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Once the subarachnoid space has been entered, the pressure and in special cases dynamics of the CSF are determined (see below) and samples of uid obtained The gross appearance of the uid is noted, after which the CSF, in separate tubes, can be examined for (1) number and type of cells and presence of microorganisms; (2) protein and glucose content; (3) tumor cells, using a Millipore lter or similar technique; (4) content of gamma globulin and other protein fractions and presence of oligoclonal bands;
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(5) pigments, lactate, NH3, pH, CO2, enzymes, and substances elaborated by tumors; and (6) bacteria and fungi (by culture), cryptococcal antigen, mycobacteria, herpesvirus and cytomegalovirus DNA (by polymerase chain reaction), and viral isolation Pressure and Dynamics With the patient in the lateral decubitus position, the CSF pressure is measured by a manometer attached to the needle in the subarachnoid space In the normal adult, the opening pressure varies from 100 to 180 mmH2O, or 8 to 14 mmHg In children, the pressure is in the range of 30 to 60 mmH2O A pressure above 200 mmH2O with the patient relaxed and legs straightened re ects the presence of increased intracranial pressure In an adult, a pressure of 50 mmH2O or below indicates intracranial hypotension, generally due to leakage of spinal uid or to systemic dehydration When measured with the needle in the lumbar sac and the patient in a sitting position, the uid in the manometer rises to the level of the cisterna magna (pressure is approximately double that obtained in the recumbent position) It fails to reach the level of the ventricles because the latter are in a closed system under slight negative pressure, whereas the uid in the manometer is in uenced by atmospheric pressure Normally, with the needle properly placed in the subarachnoid space, the uid in the manometer oscillates through a few millimeters in response to the pulse and respiration and rises promptly with coughing, straining, or abdominal compression The presence of a spinal subarachnoid block can be con rmed by jugular venous compression (Queckenstedt test) First one side of the neck is compressed, then the other, and then both sides simultaneously, with enough pressure to compress the veins but not the carotid arteries In the absence of subarachnoid block, there is a rapid rise in pressure of 100 to 200 mmH2O and a return to its original level within a few seconds after release Failure of the pressure to rise with this maneuver usually means that the needle is improperly placed A rise in pressure in response to abdominal compression (or coughing or straining) but not to jugular compression indicates a spinal subarachnoid block Failure of the pressure to rise with compression of one jugular vein but not the other (Tobey-Ayer test) may indicate lateral sinus thrombosis These tests are now rarely used, having been replaced by more precise and less hazardous imaging techniques, but they remain useful in appropriate circumstances Jugular compression should not be performed when an intracranial tumor or other mass lesion is present or suspected Gross Appearance and Pigments Normally the CSF is clear and colorless, like water Minor degrees of color change are best detected by comparing tubes of CSF and water against a white background (by daylight rather than uorescent illumination) or by looking down into the tubes from above The presence of red blood cells imparts a hazy or ground-glass appearance; at least 200 red blood cells (RBCs) per cubic millimeter (mm3) must be present to detect this change The presence of 1000 to 6000 RBC per cubic millimeter imparts a hazy pink to red color, depending on the amount of blood; centrifugation of the uid or allowing it to stand causes sedimentation of the RBC Several hundred or more white blood cells in the uid (pleocytosis) may cause a slight opaque haziness A traumatic tap (in which blood from the epidural venous plexus has been introduced into the spinal uid) may seriously confuse the diagnosis if it is incorrectly interpreted to indicate a
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pre-existent subarachnoid hemorrhage To distinguish between these two types of bloody tap, two or three serial samples of uid should be taken at the time of the LP With a traumatic tap, there is usually a decreasing number of RBC in the second and third tubes Also with a traumatic tap, the CSF pressure is usually normal, and if a large amount of blood is mixed with the uid, it will clot or form brinous webs These are not seen with pre-existent hemorrhage because the blood has been greatly diluted with CSF and de brinated With subarachnoid hemorrhage, the RBC begin to hemolyze within a few hours, imparting a pink-red discoloration (erythrochromia) to the supernatant uid; allowed to stand for a day or more, the uid becomes yellow-brown (xanthocromia) Prompt centrifugation of bloody uid from a traumatic tap will yield a colorless supernatant; only with large amounts of blood (RBC over 100,000/mm3) will the supernatant uid be faintly xanthochromic due to contamination with serum bilirubin and lipochromes The uid from a traumatic tap should contain one or two white blood cells (WBCs) per 1000 RBC assuming that the hematocrit is normal, but in reality this ratio varies widely With subarachnoid hemorrhage, the proportion of WBC rises as RBC hemolyze, sometimes reaching a level of several hundred per cubic millimeter; but the vagaries of this reaction are such that it, too, cannot be relied upon to distinguish traumatic from pre-existent bleeding The same can be said for crenation of RBC, which occurs in both types of bleeding The reason that red corpuscles undergo rapid hemolysis in the CSF is not clear It is surely not due to osmotic differences, insofar as the osmolarity of plasma and CSF is essentially the same Fishman suggests that the low protein content of CSF disequilibrates the red cell membrane in some way The explanation for the rapid phagocytosis of RBC in the CSF, which begins within 48 h, is also obscure The pigments that discolor the CSF following subarachnoid hemorrhage are oxyhemoglobin, bilirubin, and methemoglobin; in pure form, these pigments are colored red (orange to orange-yellow with dilution), canary yellow, and brown, respectively Mixtures of these pigments produce combinations of these colors Oxyhemoglobin appears rst, within several hours of the hemorrhage, becomes maximal in about 36 h, and diminishes over a 7- to 9-day period Bilirubin begins to appear in 2 to 3 days and increases in amount as the oxyhemoglobin decreases Following a single brisk bleed, bilirubin persists in the CSF for 2 to 3 weeks, the duration varying with the number of RBC that were present originally Methemoglobin appears when blood is loculated or encysted and isolated from the ow of CSF Spectrophotometric techniques can be used to distinguish the various hemoglobin breakdown products and thus determine the approximate time of bleeding Not all xanthochromia of the CSF is due to hemolysis of RBC With severe jaundice, bilirubin of both the direct- and indirectreacting types will diffuse into the CSF The quantity of bilirubin is from one-tenth to one-hundredth that in the serum Elevation of CSF protein from whatever cause results in a faint opacity and xanthochromia, more or less in proportion to the albumin-bound fraction of bilirubin Only at levels of more than 150 mg/100 mL does the coloration due to protein become visible to the naked eye Hypercarotenemia and hemoglobinemia (through hemoglobin breakdown products, particularly oxyhemoglobin) also impart a yellow tint to the CSF, as do blood clots in the subdural or epidural space of the cranium or spinal column Myoglobin does not enter
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