The chronic subdural hematoma becomes gradually encysted by fibrous membranes (pseudomembranes) that grow from the dura. Some hematomas, probably those in which the initial bleeding was slight (see below), resorb spontaneously. Others expand slowly and act as space-occupying masses (Fig. 34-11). Gardner, in 1932, first postulated that the gradual enlargement of the hematoma was a result of the accession of fluid, particularly CSF, which was drawn into the hemorrhagic cyst by its increasing osmotic tension as red blood cells (RBCs) hemolyzed and protein was liberated. This hypothesis, which came to be widely accepted, is not supported by the available data. It had been demonstrated that the breakdown of RBCs contributes little, if at all, to the accumulation of fluid in the subdural space. According to the latter authors, the most important factor in the expansion of subdural fluid is a pathologic permeability of the developing capillaries in the outer pseudomembrane of the hematoma. The CSF plays no discernible role in this process, contrary to the original view of Munro and Merritt. The experimental observations of Labadie and Glover suggested that the volume of the original clot is a critical factor: The larger its initial size, the more likely it will be to enlarge. An inflammatory reaction, triggered by the breakdown products of blood elements in the clot, appears to be an additional stimulus for growth as well as for neomembrane formation and its vascularization. In any event, as the hematoma enlarges, the compressive effects increase gradually.
Treatment of subdural hematoma In most cases of acute hematoma it is sufficient to place burr holes and evacuate the clot before coma has developed. Treatment of larger hematomas, particularly after several hours have passed and the blood has clotted, consists of craniotomy to permit control of the bleeding and removal of the clot. As one would expect, the interval between loss of consciousness and the surgical drainage of the clot is perhaps the most important determinant of outcome in serious cases. Thin, crescentic clots can be observed and followed over several weeks and surgery undertaken only if focal signs or indications of increasing ICP arise (headache, vomiting, and bradycardia). Small subdural hematomas causing no symptoms and followed by CT scans will self-absorb, leaving only a deep yellow, sometimes calcified membrane attached to the inner dural surface. If the acute clot is too small to explain the coma or other symptoms, there is probably extensive contusion of the cerebrum or another lesion.
To remove more chronic hematomas, a craniotomy must be performed and an attempt made to strip the membranes that surround the clot. This is said to diminish the likelihood of reaccumulation of fluid but it is not always successful. Other causes of operative failure are postoperative swelling of the compressed hemisphere or failure of the hemisphere to expand after removal of a large clot. The difficulty of managing these patients surgically should not be underestimated. Elderly patients may be slow to recover after removal of the chronic hematoma or may have a prolonged period of confusion. Postoperative expansion of the brain can be followed by serial CT scans and may take weeks. Small, asymptomatic chronic collections are usually left alone and followed serially by clinical and CT examination, first at several week and then longer intervals.
Although no longer a common practice, the administration of glucocorticoids was an alternative to surgical removal of subacute and chronic subdural hematomas in patients with minor symptoms or with contraindications to surgery. This approach, reviewed by Bender and Christoff decades ago, has not been studied systematically but has been successful in a few of our patients (of course, they may have improved independent of the steroids).