Acute hemorrhages are more dense and appear white on CT, whereas CSDHs are hypodense and appear darker than the brain parenchyma. Subacute SDHs may have features of both acute SDHs and CSDHs or may appear isodense. While acute SDHs are often associated with trauma and are readily diagnosed, chronic and subacute SDHs present a greater diagnostic challenge. Clinically, subacute SDHs act like CSDHs and are treated similarly.11 For the purposes of this discussion, the case patient’s SDH will be considered a form of CSDH.
Pathophysiology of Chronic Subdural Hematomas
Chronic subdural hematomas form in a number of ways. Major causes are related to brain atrophy resulting from advanced age, alcoholism, brain injury, stroke, or other conditions.11 Atrophy of the brain causes the size of the subdural space to increase. This increased space causes the bridging veins between the cortical surface of the brain and the dura to become stretched and easily torn. As a result, seemingly minor trauma can easily lead to hemorrhage.
Over time, these small, acute hemorrhages in the subdural space may liquefy into CSDHs. Bleeding triggers an inflammatory response, and gradually, blood begins to break down, as with any bruise. Unlike most blood clots, however, blood in the subdural space is affected by fluid dynamics, fibrinolysis, and the formation of neomembranes.11,12 As a result, the blood may not be completely reabsorbed and may actually expand, causing patients to experience symptoms.
Potentially, SDHs can also be caused by subdural hygromas, low intracranial pressure, dehydration, or overdrainage of cerebrospinal fluid during lumbar puncture, spinal anesthesia, or shunting.13
Epidemiology
The annual incidence of CSDH is one to two cases per 100,000 persons. Incidence increases to seven cases per 100,000 among persons older than 70.13 The mortality rate for SDH is 31% to 36%.14,15 The mortality rate for CSDH is approximately 6%. For patients older than 60, the rate increases to 8.8%.16 Rates of morbidity (ie, severe disability or persistent vegetative state) associated with CSDHs have been reported at about 10%.16,17
Men are affected more commonly than are women (accounting for 61% to 70% of cases), and median ages between 71 and 78 have been reported.4,12,18,19
The risk factors for CSDH are listed in Table 1.4,10 SDHs frequently occur in the context of trauma, but they can occur spontaneously, especially in coagulopathic patients. Among patients with CSDHs who are taking warfarin, 45.5% to 52% deny recent experiences of trauma.4,14
Signs and Symptoms of Chronic Subdural Hematomas
The clinical onset of CSDH is insidious. Possible presenting symptoms are listed in Table 2.14,18,20,21 Frequently, the neurologic examination fails to reveal any focal deficits. Many of the symptoms are vague and nonspecific and may mimic those of other conditions that are common in the elderly, thus making diagnosis difficult. Despite clinical suspicion, the definitive diagnosis of SDH is based on CT results.
Reversing Warfarin-Induced Coagulopathy
In all patients with intracranial hemorrhages who are taking warfarin, the coagulopathy must be reversed. The agents commonly used to reverse the effects of warfarin include vitamin K, FFP, and rFVIIa.9,22-24 The choice of agents depends on the timing of intervention.
Vitamin K is commonly given to patients either intravenously or orally in combination with FFP and/or rFVIIa to promote the reversal of warfarin-induced coagulopathy. Vitamin K is seldom used alone, as its effects may not be seen for 24 hours or longer, and may not completely reverse the effects of warfarin.25
Another frequently used product is FFP. Unfortunately, FFP has been associated with complications such as fluid overload, infectious disease transmission, and anaphylaxis. Additionally, FFP too reverses coagulopathy very slowly. Boulis et al26 found that in patients given FFP with single-dose vitamin K, INR reduction averaged 0.18/hour. At this rate, it would take approximately 11 hours to correct an INR of 3.0 to the desired target of 1.0.
In contrast, rFVIIa, used off-label, has proved highly effective in rapidly reversing coagulopathy and allowing patients to safely undergo immediate surgical treatment.23,24 To its disadvantage, rFVIIa increases the risk of thromboembolism and is significantly more expensive than FFP. Compared with $105 for one unit of FFP, the cost of an 80-mcg/kg dose of rFVIIa for a patient weighing 80 kg is about $6,400.27
Factors Predicting Outcome for Subdural Hematomas
A number of factors determine post-SDH outcome. Rozzelle et al14 found that a Glasgow Coma Scale score below 7, age greater than 80, more acute hemorrhages, and hemorrhages requiring craniotomy rather than burr-hole drainage were associated with significantly higher mortality rates than when these factors were absent.
Other studies have revealed that patients with poor clinical status and larger hematomas with more midline shift are also prone to higher mortality rates.20,28 Merlicco et al29 found that younger, nonalcoholic patients without severe trauma whose hematomas were under high pressure had better chances for full recovery than other patients.