe jaundice. Conjugated bilirubin comes mostly from serum.
Links
Related articles
- Cerebrospinal fluid
- Biochemical examination of cerebrospinal fluid
- Proteins in cerebrospinal fluid
- Cytological examination of cerebrospinal fluid
- Cerebrospinal fluid syndromes
External links
- AMBLER, Zdeněk. Basics of neurology. 6th edition. Prague: Galén, 2006. pp. 171-181. ISBN 80-7262-433-4 .
- {{#switch: web
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Incomplete publication citation. FIALOVÁ, L. and M VEJRAŽKA2005. Also available from <https://el.lf1.cuni.cz>.
|collection =
Incomplete citation of contribution in proceedings. FIALOVÁ, L. and M VEJRAŽKA. 2005. Also available from <https://el.lf1.cuni.cz>. {{ #if: |978-80-7262-438-6} } |article = Incomplete article citation. FIALOVÁ, L. and M VEJRAŽKA. 2005, year 2005, also available from <https://el.lf1.cuni.cz>.
|web =
Incomplete site citation. FIALOVÁ, L. and M VEJRAŽKA. ©2005. [cit. 8. 9. 2009]. <https://el.lf1.cuni.cz>.
|cd =
Incomplete carrier citation. FIALOVÁ, L. and M VEJRAŽKA. ©2005. [cit. 8. 9. 2009].
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Incomplete database citation. ©2005. [cit. 8. 9. 2009]. <https://el.lf1.cuni.cz>.
|corporate_literature =
Incomplete citation of company literature. FIALOVÁ, L. and M VEJRAŽKA. 2005. Also available from <https://el.lf1.cuni.cz>. legislative_document = Incomplete citation of legislative document. 2005. Also available from URL <https://el.lf1.cuni.cz>.
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Incomplete publication citation. ADAM, P. Cytologie mozkomíšního moku (CD-ROM). SEKK, 2000. 1;
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Incomplete citation of contribution in proceedings. ADAM, P. Cytologie mozkomíšního moku (CD-ROM). SEKK, 2000. 1; {{
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|article =
Incomplete article citation. ADAM, P. 2000, year 2000,
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Incomplete site citation. ADAM, P. SEKK, ©2000.
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Incomplete carrier citation. ADAM, P. SEKK, ©2000.
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Incomplete database citation. SEKK, ©2000.
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ADAM, P. Cytologie mozkomíšního moku (CD-ROM). SEKK, 2000. 1;
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Incomplete publication citation. AMBLER, Z, J BEDNAŘÍK and E RŮŽIČKA. Klinická neurologie – část obecná. Triton, 2004. 1; 978-80-7262-438-6.
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Incomplete citation of contribution in proceedings. AMBLER, Z, J BEDNAŘÍK and E RŮŽIČKA. Klinická neurologie – část obecná. Triton, 2004. 1; {{
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Incomplete article citation. AMBLER, Z, J BEDNAŘÍK and E RŮŽIČKA. 2004, year 2004,
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Incomplete site citation. AMBLER, Z, J BEDNAŘÍK and E RŮŽIČKA. Triton, ©2004.
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Incomplete carrier citation. AMBLER, Z, J BEDNAŘÍK and E RŮŽIČKA. Triton, ©2004.
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Incomplete database citation. Triton, ©2004.
|corporate_literature =
AMBLER, Z, J BEDNAŘÍK and E RŮŽIČKA. Klinická neurologie – část obecná. Triton, 2004. 1; 978-80-7262-438-6} }
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Incomplete publication citation. GLOSOVÁ, L. Cytologický atlas mozkomíšního moku. 1998. 1; 978-80-7262-438-6.
|collection =
Incomplete citation of contribution in proceedings. GLOSOVÁ, L. Cytologický atlas mozkomíšního moku. 1998. 1; {{
#if: 80-85824-70-1 |978-80-7262-438-6} }
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Incomplete article citation. GLOSOVÁ, L. 1998, year 1998,
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Incomplete site citation. GLOSOVÁ, L. ©1998.
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Incomplete carrier citation. GLOSOVÁ, L. ©1998.
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|corporate_literature =
Incomplete citation of company literature. GLOSOVÁ, L. Cytologický atlas mozkomíšního moku. 1998. 1; 978-80-7262-438-6} }
Kategorie:Biochemie
Kategorie:Klinická biochemie
Kategorie:Neurologie
Kategorie:Infekční lékařství
