Subdural Hematomas in the Elderly: The Great Neurological Imitator
Authors: Stephen W. Meldon, MD, Assistant Professor, Case Western Reserve University; Department of Emergency Medicine, MetroHealth Medical Center, Cleveland, OH; Sarah Delaney-Rowland, MD, Chief Resident, Department of Emergency Medicine, MetroHealth Medical Center, Cleveland, OH.
Peer-Reviewers: Roseanna Lechner, MD, Assistant Professor of Surgery, Case Western Reserve University; Department of Neurosurgery, MetroHealth Medical Center, Cleveland, OH; O. John Ma, MD, Assistant Professor of Emergency Medicine, University of Missouri-Kansas City School of Medicine; Research Director, Department of Emergency Medicine, Truman Medical Center, Kansas City, MO.
Due to advancements in medical technology, better access to health care, and improved living conditions, the geriatric population in the United States is rapidly expanding. This dramatic increase in the number of older persons will put a much larger population at risk for injury. Improving outcomes in this fragile population requires the need for a better understanding in the diagnosis, treatment, and management of geriatric injuries. Elderly trauma patients have an increased mortality rate and worse outcomes despite similar or less injury severity than nonelders.1,2 The explanation for this difference lies in those factors unique to the older patient. Diminished physiologic reserve associated with aging, atypical clinical presentations, and comorbidities contribute to worse trauma outcomes in this age group. Important comorbidities include preexisting central nervous system (CNS) disease and other concurrent medical illnesses such as cardiovascular disease, lung disease, and coagulopathy. Geriatric trauma, though not completely distinct from nongeriatric trauma, does require an expanded fund of knowledge and specialized skills.
Head trauma is a significant contributor to poor outcomes in the elderly. As a cause of trauma-related deaths, it is second only to shock. Several differences exist when head injuries are compared in elder and nonelder populations. These include mechanism of injury, clinical presentation, operative intervention, and radiographic findings on neuroimaging. The sex ratio of head injuries in the elderly is approximately 1:1, whereas in nonelder head-injured patients there is a much higher incidence with males. The most common mechanism of injury in the elderly is falls, compared with motor vehicle crashes (MVC) in the younger population. 3-6 Alcohol is involved less frequently in older injured patients. The elderly have a higher rate of positive computerized tomography (CT) scans and an increased need for neurosurgical intervention. Clinical presentations also differ, with 12% of older patients having a normal neurological examination and a positive CT scan, compared with 7% in the younger age group.3 Overall, elderly patients have worse outcomes, with increased hospital admissions, worse functional outcomes, and increased injury-related deaths.7,8 Elderly patients with head injuries and Glasgow Coma Scale (GCS) score less than 8 have greater than 80% mortality rate.9
With this background in mind, this issue will focus on subdural hematomas, the most common, significant intracranial injury in elders. Etiologies, diagnosis, and management of acute and chronic subdural hematomas will be discussed. In addition, atypical clinical presentations and CT findings will be emphasized.
— The Editor
A subdural hematoma (SDH) refers to a collection of blood between the dura and the brain. SDHs are three times more frequent in the elderly population.10 Most result from bleeding originating from bridging veins, which are prone to injury following acceleration/deceleration movement of the brain. Prognosis depends on several factors: the degree of underlying brain injury; the size and pressure of the expanding hematoma; and the patient’s age. Prognosis is especially poor in the elderly.
SDHs are commonly classified into three types, depending on the time of symptom onset following the initial injury. Although these time frames are somewhat arbitrary, the significant differences in CT findings, treatment, and outcome make this classification useful.
Acute subdurals are symptomatic within 24 hours after injury. Usually there is an associated decreased level of consciousness on presentation. CT scan demonstrates a hyperdense, crescent-shaped collection between the calvarium and the cortex. Acute subdurals are more common in younger patients and tend to be associated with major trauma.11 Approximately one-third of acute subdurals have other associated focal brain injuries. They may occur in association with cortical contusions, subarachnoid hemorrhages, and diffuse axonal injury.11 Morbidity and mortality are much higher when compared to chronic SDHs.
Subacute SDHs are symptomatic between 24 hours and two weeks after the injury. Presentations include complaints of headache, altered mental status, motor weakness, or hemiparesis. CT scan demonstrates a hypodense or isodense (when compared to brain parenychma) fluid collection.
Chronic subdurals generally become symptomatic more than two weeks after the initial injury. The signs and symptoms may be nonspecific, such as mild mental status changes and difficulty walking, or more dramatic, such as focal weakness, hemiparesis, and altered level of consciousness. Chronic subdurals occur in older individuals, are often associated with trivial trauma, and are seldom associated with injury to underlying brain. One study found that the majority of chronic subdurals occurred in patients older than 50 years of age and none had associated focal brain injuries.11
After review of the literature, one study defined chronic SDH by the following criteria: hematomas resulting in urgent neurologic deficits 20 days after trauma, or if no trauma has taken place, hematomas that have existed for at least three weeks; hematomas not accompanied by evidence of fresh cerebral injury or cerebral injury that has failed to heal; or hematomas with pronounced, neomembranous organization.12
A subdural hygroma, also referred to as a traumatic subdural effusion, is a collection of blood-tinged fluid in the subdural space. Absolute distinction between chronic SDHs and subdural hygromas is not always possible because the subdural fluid is often a mixture of CSF and blood. Evidence exists to indicate that subdural hygromas may become chronic SDHs.13-15 The mechanism of formation is not entirely understood. They may result from tears in the subarachnoid space that permit CSF to escape into the subdural space, or from effusions from injured vessels with abnormal permeability. The most common signs and symptoms are headache, nausea, and vomiting; decreased level of consciousness; and focal deficits. CT scan demonstrates a crescent-shaped collection that has the same density as CSF. Subdural hygromas are usually associated with minor or trivial trauma. They occur more frequently in older patients, with the majority of patients in their sixth decade.16
Accurate incidences of acute and chronic SDHs are difficult to assess. The number of elders is rapidly increasing, placing more patients at risk for these injuries. A recent epidemiologic study found that fall-induced severe head injuries in elders was increasing at a rate that was not due simply to demographic changes.17 In addition, reported incidences of small acute and chronic SDH have clearly increased secondary to widespread use of CT scanning.
One prospective U.S. population-based study found the average annual incidence of clinically important SDH to be 46.7 per 100,000. Using the 65-74 year old group as a reference, the relative risk for SDH was five times higher in 75- to 84-year-olds and 13 times greater in those older than 85.18
A retrospective study covering a seven-year period found the overall incidence of chronic SDHs was 1.72 cases/100,000 population/year. The study also reported that the incidence was greatly influenced by increasing age. In patients aged 60 to 69 years, the incidence rose to 8.4 cases/100,000 population/year, and the incidence further doubled for populations older than 70 years of age.19 Kudo et al assessed the epidemiological trends on Awaji Island in 1992 and found the overall incidence of chronic subdural was 13.1 (per 100,000 population/year); the incidence was 17 times greater in people 65 years or older (58.1 compared to 3.4 in younger persons). If these numbers were extrapolated to all of Japan by the year 2020, the incidence would increase to 16.3/100,000 population/year.20
Falls remain the most significant mechanism of injury in this group. An increasing number and incidence of fall-induced severe head injuries exists in the geriatric population.17 One study found that 59% of their elderly population who required CT scans for evaluation of closed head trauma sustained their trauma from falls.21 The study found MVCs responsible for closed head injuries in the elderly in only 20% of the population studied. Other investigators have found similar results.22,23 However, the increasing number of older drivers may have a significant effect on both the prevalence of older patients involved in MVCs and the incidence of head injuries and SDH.
Common predisposing conditions for the development of SDHs include coagulopathy, vascular malformations, renal dialysis, CSF shunts, and head trauma. Head trauma is the most frequent causative factor leading to the development of SDHs. Although direct trauma to the dura, brain, or skull or a pre-existing arachnoid cyst can lead to the formation of a SDH, the most common mechanism is traumatic acceleration/deceleration injury.
The trauma required to produce a chronic SDH is often mild and is usually not accompanied by period of unconsciousness.19,24-26 The interval from time of trauma to presentation is variable, ranging from three weeks to 12 years.24,26 However, a history of trauma often is not elicited from the patient or the patient’s family. In multiple studies, a history of trauma was documented in only 55-65% of patients with chronic SDHs.27,28
This is in contrast to acute SDHs in which the trauma required to produce an acute subdural is usually severe. Most patients present within hours of the initial injury.
Anticoagulation plays a significant role in the predisposition for SDH. In one review of 116 anticoagulant-related intracranial hemorrhages, approximately 40% were chronic subdurals and nearly 80% of patients were older than 80 years of age.29 Since warfarin use has increased steadily during the last decade, consideration of anticoagulant-related SDH in the elderly becomes even more important.30 The risk of SDH also is increased with other bleeding diatheses such as hemophilia, thrombocytopenia, and hepatogenic coagulopathies.24
Uncommon etiologies for subdural bleeding other than trauma include rupture of a cerebral aneurysm or arteriovenous malformation (AVM), brain tumors, meningeal carcinomatosis, and sarcoidosis.31-34 A rare cause of chronic SDHs is local infection.35
Other at-risk populations include renal dialysis patients and alcoholics. Renal dialysis patients’ predisposition stems from platelet dysfunction, anticoagulation, and intracranial hypotension.36 Alcoholic patients are predisposed to the development of SDHs because of frequent trauma (such as falls), cerebral atrophy, and coagulopathies associated with cirrhosis. Alcohol abusers have a significantly higher incidence of acute SDH and have increased postoperative morbidity and mortality compared to non-alcoholics.37
Acute SDHs usually occur when the brain is subjected to a high-energy, short-duration force from trauma.38 This mechanism produces shearing forces that not only tear the bridging veins and result in an acute SDH, but also often produce frontal and temporal cerebral contusions. Shear forces also damage the cerebral vasculature and disturb cerebral autoregulation.38 Cerebral vascular damage may be responsible for the high incidence of associated cerebral edema, which predisposes to secondary ischemic brain damage.39
The mechanism responsible for the development of subdural hemorrhage is a traumatic acceleration/deceleration of the head. This results in differential movement of the brain relative to the skull and in tearing or stretching of cortical bridging veins.40 The elderly are predisposed to bleeding via this mechanism because of generalized cerebral atrophy and an increase in venous fragility. Cortical bridging veins are short, straight trunks that pass directly from the dura to the brain. These bridging veins are placed under stress as the atrophying brain separates from the dura. Since these thin, fragile veins are firmly adherent to both the dura and the mobile cerebral hemisphere, they are intolerant of significant movement and bleed easily when injured.41 Acute subdurals also may develop from chronic SDHs as a result of recurrent trauma or following surgical evacuation of a chronic subdural hemtoma.42
In contrast, the pathophysiology of chronic SDHs is complex and involves slow evolution and development of the hematoma over a prolonged time period.35 The unique pathophysiology characterizing chronic SDHs was initially described using light microscopy more than half a century ago.43 On the first day, the outer surface of the developing hematoma is covered with a thin layer of fibrin and fibroblasts begin to migrate from the undersurface of the dura toward the clot. On day four, a membrane forms on the outer surface of the clot and subsequently enlarges. After approximately two weeks, there exists a thin inner membrane covering the liquefied hematoma. Some subdurals will reabsorb spontaneously, while others will create a chronic SDH by gradual increase in the volume of the encapsulated fluid.
Two theories have been proposed to explain the growth of chronic SDHs. Gardner postulated that partial clot liquefaction increased the protein content within the encapsulated space and thus increased the oncotic pressure within the chronic subdural. The resulting osmotic gradient then caused SDH enlargement.44 Flaws with Gardner’s hypothesis include a normal oncotic pressure following breakdown of red blood cells and identical osmolality of surgically removed SDH, venous blood, and CSF.45,46
The second hypothesis suggests that recurrent bleedings account for the expansion of chronic SDHs.24,47 Ito et al administered Cr51-labeled red blood cells intravenously 6-24 hours prior to the evacuation of SDHs and found up to a 28% concentration of fresh blood within the subdural.48 The recurrent hemorrhage appears to originate from dilated, abnormal vessels contained in the outer membrane of the hematoma.49 Angiogenesis factor, found in increased quantities in chronic SDH, contributes to the development of the increased vascularity of the outer membrane. A coagulopathic environment exists within chronic SDHs, and abnormal levels of fibrinolytic enzymes and increased fibrinolytic activity increase the likelihood of hemorrhage.50-52
Another mechanism to explain the development of a chronic SDH is transformation of a subdural hygroma into chronic SDH. In one study, this was a common occurrence, with one-fourth of patients with traumatic subdural effusion developing a chronic SDH.16 This may occur as a result of new head trauma, which causes a tear in the bridging veins within or external to the subdural fluid collection. However, most patients with such a transformation deny any recent head trauma.15,40 Another plausible mechanism involves multiple, recurrent microhemorrhages occurring from the subdural hygroma membrane.15 It is hypothesized that brain atrophy may predispose patients to this transformation; however, it has been observed in patients as young as 18 years of age.13,15
The pathogenesis of subdural hygromas is still unknown but is believed to involve minor trauma that results in the separation of the dura-arachnoid interface, producing a potential subdural space. Proliferation of the dural border cell layer results in a neomembrane with hyper-permeable capillaries.53,54 A subsequent efflux of CSF or leakage of serous fluid into the subdural space occurs, creating the subdural hygroma.54,55 Repeated microhemorrhages in the subdural hygroma may occur from either bridging vein trauma or bleeding from the neomembranes, resulting in a chronic SDH.
Clinical Presentations and Differential Diagnosis
SDH has been referred to as the "great neurologic imitator."56,57 SDHs can mimic stroke, dementia, and other neurological diseases such as Parkinson’s. Symptoms may be insidious and nonspecific, and a history of head trauma is often lacking. Subtle presentations include mild headache, subtle mental status change, and gait disturbances. SDH must be considered in any older person with an alteration in mental status, especially in those prone to falls or on anticoagulants. Acute changes in a patient’s activities of daily living (ADLs: bathing, dressing, continence, toileting, feeding, and transfers) may be indicative of an acute medical event such as a SDH.
Acute SDHs often present with a clear history of trauma followed by headache and altered level of consciousness. Evidence of direct head trauma such as cephalohematomas or scalp lacerations, however, may be mild or absent. Patients commonly present with a lucid interval and then acutely deteriorate. Acute SDH were present in 17-38% of cases involving "talk and die" patients.58,59 Focal neurological deficits and new gait disturbances may occur. Signs of increased intracranial pressure (ICP) may be noted, but are less likely to be present initially in the elderly because of preexisting brain atrophy. Pupillary changes and posturing are ominous signs. It should be reemphasized that the precipitating trauma, such as a fall from a standing height, may be mild. Patients with subacute SDH often complain of worsening headaches 7-14 days after trauma.60 There may be evidence of old injuries including healing lacerations or abrasions.
The presenting symptoms of chronic SDH are highly variable. Symptoms may occur acutely and suggest other cerebrovascular events. The difficulty in diagnosis is compounded in patients with multiple comorbid conditions and in those who are unable to give a detailed history. The most common presenting symptoms are headache, mental status changes, and hemiparesis.25,27,61 Headache is the presenting complaint in 30-90% of patients.19,28,57,62 The description of the headache ranges from mild and generalized to severe with sudden onset. Headache severity may increase with coughing, straining, and exercise. Nausea and vomiting may occur. Mental status changes can present as dementia, mild confusion, and various levels of decreased consciousness, including obtundation.19,57,62
A recent retrospective analysis found the three most common presentations of chronic subdurals to be symptoms of increased ICP, fluctuating drowsiness, and progressive dementia.26
Presenting complaints may mimic stroke or transient ischemic attacks (TIA). Symptoms vary and include aphasia, hemiparesis, and hemisensory defects.63-66 Possible mechanisms to explain this presentation include decreased regional blood flow from intermittent vessel compression, vascular displacement from parenchymal swelling, and electrophysiologic aberrations such as seizures or cortical depression.63,65,67 Given that the elderly population has higher rates of atherosclerotic disease, focal deficits resulting from decreased cerebral blood flow are more likely. One study hypothesized that these events are temporally associated with repeated episodes of bleeding into the hematoma.65
Patients with chronic SDHs may present with psychiatric symptoms of depression, paranoia, schizophreniform psychosis, manic-depressive psychosis, catatonia, and vague personality and intellectual changes.35,68,69 Although geriatric depression is becoming increasingly recognized, other acute or new-onset psychiatric illnesses are uncommon in this age group, and organic etiologies such as SDH should be sought.
Chronic SDHs also may mimic Parkinson’s disease in their presentation or cause an exacerbation of symptoms in patients who have Parkinson’s. Explanations for this finding include dysfunction of the frontopontine pathways or disturbances of basal ganglia function.70,71
Seizures are both an initial symptom and a risk factor for the development of a SDH. The incidence of seizures with chronic SDHs is approximately 4-6% and decreases to 2-3% following neurosurgical treatment.57,62,72
Although the physical findings of chronic SDH may be varied, the findings tend to correspond to the patient’s presenting symptoms. Papilledema is indicative of increased ICP, but is found less commonly in geriatric patients since any underlying brain atrophy can accommodate a large expanding mass before ICP raises significantly. Common neurological signs include aphasia, cranial nerve palsies, hemiparesis, hemisensory deficits, gait disturbances, and hemianopsia.19,25,28,62
Posterior fossa SDH represent a very rare clinical entity, if newborns are excluded. They occur in less than 2% of all SDHs.25,73 Posterior fossa SDHs result from occipital trauma that injures bridging vessels or venous sinuses. Clinical presentations include complaints of nausea, vomiting, headache, decreased level of consciousness, cranial nerve palsies, nuchal rigidity, cerebellar signs and symptoms, and papilledema. There are often signs of brainstem compression: miosis, mydriasis, nystagmus, anisocoria, flaccid or hypertonic limbs, and eye deviation. The clinical course is rapid and decline usually occurs within the first nine hours after injury.73 Prognosis is dismal; less than 5% of patients survive. Negative outcome predictors include: advanced age, rapid clinical deterioration, brainstem compression, associated intracranial lesions, delayed surgery, and completely obliterated posterior fossa cisterns on head CT.73,74
Epidural hematomas are seen much less commonly than subdurals in the elderly. This is thought to be the result of the close attachment of the dura to the periosteum of the inner table, which obliterates the potential space and prevents the hematoma from developing.
Differential diagnosis of SDH includes dementia, stroke, TIA, encephalitis, adverse drug reactions, psychiatric disorders, brain tumors, and subarachnoid hemorrhage. (See Table 1.) Careful history and physical examination can help differentiate these conditions.18 Older patients, however, often have underlying neurological disease and differentiating acute findings; cognitive impairment and changes from the patient’s baseline may be difficult. Liberal use of CT scanning is recommended in this population.41 Antiplatelet and anticoagulant therapy should not be instituted in patients with focal or transient neurological deficits until SDH is excluded.64,75
|Table 1. Differential Diagnosis for SDH|
|- Normal pressure hydrocephalus|
|- Parkinson's disease|
|- Infection (meningitis, brain abscess)|
|- Psychiatric illness|
|- CNS tumor|
|- Adverse drug reactions|
The diagnosis of acute and chronic SDHs has changed considerably since the advent of CT scanning. Prior to this, the diagnosis was suggested by abnormal skull radiographs and confirmed by cerebral angiography. Plain films were abnormal in up to 50% of cases (demonstrating depression or lateral displacement of the pineal gland); however, this finding was neither sensitive nor specific.25,57,62 Angiography was the standard means for diagnosing SDHs for many years, with accuracy approaching 99%. Subdurals would appear as an avascular region between the cortical surface of the brain and the inner table of the skull.25,28,62 Angiography, still in use just two decades ago, was invasive, time consuming, and not without risk. Radioisotope brain scans have also been used in the past to detect SDHs. They were only reliable in well-developed hematomas and had high false-negative rates in patients with scalp trauma, Paget’s disease, infection, and tumor.56,76-78
Noncontrast head CT scans provide a reliable, noninvasive means for detecting acute and chronic SDHs. A peripheral area of either high or low density, when contrasted with normal brain tissue, is easily identified. As was alluded to above, a SDH is a dynamic entity; therefore, its appearance on CT scans depends upon the phase of its development.79-81
In the acute setting, SDHs usually appear as a hyperdense crescentic-shaped mass overlying the cortical surface. (See Figure 1.) Since the subdural space is continuous around each hemisphere, the hematoma is free to completely surround these structures while respecting the midline and tentorial margins.81 Occasionally, a hyperacute SDH may appear hypodense if imaged prior to clot formation. Hypodense areas may also appear within an acute SDH (mixed-density SDH) because of active bleeding.82 Acute SDH can also appear hypodense in patients with significant underlying anemia (hemoglobin concentrations less than 8-10 g/dL).83 Although usually easily visualized, acute SDH can be difficult to appreciate if the collection occurs under the temporal lobe or along tentorial surfaces. (See Figure 2.)
Between the first and third weeks after formation, a SDH may become isodense to brain tissue because of lysis of red blood cells and resorption of hemoglobin. (See Figure 3.) Effacement of sulci, inward displacement of the normal gray-white junction, deformation of normal ventricular anatomy, and obliteration of basal cisterns may indirectly identify these isodense collections.79,84,85 Medial displacement of cortical sulci away from the inner table of the skull is highly suggestive of isodense SDH. Conversely, good visualization of the cortical sulci extending to the inner table of the skull rules out an isodense SDH.86 Bilateral isodense subdurals are more difficult to detect but may appear as obliteration of basal cisterns and blunting of the normal gyral and sulcal anatomy.84 In addition, small compressed ventricles, although not a specific finding, should suggest the possibility of bilateral isodense SDHs.86 Contrast-enhanced CT scans are useful for visualization of isodense subdurals. Contrast enhancement of the cortical surface and inner membrane of the SDH, which are displaced from the inner table of the skull, allows for easier detection.85,87,88 A scanning delay of 3-6 hours allows for visualization of the hematoma itself.89
In the third week, the clot becomes hypodense relative to brain tissue and is usually readily apparent on CT scan. (See Figures 4 and 5.) Chronic SDH commonly occur bilaterally, especially in the very elderly (older than 75 years).90 Acute hemorrhage can occur in a chronic SDH after only minor trauma. Blood tends to layer on the fibrovascular membranes that bridge the subdural space, creating a multilocular appearance.81 (See Figure 6.) This should be differentiated from the layering of blood products (hematocrit effect) seen in acute subdurals when patients are left undisturbed for several hours.
Subdural hygromas, which are often frontal, are also hypodense fluid collections. (See Figure 7.) Differential diagnosis includes chronic SDH or brain atrophy with enlargement of the subarachnoid space.91 Hygromas usually arise 1-2 weeks after trauma, which helps differentiate them from chronic SDH. As with chronic SDHs, fluid in the subdural space tends to collect anteriorly, especially in elderly patients. The distinction between these two entities is not always possible radiographically, unless a CT scan was performed at the time of the initial trauma.
Although CT remains the imaging modality of choice for detecting SDHs in the acute setting, magnetic resonance imaging (MRI) has better sensitivity.69 SDHs have shorter T1 and longer T2 values when compared to normal brain. Chronic SDH are often hyperintense on T1 and T2 weighted scans and are rarely isodense on T1 images.61,92,93 Low intensity T2 images due to recurrent bleeding are common in symptomatic chronic SDH, and MRI findings correlate well with the age of the hematoma and onset of symptoms.94 MRI also clearly demonstrates isodense SDH better than CT. It is also significantly better at identifying small or transversely oriented SDH collections, interhemispheric SDH, and SDH at the base of the skull and in the posterior fossa, since it eliminates the bone artifact seen on CT.95,96 Postcontrast MRI can predict progression of acute SDH. Diffuse enhancement, which indicates active bleeding, has been shown to be very sensitive in predicting enlarging hematomas.97
Chronic SDHs can also be detected on EEG by diffuse or unilateral voltage suppression, delta activity, or depression of a rhythm; however, the EEG may also be normal or demonstrate nonspecific findings and imaging is still required to make the diagnosis.43,56,77
Accurate and rapid diagnosis of SDHs is imperative for successful management. The size (measured in mm) and density of the SDH should be noted. Other important CT findings include the degree of midline shift (also noted in mm), effacement of ventricles and cisterns, and associated intracranial hematomas or subarachnoid hemorrhage.
As with all acutely ill or injured patients, initial management of head injuries begins with rapid assessment and attention to airway, breathing, and circulation (ABCs). Attention to the ABCs will limit secondary insults from hypoxemia and increased ICP. Initial assessment should assess the patient’s level of consciousness and responsiveness and pupillary reactivity. The GCS is a rapid, reliable, and reproducible score for head injury patients. It is useful both for predicting prognosis and for frequent reassessment of these patients. (See Table 2.)
|Table 2. Glasgow Coma Scale (GCS)|
Indications for endotracheal intubation include airway control and hyperventilation. Although a GCS of 8 or less often indicates loss of airway protection, snoring respirations, accumulation of secretions in the oral pharynx, and lack of cough or gag response provide more direct evidence of the need for airway protection. In the setting of normal respiratory function, intubation will also ensure adequate oxygenation. Since critical management decisions are often based on serial neurological examinations and GCS scores, routine use of long acting paralytic agents is not advocated.98
The role of hyperventilation in the management of acute head injury is somewhat controversial.99,100 The benefit of hyper- ventilation is that it reduces PC02, causing a subsequent cerebral vasoconstriction, which in turn reduces ICP. The goal is a PC02 of approximately 30-35 mmHg; levels less than 35 mmHg should be avoided in the first 24 hours post-injury. However, it is now recognized that maintaining cerebral perfusion pressure (CPP) should guide therapy in traumatic brain injuries. CPP is defined as the mean arterial pressure (MAP) minus ICP. Ideally, CPP should be kept at approximately 70 mmHg.101 The beneficial affects of hyperventilation appear short-lived, and hyperventilation can actually lower cerebral blood volumes and thus reduce CPP. Despite these controversies, hyperventilation remains commonly used in patients with documented or suspected increased ICP.
Osmotic diuresis, another common means of ICP management, is also controversial.101-103 Mannitol at doses of 0.5-1.0 gm/kg IV is commonly used as a temporizing measure in the setting of acute changes in the neurologic exam (such as posturing or other evidence of herniation), increasing hematoma size, or uncontrollable ICP. Osmotic diuretics, such as mannitol, should be used to maintain CPP greater than or equal to 70 mmHg in the euvolemic or hypervolemic patient. Injudicious use in the hypovolemic patient can result in lowering the MAP with a resulting decrease in CPP. This may be especially critical in the elderly trauma patient, since accurate evaluation of volume status can be difficult.104 If hypovolemia is present or suspected, volume replacement should be employed, and followed by pressors if necessary to maintain the MAP. The most commonly used pressors include norepinephrine (Levophed; 3-12 micrograms/minute IV) or phenylephrine (Neo-Synephrine; 40-180 micrograms/minute IV). Pressor agents should not be used for neurological resuscitation without ICP and MAP monitoring.101
Specific management of acute and chronic subdurals, including indications for neurosurgical interventions, will be discussed below.
Management of acute SDHs depends on the patient’s neurological exam, including GCS and CT findings, with attention to SDH size, midline shift, and cistern effacement. Patients who have an acute SDH with a thickness of 10 mm or less and a shift of the midline structures of 5 mm or less can often be treated nonoperatively.
In one large, retrospective series of patients with acute SDH, 61% were managed nonoperatively.105 These patients tended to have small SDH (< 10 mm), higher GCS scores (mean of 11), and less evidence of associated brain injury (open paramesencephalic cisterns and less midline shift). For patients with GCS scores of 9-15, craniotomy was not associated with a difference in outcome. The importance of the pre-hospital and admitting GCS scores for determining treatment also has been examined. Patients with stable GCS scores who did not meet CT criteria for surgery were treated conservatively in one prospective study. Fifteen of 65 patients were managed nonoperatively; two required subsequent operations. Functional outcomes were achieved in two-thirds of patients treated with nonoperative management.98 In another series of acute SDH patients with GCS scores between 11 and 15, 93% achieved a good outcome with nonoperative treatment.106 As these studies suggest, if a small hematoma is not a source of intracranial hypertension or significant neurologic dysfunction, then evacuation provides no advantage.
Conversely, large SDH with shift greater than 5 mm are usually associated with an elevated ICP. In these instances, prompt craniotomy and evacuation is necessary and management of the acute SDH generally takes precedence over other injuries. Early surgery is most important for a subset of patients with pure acute SDHs and a lucid interval after injury. In these cases, associated cerebral damage is mild and neurologic deterioration results from increased ICP due to the hematoma itself. Numerous studies have demonstrated lower mortality (approximately 50% survival) in this group of patients with prompt surgical treatment.107-109
Operative treatment of acute SDHs consists of craniotomy for evacuation of the clot and may include subsequent placement of subdural or intraventricular pressure-monitoring devices. Overall surgical mortality rates range from 33% to 100%.73,110,111 Emergency department burr holes are not useful for the diagnosis or treatment of acute SDH. The thick, nonliquid nature of the clot often prohibits evacuation through a small burr hole and generally requires a craniotomy in most cases.112
If not surgically removed, the SDH may be expected to resolve into liquefied clot within 4-6 weeks and eventually be completely absorbed.39,113 Resolution of acute SDH is primarily seen in young, healthy adults with relatively small hematomas.
The treatment of chronic SDHs is a matter of debate; however, a simplified approach consists of either conservative or operative management. Since chronic SDH is a primary disease of the elderly, treatment modalities ideally should be minimally invasive, expedient, and have the best therapeutic result. Conservative medical management involves mannitol and glucocorticoid administration.114 Surgical evacuation involves craniotomies, burr holes, twist drill craniotomies, or small trephine. The method is determined by the amount of hemorrhage and consistency of the hematoma as assessed by CT or MRI. Morbidity and mortality following surgical evacuation ranges from 5% to 11% and is affected by type of surgical procedure.35
Burr hole craniotomy is the most accepted surgical treatment of chronic SDHs. It has been shown to be an effective treatment with a low incidence of complications in spite of patients’ advanced age and associated comorbid diseases.24,27,28 Recent technical advances have resulted in lower mortality, reduced re-operative rate, and shorter duration of in-patient stay.115,116
Craniotomy with extensive membranectomy is a more invasive surgical technique with a higher rate of complication.24 The use of this technique as the initial treatment of chronic SDH has declined and it is now reserved as a secondary treatment following unsuccessful initial procedures.27,28,117
Re-accumulation of chronic SDH after burr hole craniotomy is a known complication.24,27,118 Re-accumulation of hematoma with fresh blood is more likely with large excisions of the external membrane and may be related to excessive drainage volume.118 A recent study involving very elderly patients recommends that re-operation for persistent fluid collections not be performed if there is clinical improvement in the patient.115
Spontaneous resolution of chronic SDHs is rarely observed. CT findings associated with spontaneous resolution include chronic subdurals that are low density or isodense, that are small in size and associated with ventricular dilation, and those that are found in patients with mild or no clinical signs or symptoms.15,119,120 The mechanism responsible for this spontaneous resolution is hypothesized to involve decreased fibrinolytic activity of the hematoma capsule and of the fluid.119
Other complications from surgical evacuations include subdural empyema, brain abscess, cellulitis, bone-flap infection, and meningitis. Seizures are also a postoperative complication so anticonvulsants are begun preoperatively and continued for six months. Further complications include acute intracerebral hematoma after evacuation. This may occur by hemorrhage into previously undetected areas of contusion, a sudden increase in cerebral blood flow coupled with faulty autoregulation, and damage to parenchymal vessels secondary to rapid shift of cranial contents. Complications also include brain stem hemorrhage, cerebral edema, tension pneumocephalus, and SIADH.
Post-op results of chronic SDH evacuation are dependent on neurologic condition of patients at the time of admission.27
Acute SDHs generally carry a poor prognosis, especially in the elderly. Mortality rates range from 50% to 80% and have not changed significantly in four decades.25,121-124 One study found mortality to be four times higher in older patients than in younger ones.125 Important prognostic factors in addition to age include neurologic presentation, CT scan findings, and delays in craniotomy and hematoma evacuation.
One group examined 315 patients with severe head injuries.126 Patients with SDH had 66% mortality and worse outcomes as measured by the Glasgow Outcome Scale. Predictors of mortality included older age, low motor score on the GCS, and CT scan findings of cerebral edema and midline shift. Pennings found not only significantly worse survival (79% mortality vs 36% mortality for younger patients) in older patients with severe brain injuries, but also significantly worse outcomes, with only one older patient making a favorable recovery. Older patients had both early and late hospital deaths and one-third were attributed to pulmonary, cardiac, or multi-system organ failure.127
Important prognostic factors that are available to the ED physician include pupillary response and GCS. Although bilateral fixed pupils is typically an ominous sign in patients with traumatic intracranial hemorrhage, in one series a full 25% of patients with this finding made a good recovery.128 In this study, however, no patients older than the age of 65 survived and the most important predictor of negative outcome in these patients was the presence of an acute SDH. One recent series examined the initial GCS score and outcome.121 Ninety-one percent of patients with a high GCS (9-15) achieved functional recovery, compared with 23% of patients with a low GCS (3-8). Others have shown that the simple combination of GCS and age can be predictive of poor outcomes (death or persistent vegetative state). In one study, there were no functional survivors in patients with an age older than 60 and a GCS score of less than 5.129 As the authors note, these findings should not be used to decide if treatment is warranted, but instead should be used to guide clinicians and families toward rational treatments and realistic expectations.
CT findings can also help predict outcomes in patients with acute SDH. One report showed that a hematoma thickness less than 10 mm had only a 10% mortality, while mortality rose to 90% with hematomas greater than 30 mm.123 The authors noted a significant increase in mortality (less than 50% survival) with a hematoma thickness greater than 18 mm and a mid-line shift greater than 20 mm. Just as importantly, evidence of brain swelling (additional mid-line shift not explained by hematoma size alone) was a significant factor in outcome. Fifty percent mortality was associated with brain swelling displacement of only 3 mm and patients with swelling greater than 5 mm had only a 25% chance of survival.
The timing of acute SDH evacuation has also been evaluated in regard to prognosis. One group reviewed 82 patients with acute SDH and coma and found that time from injury to operation was the most significant factor in reducing mortality.130 Patients who underwent surgery within four hours had a 30% mortality compared to 90% who had surgery after four hours. Interestingly, patient age did not affect survival. Others have noted improved survival if extra-axial hematomas are evacuated within two hours of neurologic deterioration.124 Functional outcome was also improved with early operation. Not all studies have shown such improvement with early surgery. Another group found age older than 65, low GCS scores, and elevated ICPs, but not timing of surgery, to be associated with poor outcome.109 A recent, larger study examined 211 patients with acute SDH and GCS ranging from 3 to 15. Factors found to be independently associated with outcome were age, admission GCS scores, overall injury severity, and pupillary reactivity.105 In a small subset of patients with large acute SDH and coma, mortality was much lower in those undergoing early craniotomy (30% vs 59%); however, small numbers accounted for the lack of statistical significance.
These studies suggest that although age is an important factor in outcomes in patients with acute SDHs, the extent of the primary underlying brain injury is the most important factor affecting outcome. Functional recovery is possible, even in very elderly patients, if their initial presentation shows only mild impairment in consciousness (i.e., GCS scores of 12 or higher).131,132
In contrast to acute SDH, chronic SDH have a much better outcome. Prognosis is often determined by the patient’s condition on admission, general health, and comorbid diseases.15,25,120 Mortality of patients surgically treated for chronic SDH is approximately 10%. Three-fourths of patients return to their baseline functional level postoperatively.133 The use of burr hole craniotomy and closed-system drainage also limits the surgical risk and can be offered even to very elderly and frail patients. Good outcomes (absent or only mild neurological deficits) have been reported in 76% of older patients treated for chronic SDH by this method.134 These findings reflect the pathophysiology of this entity and the low incidence of significant underlying brain injury.
Few studies have addressed factors influencing function and independence as a long-term outcome in the geriatric head-injured population. One study found that in geriatric trauma patients with a GCS of less than 8, none returned to independent living.135 Another study found that 33% of head-injured elderly patients had a change in domicile following their discharge from the hospital.136
Older adults sustaining mild and moderate head injury show cognitive and behavioral changes and disturbances in mood persisting for greater than one year post-injury.137,138 A review examining cognitive performance in geriatric patients following a closed head injury found that 50% had generalized deterioration and dementia thought to be a consequence of their head trauma.139 Elderly head injured patients perform more poorly at word naming and word fluency, memory testing, and other cognitive abilities than age-matched controls.137,140 These cognitive disturbances may predispose these patients to more falls and as a consequence increase the risk of subsequent head injuries.
Pitfalls. Several pitfalls can occur in the evaluation of elderly patients with SDHs. The most important pitfall is simply not considering the diagnosis. In the elderly, acute SDHs can occur after seemingly minor head trauma or following insignificant injury mechanisms such as a fall. Chronic subdurals may be especially hard to diagnose since there is often no history or seemingly remote history of head trauma. As noted above, presentations can be subtle or can mimic other disease processes such as worsening Parkinson’s disease or dementia. Histories should be obtained or confirmed with family members or caregivers. A history of acute changes in mentation, behavior, or ADLs is potentially significant. The possibility of a SDH in these patients should be kept in mind and if suspected, a CT scan should be obtained.
Conversely, the presence of a small chronic SDH or subdural hygroma may be found in older patients who have other causes for acute mental status change, such as severe hyporthyroidism or hyperosmolar coma. Although beyond the scope of this article, other common etiologies for altered mental status or delirium in older patients such as infection, congestive heart failure, or electrolyte abnormalities should be sought. Careful attention to the history, physical examination (such as signs of hypothyroidism), and laboratory evaluation (electrolytes, renal function, and glucose levels) can be very helpful in assessing these complex patients.
As noted above, CT scans are very sensitive at detecting acute and chronic SDHs. Two pitfalls in CT diagnosis can occur, however. The first, as noted previously, is missing a subacute SDH. The other is missing an acute SDH in an unusual location, such as a parafalcine or tentorial SDH. Careful review, along with neuroradiological consultation (using tele-radiology if necessary), should limit these occurrences.
In addition, the possibility of a cervical spine injury (CSI) should be considered in all patients with a history of trauma and SDH. CSI are not uncommon in the older patient. These injuries most often occur following minor trauma, with falls (70%) being the most common mechanism. CSI in the elderly often involve the upper cervical spine (C1 and C2) and spinal cord injury is either absent or incomplete.141 Radiographic evaluation should include an adequate view of the odontoid. CT scans may be necessary if plain films are not conclusive or suspicious for acute injury.
Disposition of older patients with SDH is fairly straightforward. Absolute indications for emergent neurosurgical consultation include GCS score of 8 or less in the setting of trauma, and CT findings of acute SDH with or without mass affect or obliteration of basal cisterns.101 Patients with acute SDH require admission to an intensive care unit (ICU) setting. If neurosurgical care is not immediately available, patients should be promptly transferred.
Patients with chronic SDH also require neurosurgical consultation, with the urgency of the evaluation depending on the patient presentation, such as the presence of neurologic deficits or an abnormal GCS score. Patients with small chronic SDH and minimal abnormalities on neurologic examination warrant admission for observation and neurosurgical consultation. Patients found to have cystic hygromas are at risk for development of chronic SDH and should followup with their primary care physician who can arrange neurosurgical evaluation as appropriate. Other important factors in disposition include the patient’s living arrangements and consideration of elder abuse.
SDHs are common in elder persons and will increase in incidence as our population grows older. Acute SDHs can occur after varying degrees of trauma and often have devastating outcomes in this age group, especially if diagnosis and treatment are delayed. Initial management of acute head injuries and SDH should be familiar to all emergency physicians. Chronic SDHs are more insidious and can mimic a number of other disease processes in the very elderly. Maintaining a high index of suspicion and liberal use of CT scanning can allow one to make this difficult diagnosis and thus maximize outcomes for this at-risk population.
1. Osler T, Hales K, Baack B, et al. Trauma in the elderly. Am J Surg 1988;156:537-543.
2. Finelli FC, Jonsson J, Champion HR, et al. A case control study for major trauma in geriatric patients. J Trauma 1989;29:541-548.
3. Nagurney JT, Borczuk P, Thomas SH. Elder patients with closed head trauma: A comparison with nonelder patients. Acad Emer Med 1998;5:678-684.
4. Baker SP, O'Neill B, Ginsberg MJ, et al. The Injury Fact Book, 2nd ed. New York: Oxford University Press; 1992.
5. Sattin RW, Huber DAL, DeVito CA, et al. The incidence of fall injury events among the elderly in a defined population. Am J Epidem 1990;131:1028-1037.
6. Rakier A, Guilburd JN, Soustiel JF, et al. Head injuries in the elderly. Brain Inj 1995;9:187-193.
7. Champion HR, Copes WS, Buyer D, et al. Major trauma in geriatric patients. Am J Pub Health 1989;79:1278-1282.
8. van der Sluis CK, Timmer HW, Eisma WH, et al. Outcome in elderly injured patients: Injury severity versus host factors. Injury 1997;28:588-592.
9. Levy DB, Hanlon DP, Townsend RN. Geriatric trauma. Clin Geriatr Med 1993;9:601-620.
10. Evans R. Trauma and Falls. In: Sanders AB, ed. Emergency Care of the Elder Person. St. Louis: Beverly Cracon Publications; 1996:150-170.
11. Lee KS, Park YT, Bae HG, et al. Pathogenesis and fate of traumatic subdural hygroma. Br J Neurosurg 1994;8:551-558.
12. Yamashima T, Yamamoto S. Clinicopathological classification of chronic subdural hematoma. Zent bl Fneurochir 1985;46:304-314.
13. Lee KS, Doh JW, Bae HG, et al. Relations among traumatic subdural lesions. J Korean Med Sci 1996 Feb;11:55-63.
14. Lee KS, Bae WK, Doh JW, et al. Origin of chronic subdural hematoma and relation to traumatic subdural lesions. Brain Inj 1998;12:901-910.
15. Park C, Choi KH, Kim MC, et al. Spontaneous evolution of posttraumatic subdural hygroma into chronic subdural hematoma. Acta Neurochir (Wien) 1994;127;41-47.
16. Murata K. Chronic subdural hematoma may be preceded by persistent traumatic subdural effusion. Neurl Med Chir (Tokyo) 1993;33:691-696.
17. Kannus P, Palvanen M, Niemi S, et al. Increasing number and incidence of fall-induced severe head injuries in older adults: Nationwide statistics in Finland in 1970-1995 and prediction for the future. Am J Epidemiol 1999;149:143-150.
18. Alexander EM, Wagner EH, Buchner DM, et al. Do surgical brain lesions present as isolated dementia: A population-based study. J Am Geriatr Soc 1995 Feb;43:138-143.
19. Fogelholm R, Heiskanen O, Waltimo O. Chronic subdural hematoma in adults. Influence of patient’s age on symptoms, signs and thickness of hematoma. J Neurosurg 1975;42:43-46.
20. Kudo H, Kuwamura K, Izawa I, et al. Chronic subdural hematoma in elderly people: Present status on Awaji Island and epidemiological prospect. Neurol Med Chir (Tokyo) 1992;32:207-209.
21. Nagurney JT, Borczuk P, Thomas SH. Elderly patients with closed head trauma after a fall: Mechanisms and outcomes. J Emer Med 1998;16:709-713.
22. Oreskovich MR, Howard JD, Copass MK, et al. Geriatric trauma: Injury patterns and outcome. J Trauma 1984;24:565.
23. Roy CW, Pentland B, Miller JD. The causes and consequences of minor head injury in the elderly. Injury 1986;17:220-223.
24. Markwalder T-M. Chronic subdural hematomas: A review. J Neurosurg 1981;54:637-645.
25. McKissock W, Richardson A, Bloom WH. Subdural hematoma: A review of 389 cases. Lancet 1960;1:1365-1369.
26. Kotwica Z, Brzezinski J. Clinical pattern of chronic subdural hematoma. Neurochirurgia (Stuttg) 1991;34:148-150.
27. Krupp WF, Jans PJ. Treatment of chronic subdural hematoma with Burr-hole craniostomy and closed drainage. Br J Neurosurg 1995;9:619-627.
28. Richter HP, Klein HJ, Schafer M. Chronic subdural hematomas treated by enlarged Burr hole craniotomy and closed system drainage retrospective study of 120 patients. Acta Neurochir (Wien) 1984;71:179-188.
29. Mattle H, Kohler S, Huber P, et al. Anticoagulation-related intracranial extracerebral hemorrhage. J Neurol Neurosurg Psychiatry 1989;52:829-837.
30. Smith NL, Psaty BM, Furgerg CD, et al. Temporal trends in the use of anticoagulants among older adults with atrial fibrillation. Arch Intern Med 1999;159:1574-1578.
31. Bassett RC, Lemmen LJ. Subdural hematoma associated with bleeding intracranial aneurysm. J Neurosurg 1952;9:443-450.
32. Boop WC Jr, Chou SN, French LA. Ruptured intracranial aneurysm complicated by subdural hematoma. J Neurosurg 1961;18:834-836.
33. Russell DS, Cairns H. Subdural false membrane or hematoma (pachymeningitis internal iaemorrhagica) in carcinomatosis and sarcomatosis of the dura mater. Brain 1934;57:32-48.
34. Modesti LM, Binet EF, Collins GH. Meningtomas causing spontaneous intracranial hematomas. J Neurosurg 1976;45:437-441.
35. Traynelis VC. Chronic subdural hematoma in the elderly. Clin Geriatr Med 1991;7:583-598.
36. Kopitnik TA, deAndrade R Jr, Gold MA, et al. Pressure changes within a chronic subdural hematoma during hemodialysis. Surg Neurol 1989;32:289-293.
37. Sonne NM, Tonnesen H. The influence of alcoholism on outcome after evacuation of subdural hematoma. Br J Neurosurg 1992;6:125-130.
38. Gennarelli TA, Speilman GM, Langfitt TW, et al. Influence of the type of intracranial lesion on outcome from severe head injury. A multicenter study using a new classification system. J Neurosurg 1982;56:26-32.
39. Adams JH. Brain Damage in Fatal Non-missile Head Injury. In: Vinken PJ, Bruyn GW, Klawans HL, eds. Handbook of Clinical Neurology, Vol 57. Amsterdam: Elsevier Science Publishers; 1990;43-63.
40. Cooper PR. Post-traumatic Intracranial Mass Lesion. In: Cooper PR, ed. Head Injury, 3rd ed. Baltimore: Williams & Wilkins; 1993:275-329.
41. Mandavia D. Newton K. Geriatric trauma. Emerg Med Clin North Am 1998;16:257-274.
42. Turgut M, Akalan N, Saglam S. A fatal acute subdural hematoma occurring after evacuation of "contralateral" chronic subdural hematoma. J Neurosurg Sci 1998;42:61-63.
43. Munro D, Merritt HH. Surgical pathology of subdural hematomas. Based on a study of one hundred and five cases. Arch Neurol 1936;35:64-78.
44. Gardner WJ. Traumatic subdural hematoma with particular reference to the latent interval. Arch Neurol Psych 1932;27:847-858.
45. Rabe EF, Flynn RE, Dodge, PR. A study of subdural effusions in an infant with particular reference to the mechanisms of their persistence. Neurology 1962;12:79-92.
46. Weir B. The osmolality of subdural hematoma fluid. J Neurosurg 1971;34:528-533.
47. Putnam TJ, Cushing H. Chronic subdural hematoma: Its pathology, its relations to pachymeningitis hemorrhagica and its surgical treatment. Arch Surg 1925;11:329-393.
48. Ito H, Yamamoto S, Saito K, et al. Quantitative estimation of hemorrhage in chronic subdural hematoma using the 51Cr erythrocyte labeling method. J Neurosurg 1987;66:862-864.
49. Sato S, Suzuki J. Ultrastructural observations of the capsule of chronic subdural hematoma in various clinical stages. J Neurosurg 1975;43:569-578.
50. Ito H, Komai T, Yamamoto S. Fibrinolytic enzyme in the lining walls of chronic subdural hemtoma. J Neurosurg 1978;48:197-200.
51. Kawakami Y, Chikama M. Tamiya T, et al. Coagulation and fibrinolysis in chronic subdural hematoma. Neurosurgery 1989;25:25-29.
52. Saito K, Ito H, Hasegawa T, et al. Plasmin-02-plasmin inhibitor complex and 02-plasmin inhibitor in chronic subdural hematoma. J Neursurg 1989;70:68-72.
53. Friede RL, Schachenmayr W. The origin of subdural neomembranes: II. Fine structure of neomembranes. Am J Pathol 1978;92:69-84.
54. Hasegawa M, Yamashima T, Yamashita J, et al. Traumatic subdural hygroma: Pathology and meningeal enhancement on magnetic resonance imaging. Neurosurgery 1992;31:580-585.
55. Fobben ES, Grossman RI, Hackney DB, et al. MR characteristics of subdural hematomas and hygromas at 1.5 T. AJR 1989;153:589-595.
56. Potter JF, Fruin AH. Chronic subdural hematoma—The Great Imitator. Geriatrics 1977;32:61-66.
57. Luxon LM, Harrison MJ. Chronic subdural hematoma. Q J Med 1979;48:43-53.
58. Lobato RD, Rivas JJ, Gomez PA, et al. Head-injured patients who talk and deteriorate into coma. J Neurosurg 1991;75:256-261.
59. Marshall LF, Gautile T, Klauber MR, et a.: The outcome of severe closed head injury. J Neurosurg 1991;75:S28-S36.
60. Nomura S, Oritz T, Tsurutani T, et al. Subacute subdural hematoma: Report of 3 cases. Nippon Geka Hokan 1996;65:30-35.
61. Maggio WW. Chronic Subdural Hematoma in Adults. In: Apuzzo MLJ, ed. Brain Surgery, Vol 2. New York: Churchill Livingstone, 1993;1299-1314.
62. Cameron MM. Chronic subdural hematoma: A review of 114 cases. J Neurol Neurosurg Psychiatry 1978;41:834-839.
63. Mishriki YY. Subdural hematoma mimicking a transient ischemic attack due to antihypertensive medication. South Med J 1999;92:905-906.
64. Cher LM, White OB. Subdural hematoma presenting with transient neurological deficits. Med J Aust 1992;156:654-655.
65. Moster ML, Johnston DE, Retnmuth OM. Chronic subdural hematoma with transient neurological deficits: A review of 15 cases. Ann Neurol 1983;14:539-542.
66. Russell NA, Goumnerova L, Atack EA, et al. Chronic subdural hematoma mimicking transient ischemic attack. J Trauma 1985;25:1113-1114.
67. Ikeda K, Ito H, Yamashita J. Relation of regional cerebral blood flow to hemiparesis in chronic subdural hematoma. Surg Neurol 1990;33:87-95.
68. Black DW. Subdural hematoma: A retrospective study of the great neurologic imitator. Postgrad Med 1985;78:107-115.
69. Elie M, Primeau F, Cole MG. Chronic subdural hematoma in the elderly: A case report. J Geriatr Psychiatry Neurol 1996;9:100-101.
70. Wiest RG, Burgunder JM, Krauss JK. Chronic subdural haematomas and Parkinsonian syndromes. Acta Neurochir (Wien) 1999;141:753-758.
71. Ellis GL. Subdural hematoma in the elderly. Emerg Med Clin North Am 1990;8:281-294.
72. Rubin G, Rappaport ZH. Epilepsy in chronic subdural hematoma. Acta Neurochir (Wien) 1993;123:39-42.
73. Borzone M, Rivano C, Altomonte M, et al. Acute traumatic posterior fossa subdural hematomas. Acta Neurochir (Wien) 1995;135:32-37.
74. Tsai FY, Teal JS, Itabashi HH, et al. Computed tomography of posterior fossa trauma. J Comput Assist Tomog 1980;4:291-305.
75. Ferro JM, Pinto AN, Falcao I, et al. Diagnosis of stroke by the noneurologist. A validation study. Stroke 1998;29:1106-1109.
76. Cowan RJ, Maynard CD, Lassiter KR. Technetium-99m pertechnetate brain scans in the detection of subdural hematomas: A study of the age of the lesion as related to the development of a positive scan. J Neurosurg 1970;32:30-34.
77. Lusins J, Jaffe R, Bender MB. Unoperated subdural hematomas: Long-term follow-up study by brain scan and electroencephalography. J Neurosurg 1976;44:601-607.
78. Raskind R, Glover MB, Weiss SR. Chronic subdural hematoma in the elderly: A challenge in diagnosis and treatment. J Am Geriatr Soc 1972;20:330-334.
79. Haar Fl, Lott TM, Nicholas P Jr. The usefulness of CT scanning for subdural hematomas. Neurosurgery 1977;1:272-275.
80. Scotti G, Terbrugge K, Melancon D, et al. Evaluation of the age of subdural hematomas by computerized tomography. J Neurosurg 1977;47:311-315.
81. Klufas RA, Hsu L, Patel MR, et al. Unusual manifestations of head trauma. AJR 1996;166:675-681.
82. Reed D, Robertson WD, Graeb DA, et al. Acute subdural hematomas: Atypical CT findings. AJNR 1986;7:417-421.
83. Smith WP, Batnitzky S, Rengachary SS. Acute isodense subdural hematomas: A problem in anemic patients. AJR 1981;136:543-546.
84. Weisberg LA. The significance of nonvisualization of the cortical sulcal spaces on computed tomography. Comput Radiol 1982;6:337-341.
85. Weisberg LA. Analysis of the clinical and computed tomographic findings in isodense subdural hematoma. Comput Radiol 1986;10:245-252.
86. Kim KS, Hemmati M, Weinberg PE. Computed tomography in isodense subdural hematoma. Radiology 1978;128:71-74.
87. Hayman LA, Evans RA, Hinck VC. Rapid-high-dose contrast computed tomography of isodense subdural hematoma and cerebral swelling. Radiology 1979;131:381-383.
88. Marcu H, Becker H. Computed-tomography of bilateral isodense chronic subdural hematomas. Neuroradiology 1977;14:81-83.
89. Karasawa H, Tomita S, Suzuki S. Chronic subdural hematomas: Time-density curve and iodine concentration in enhanced CT. Neruoradiology 1987;29:36-39.
90. Spallone A, Giuffre R, Gagliardi FM, et al. Chronic subdural hematoma in extremely aged patients. Eur Neurol 1989;29:18-22.
91. Deltour P, Lemmerling M, Bauters W, et al. Posttraumatic subdural hygroma: CT findings and differential diagnosis. JBR-BTR 1999;82:155-156.
92. Hosoda K, Tamaki N, Masumura M, et al. Magnetic resonance images of chronic subdural hematomas. J Neurosurg 1987;67:677-683.
93. Sipponen JT, Sepponen RE, Sivula A. Chronic subdural hematoma: Demonstration by magnetic resonance. Radiology 1984;150:79-85.
94. Kaminogo M, Moroki J, Ochi A, et al. Characteristics of symptomatic chronic subdural haematomas on high-field MRI. Neurorad 1999;41:109-116.
95. Kelly AB, Zimmerman RD, Snow RB, et al. Head trauma: Comparison of MR and CT experience in 100 patients. AJNR 1988;9:699-708.
96. Romano VA, Toffol GJ. Confirmation of traumatic interhemispheric subdural hematoma by magnetic resonance imaging. J Emerg Med 1994;12:369-373.
97. Tomida M, Muraki M, Uemura K, et al. Post contrast magnetic resonance imaging to predict progression of traumatic epidural and subdural hematomas in the acute stage. Neurosurgery 1998;43:66-71.
98. Servadei F, Nasi MT, Cremonini AM, et al. Importance of a reliable admission Glasgow Coma Scale score for determining the need for evacuation of posttraumatic subdural hematomas: A prospective study of 65 patients. J Trauma 1998;44:868-873.
99. Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: A randomized clinical trial. J Neurosurg 1991;75:731-739.
100. Obrist WD, Langfitt TW, Jaggi JL, et al. Cerebral blood flow and metabolism in comatose patients with acute head injury. J Neurosurg 1984;61:241-253.
101. Gruen P, Liu C. Current trends in the management of head injury. Emerg Med Clin North Am 1998;16:63-83.
102. Cruz J, Miner ME, Allen SJ, et al. Continuous monitoring of cerebral oxygenation in acute brain injury: Injection of mannitol during hyperventilation. J Neurosurg 1990;73:725-730.
103. Mendelow AD, Teasdale GM, Russell T, et al. Effect of mannitol on cerebral blood flow and cerebral perfusion pressure in human head injury. J Neurosurg 1985;63:43-48.
104. Scalea TM, Simon HM, Duncan AO, et al. Geriatric blunt multiple trauma: Improved survival with invasive monitoring. J Trauma 1990;30:129-136.
105. Dent DL, Croce MA, Menke PG, et al. Prognostic factors after acute subdural hematoma. J Trauma 1995;39:36-42.
106. Croce MA, Dent DL, Menke PG, et al. Acute subdural hematoma: Non-surgical management of selected patients. J Trauma 1994;36:820.
107. Stone JL, Lowe RJ, Jonasson O, et al. Acute subdural hematoma: Direct admission to a trauma center yields improved results. J Trauma 1986;26:445-450.
108. Singounas EG, Sfakianos G, Sourtzis I, et al. "Benign" acute subdural haematomas. Acta Neurochir (Wien) 1990;106:140-144.
109. Wilberger JE, Harris M, Diamond DL. Acute subdural hematoma: Morbidity and mortality related to timing of operative intervention. J Trauma 1990;30:733-736.
110. St. John JN, French BN. Traumatic hematomas of the posterior fossa. A clinicopathological spectrum. Surg Neurol 1986;25:457-466.
111. Hecimovic I, Blagus G, Kristek B, et al. Successful treatment of traumatic acute posterior fossa subdural hematoma: Report of two cases. Surg Neurol 1999;51:247-251.
112. Lowe JG, Northrup BE. Traumatic Intracranial Hemorrhage. In: Evans RW, ed. Neurology and Trauma. Philadelphia: WB Saunders; 1996;140-150.
113. McCorrnick WF. Pathology of Closed Head Injury. In: Wilkins WH, Rengachay SS, ed. Neurosurgery. Vol 2. New York: McGraw-Hill; 1965:1544-70.
114. Drapkin AJ. Chronic subdural hematoma: Pathophysiological basis for treatment. Br J Neursurg 1991;5:467-473.
115. Zingale A, Albanese V, Romano A, et al. Traumatic chronic subdural hematoma over 80 years. A preliminary prospective study. J Neurosurg Sci 1997;41:169-173.
116. Smely C, Madlinger A, Scheremet R. Chronic subdural hematoma - A comparison of two different treatment modalities. Acta Neurochir (Wien) 1997;139:818-825.
117. Tyson G, Strachan WE, Newman P, et al. The role of craniectomy in the treatment of chronic subdural hematomas. J Nuerosurg 1980;52:776-781.
118. Matsumoto K, Akagi K, Abekura M, et al. Recurrence factors for chronic subdural hematomas after burrhole craniostomy and closed system drainage. Neurol Res 1999 Apr;21:277-280.
119. Nakamura H, Ogawa T, Hashimoto T, et al. Reevaluation on resolving subdural hematoma. Neurol 1981;21:491-500.
120. Naganuma H, Fukamachi A, Kawakami M, et al. Spontaneous resolution of chronic subdural hematomas. Neurosurgery 1986;19:794-798.
121. Koc RK, Akdemir H, Oktem IS, et al. Acute subdural hematoma: Outcome and outcome prediction. Neurosurg Rev 1997;20:239-244.
122. Massaro F, Lanotte M, Faccani G, et al. One hundred and twenty-seven cases of acute subdural hematoma operated on. Correlation between CT scan findings and outcome. Acta Neurochir (Wien) 1996;138:185-191.
123. Zumkeller M, Behrmann R, Heissler HE, et al. Computed tomographic criteria and survival rate for patients with acute subdural hematoma. Neurosurgery 1996;39:708-712.
124. Haselberger K, Pucher R, Auer LM. Prognosis after acute subdural or epidural hemorrhage. Acta Neurochir (Wien) 1988;90:111-116.
125. Howard III MA, Gross AS, Dacey RJ, et al. Acute subdural hematomas: An age-dependent clinical entity. J Neurosurg 1989;71:858-863.
126. Fearnside MR, Cook RJ, McDougal P, et al. The Westmead Head Injury Project outcome in severe head injury. A comparative analysis of pre-hospital, clinical and CT variables. Br J Neurosurg 1993;7:267-279.
127. Pennings JL, Bachulis BL, Simons CT, et al. Survival after severe brain injury in the aged. Arch Surg 1993;128:787-794.
128. Sakas DE, Bullock MR, Teasdale GM. One-year outcome following craniotomy for traumatic hematoma in patients with fixed dilated pupils. J Neurosurg 1995;82:961-965.
129. Quigley MR, Vidovich D, Cantella D, et al. Defining the limits of survivorship after very severe head injury. J Trauma 1997;42:7-10.
130. Seelig JM, Becker DP, Miller JD, et al. Traumatic acute subdural hematoma. Major mortality reduction in comatose patients treated within four hours. N Engl J Med 1981;304:1511-1518.
131. Caggetti B, Cossu M, Pau A, et al. The outcome from acute subdural and epidural intracranial hematomas in very elderly patients. Br J Neurosurg 1992;6:227-232.
132. Jamjoom A. Justification for evacuating acute subdural hematomas in patients above the age of 75 years. Injury 1992;23:518-520.
133. Bollmer D, et al. Age and outcome following traumatic coma: Why do older patients fare worse, in report on Traumatic Coma Data Bank. J Neurosurg 1991;75(suppl):537-549.
134. Ernestus RI, Beldzinski P, Lanfermann H, et al. Chronic subdural hematoma: Surgical treatment and outcome in 104 patients. Surg Neurol 1997 Sep;48:220-225.
135. VanAalst JA, Morris JA, Kendle H, et al. Severely injured geriatric patients return to independent living: A study of factors influencing function and independence. J Trauma 1991;31:1096-1102.
136. Wilson JA, Pentland B, Currie CT, et al. The functional effects of head injury in the elderly. Brain Inj 1987;1:183-188.
137. Goldstein FC, Levin HS, Goldman WP, et al. Cognitive and behavioral sequelae of closed head injury in older adults according to their significant others. J Neuropsy Clin Neurosci 1999;11:38-44.
138. Luukinen H, Viramo P, Koski K, et al. Head injuries and cognitive decline among older adults. Neurol 1999;52:557-562.
139. Mazzucchi A, Cattelani R, Massale G, et al. Head injured subjects aged over 50 years: Correlation between variables of trauma and neuropsychological follow-up. J Neurology 1992;239:256-260.
140. Aharon-Peretz J, Kliot D, Amyel-Zvi E, et al. Neurobehavioral consequences of closed head injury in the elderly. Brain Injury 1997;11:871-875.
141. Spivak JM, Weiss MA, Cotler JM, et al. Cervical spine injuries in patients 65 and older. Spine 1994;19:2302-2306.
Physician CME Questions
14. Which of the following statements about acute SDH is correct?
A. Acute SDH are more common in elder patients.
B. Acute SDH develop from traumatic subdural effusions.
C. Acute SDH have a mortality of 50-80%.
D. Acute SDH require a craniotomy and evacuation.
15. Epidemiologic studies of chronic SDH reveal that:
A. chronic SDH increase in incidence with advancing age.
B. it has an annual incidence of 172 cases/100,000/year.
C. it is most commonly caused by MVCs in all age groups.
D. it occurs just as frequently in non-geriatric persons.
16. The pathophysiology of SDH and hygromas has been extensively studied. Which of the following are true?
A. Acute SDH result from direct trauma causing a skull fracture overlying the bridging veins.
B. Transformation of subdural hygromas into chronic SDH is a rare occurrence.
C. Chronic SDH develop from both osmotic gradients and re-bleeding from bridging veins.
D. Subdural hygromas typically occur in older patients and are associated with minor head injuries.