FIGURE 1. A 76-year-old male with a three-month history of cognitive decline, increasing agitation, and worsening gait instability after sustaining a fall three months prior to presentation. (A) CT of the head demonstrating bilateral chronic subdural hematomas of mixed density with significant cerebral and ventricular compression. (B) CT of the head at two months post-bilateral bur hole drainage, demonstrating almost complete resolution of the subdural hematomas and restoration of normal ventricular volume. The patient experienced a nearcomplete resolution of symptoms.
sciences. Modern surgical treatment of traumatic brain injury is only 130 years old, at most, with the most dramatic changes in diagnosis and treatment occurring within the last 40 years with the advent of modern medical imaging (CT and MRI). In modern neurosurgical practice, the role of opening the skull via a craniotomy (trephination) or bur hole is to relieve pressure on the brain and restore a state of normal brain physiology and metabolism. With the exception of decompressive craniectomies (removal of part of the skull) done for treatment of severe cerebral edema, this usually involves the removal of a mass lesion. Types of hematomas
Traumatic mass lesions may occur from a variety of sources. Epidural hematomas occur due to a hemorrhage between the skull and lining of the brain (dura) and are usually associated with a skull fracture. The extent of the hemorrhagic collection is usually confined by the suture lines of the skull. The presentation is usually acute and requires rapid evaluation and potential surgical intervention. Intraparenchymal hematomas (contusions) are due to injury of the small perforating capillaries within the brain. They may present either acutely or in a delayed fashion within the first 24 to 96 hours of injury. Although surgical treatment may be required, they are often treated with intensive medical support of the patient. They are considered to be an indication of severe underlying injury to the brain parenchyma. Subdural hematomas (SDHs) are due to a hemorrhage between the brain and the dura. They are usually caused by a tear in a bridging vein that runs between the surface of the brain and a dural venous sinus but may also be caused by arterial injury. The extent of hemorrhage is not confined by the sutures lines of the skull. The presentation may be either acute, requiring emergent surgical evacuation, or
insidious over a period of weeks to months. SDHs developing between three days and three weeks after head injury are termed “subacute”; those that are manifest later than three weeks after injury are defined as “chronic.” The discussion below centers on chronic subdural hematomas in elderly patients. Etiology of chronic SDH
The incidence of chronic SDHs in the elderly is 7.4 per 100,000 people per year. Between 25 percent and 50 percent of these patients will have no history of head injury, and in those with a history of trauma, the injury is often mild. A significant proportion of patients are predisposed to SDHs because of chronic alcoholism, epilepsy, or coagulopathies (often related to Coumadin or antiplatelet agents, e.g., ASA and/or clopidogrel). Small amounts of hemorrhage into the subdural space or larger hematomas in patients with underlying brain atrophy may fail to produce symptoms within a week to 10 days. The initial hematoma is covered by an outer membrane beneath the dura. By three to four weeks, an inner membrane forms between the hematoma and the pial surface of the brain, completely enclosing the hematoma. During this period the
hematoma liquifies and becomes progressively more hypodense on CT scans. In the next weeks, in some patients the hematoma gradually enlarges, and in other patients there is a gradual re-absorption of the liquefied blood. An etiology of chronic SDH enlargement within the capsule has been postulated. The albumin/gamma globulin and total protein concentrations within the hematoma are much higher than in the serum, resulting in
a higher osmotic pressure within the hematoma. The higher osmotic pressure will draw water out of the serum into the hematoma via diffusion, thus enlarging the mass. A chronic SDH may also enlarge from recurrent smaller hemorrhages into its surrounding membranes. It is likely that a combination of the two mechanisms is at work in most large, expanding chronic SDHs. There is considerable CT evidence that some hematomas regress in size and do not need surgical treatment. It is likely there is a balance between hematoma production and re-absorption. If re-absorption exceeds production, the hematoma will shrink, and when production exceeds re-absorption, the hematoma will enlarge. Diagnosis and treatment of chronic SDH
The symptoms and signs of chronic SDH are extremely variable and are not necessarily pathognomonic. In elderly patients the insidious onset of BRAIN INJURY to page 38
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