Author(s): Bryce Weir
In 23 patients with subdural hematomas the osmolality of the hematoma fluid was compared with that of venous blood and in 11 of these cases with lumbar cerebrospinal fluid. There was no significant difference in the osmolalities of these fluids. The electrophoretic pattern of the subdural hematoma fluid resembles that of serum in that it usually does not contain prealbumins. The hemoglobin breakdown products migrate with the alpha II and beta globulins and include methemoglobin, oxyhemoglobin, and bilirubin. It is suggested that the late onset of symptoms, which often occurs, is due to either progressive bleeding from the neovascular outer membrane, effusion through it of albumin and fluid, or recurrent bleeding from a venous stump. It is also possible that very little expansion in the size of the subdural hematoma occurs following the initial formation and that late decompensation results from dynamic changes in the compressed brain. This work provides no evidence either to support or refute the concept of an osmotic mechanism for hematoma expansion.