This is a thinly encapsulated collection of clear or slightly xanthochromic fluid in the subdural space; such collections form after an injury, as well as after meningitis (in an infant or young child). As often, subdural hygromas appear without precipitant, presumably because of a ball-valve effect of an arachnoidal tear that allows cerebrospinal fluid to collect in the space between the arachnoid and the dura; brain atrophy is conducive to this process. Occasionally a hygroma originates from a tear in an arachnoidal cyst. It may be difficult to differentiate a long-standing subdural hematoma from hygroma, and some chronic subdural hematomas are probably the result of repeated small hemorrhages that arise from the membranes of hygromas. Shrinkage of the hydrocephalic brain after ventriculoperitoneal shunting is also conducive to the formation of a subdural hematoma or hygroma, in which case drowsiness, confusion, irritability, and low-grade fever are relieved when the subdural fluid is aspirated or drained. Intracranial hypotension is another cause of subdural hygromas. In adults, hygromas are usually asymptomatic and do not require treatment; they only are infrequently the cause of seizures.
Severe closed head injury is almost universally accompanied by cortical contusions and surrounding edema. The mass effect of contusional swelling, if sufficiently large, becomes a major factor in the genesis of tissue shifts and raised ICP. The CT appearance of contusion was already described (see Figs. 34-4 and 34-5). In the first few hours after injury, the bleeding points in the contused area may appear small and innocuous. The main concern, however, is the tendency for a contused area to swell or to develop into a hematoma during the first several days after injury. This may give rise to delayed clinical deterioration, sometimes abrupt in onset and concurrent with the appearance of swelling of the damaged region on the CT scan. It has been claimed, on uncertain grounds, that the swelling in the region of an acute contusion is precipitated by excessive administration of intravenous fluids (fluid management is considered further on in this chapter). Craniotomy and decompression of the swollen brain may be of benefit in selected cases with elevated ICP but it has no effect on the focal neurologic deficit.
One or several intracerebral hemorrhages may be apparent immediately after head injury, or hemorrhage may be infrequently delayed in its development by several days (the earlier mentioned spät apoplexie). The bleeding is in the subcortical white matter of one lobe of the brain or in deeper structures such as the basal ganglia or thalamus. The injury had nearly always been severe; blood vessels as well as cortical tissue are torn.
The clinical picture of traumatic intracerebral hemorrhage is similar to that of hypertensive brain hemorrhage with deepening coma with hemiplegia, a dilating pupil, bilateral Babinski signs, and stertorous and irregular respirations. The additional mass may be manifest by an abrupt rise in blood pressure and in ICP.
Craniotomy with evacuation of an acute or delayed clot has given a successful result in some cases but the advisability of surgery is governed by several factors including the level of consciousness, the time from the initial injury, and the associated damage (contusions, subdural and epidural bleeding) shown by imaging studies. Application of ICP monitoring and of CT scans at intervals after the injury facilitates diagnosis. Boto and colleagues found that basal ganglia hemorrhages were prone to enlarge in the day or two after closed head injury and that those greater than 25 mL in volume were fatal in 9 of 10 cases.