A traumatic tap, in which blood from the epidural venous plexus has been introduced into the spinal fluid, may seriously confuse the diagnosis if it is incorrectly interpreted as indicating a preexistent subarachnoid hemorrhage. To distinguish between these two types of “bloody taps,” two or three serial samples of fluid may be collected. With a traumatic tap, there is usually a decreasing number of RBCs in the subsequent tubes. Also with a traumatic tap, the CSF pressure is usually normal, and if a large amount of blood is mixed with the fluid, it will clot or form fibrinous webs. These changes are not seen with preexistent hemorrhage because the blood has been greatly diluted with CSF and defibrinated by enzymes in the CSF. In subarachnoid hemorrhage, the RBCs begin to hemolyze within a few hours, imparting a pink-red discoloration (erythrochromia) to the supernatant fluid; if the spinal fluid is sampled more than a day following the hemorrhage, the fluid will have become yellow-brown (xanthochromia). Prompt centrifugation of bloody fluid from a traumatic tap will yield a colorless supernatant; only with large amounts of venous blood (RBC >100,000/mm3) will the supernatant fluid be faintly xanthochromic due to contamination with serum bilirubin and lipochromes.
The fluid from a traumatic tap should contain approximately one or two WBCs per 1,000 RBCs assuming that the hematocrit and white blood cell count are normal, but in reality this ratio varies. With subarachnoid hemorrhage, the proportion of WBCs rises as RBCs 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 preexistent bleeding. The same can be said for crenation of RBCs, which occurs in both types of bleeding. Why red corpuscles undergo rapid hemolysis in the CSF is not clear. It is surely not because of osmotic differences, as the osmolarity of plasma and CSF is essentially the same. Fishman suggested that the low protein content of CSF disequilibrates the red cell membrane in some way.
The pigments that discolor the CSF following subarachnoid hemorrhage are oxyhemoglobin, bilirubin, and methemoglobin as described by Barrows and colleagues. In pure form, these pigments are colored red (orange to orange-yellow with dilution), canary yellow, and brown, respectively. Oxyhemoglobin appears within several hours of hemorrhage, becomes maximal in approximately 36 h, and diminishes over a 7to 9-day period. Bilirubin begins to appear in 2 to 3 days and increases in amount as the oxyhemoglobin decreases. Methemoglobin appears when blood is loculated or encysted and isolated from the flow 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 caused by hemolysis of RBCs. With severe jaundice, both conjugated and unconjugated bilirubin diffuses into the CSF. The quantity of bilirubin in the CSF ranges from one-tenth to one-hundredth that in the serum. Elevation of CSF protein from any cause results in a faint opacity and xanthochromia. Only at protein levels greater than 150 mg/100 mL does the coloration 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 appear in the CSF because a low renal threshold for this pigment permits rapid clearing from the blood.