Neurology

Subdural hematoma
Presentation and management in older adults
Bernard Karnath, MD

Subdural hematomas pose diagnostic and therapeutic difficulties in older adults. Presenting signs and symptoms of subdural hematomasheadache, confusion, ataxia, and hemiparesiscan mimic other diseases such as dementia, stroke, transient ischemic attacks, neoplasm, and normal pressure hydrocephalus. Patients with subdural hematomas and focal neurologic signs should be considered for surgical intervention, whereas asymptomatic patients or patients with only complaints of a headache can be managed medically or followed with serial neuroimaging by computed tomography. Patients who have been chronically anticoagulated pose a dilemma when they present with a subdural hematoma.
Karnath B. Subdural hematoma: Presentation and management in older adults. Geriatrics 2004; 58(July):18-23.

Key words: Chronic subdural hematoma anticoagulation falls atrial fibrillation

ubdural hematoma in older patients raises diagnostic and therapeutic difficulties. Acute subdural hematomas, which are clinically evident (ie, symptomatic) within 72 hours, usually occur in younger adults. Chronic subdural hematomas, which usually occur in older individuals with a peak incidence in the sixth and seventh decades of life, are defined as hematomas of more than 20 days of age (typically determined by patient history).1 The incidence of chronic subdural hematoma is approximately 1 in 100,000 population per year; incidence increases to approximately 7

cases per 100,000 population per year in the age 70 to 79 group.2 Significantly, subdural hematoma is a reversible cause of dementia.3
A B

pulse 86 bpm, temperature 36.8oC, and respirations 18/minute. Physical exam is remarkable for a fluctuating mental status, consistent with a delirium. He is somewhat lethargic during examination but cooperative. At other times, he is oriented to place and time. He is normocephalic and without evidence of trauma. Pupils and extraocular muscles are intact. Funduscopic exam is difficult secondary to bilateral cataracts. Cranial nerves II through XII are intact. The patients gait is unsteady. His motor exam reveals 4/5 strength in the left upper and left lower extremity. Computed tomographic (CT) imaging of the brain is shown in figure 1.
Case #2

Figure 1 CT scan of subdural hematoma (A) involving right hemisphere. Note the midline shift (B), blunting of sulci (C), and edema (D). (Visit www.geri.com for a larger image.) Source: Scan supplied by author.

Case #1

Dr. Karnath is assistant profes-

sor of medicine, University of Texas Medical Branch at Galveston, Tx.

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Disclosure: The author has no real or apparent conflicts of interest related to the content presented here. 18

A 64-year-old man presents with a onemonth history of gait ataxia, urinary incontinence, and altered mental status. His past medical history is unremarkable with the exception of chronic alcohol abuse.Vital signs on presentation are blood pressure 110/80mmHg,

A 68-year-old woman with chronic atrial fibrillation (AF),congestive heart failure, and hypertension presents with a oneweek history of worsening headaches. The patient has been on warfarin 5 mg/d for the past 5 years with the international normalized ratio (INR) maintained between 2 and 3.The patient states that she fell on her buttocks two weeks prior to presentation but denies any head trauma. Vital signs on presentation are blood pressure 145/90 mmHg,pulse 86 bpm, temperature 37.6oC, and respirations 16/minute.The patient was alert and oriented to time,place,and person.Cranial nerves II through XII are intact. Funduscopic exam is difficult due to bilateral cataracts. The patients gait is not impaired. Her strength is 5/5 throughout

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with equal deep tendon reflexes. Heart exam reveals irregularly irregular rhythm without murmurs. CT head reveals an isodense right subdural hematoma without midline brain shift.
Etiology

Older adults are at increased risk for subdural hematomas due to fragility of bridging cerebral veins. As cerebral atrophy develops, the brain shrinks away from the dura and bridging veins are predisposed to tearing due to increased stress. A history of trauma is elicited in 75% of cases. Men have a higher incidence of subdural hematoma due to a higher risk of trauma.Although trauma is the most common cause of subdural hematoma, the actual event may be so trivial that some older patients do not remember it.The etiology is undetermined in 25% of cases; these are sometimes termed spontaneous.4,5 Anticoagulant and antiplatelet therapy are associated with an increased risk for spontaneous subdural hematomas.A retrospective study of 123 patients (mean age 74, +/-5) who presented with a spontaneous subdural hematoma found that 76% (93 total patients) were on aspirin (78 patients) and warfarin (15 patients) therapy.6 Other risk factors for developing subdural hematomas include age, male gender, coagulopathy, thrombocytopenia, and alcoholism.2 Alcoholics are at particular risk due to a propensity to fall, in addition to the likely presence of underlying liver disease with secondary coagulopathy and thrombocytopenia. Many subdural hematomas resolve spontaneously before the onset of signs and symptoms.2 A subset of hematomas does progressively enlarge.Whereas several mechanisms have been proposed for the enlargement of subdural hematomas in the chronic state, only one has gained widespread acceptance. This proposed mechanism includes recurrent hemorrhage and fibrinolysis.2 The outer membrane of the hematoma contains a fine network of capillaries. There is an ongoing process of bleeding into the hematoma due to activation
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Subdural hematoma is a reversible cause of dementia. Older adults are at increased risk for subdural hematomas due to fragility of bridging cerebral veins. Presenting symptoms can be subtle and the condition may be overlooked.
Illustration for Geriatrics by Sally Cummings

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of the coagulationfibrinolytic system that results in defective hemostasis and clot formation.As a result, there is slow accumulation of hemorrhage within the subdural space causing compression of the cortex and blunting of sulci (figure 2).

Presentation

The most common presenting symptoms in patients age 60 and older are headache, altered mental status, hemiparesis, gait disturbance, and aphasia.5 In one retrospective study, 68% (30/44) of patients presented with headache,
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Subdural hematoma
ing less readily available than CT scanners and restless patients cannot be examined unless sedation is used. Neuroimaging with CT scanning as the initial diagnostic test should be considered in the presence of rapid unexplained deterioration in mental status,focal neurologic signs, gait disturbance, recent head trauma, and new onset headache. Potentially reversible causes of dementia, such as subdural hematomas, normal pressure hydrocephalus, and tumors, can be detected with CT scan or MRI of the brain. Whereas current clinical practice guidelines for dementia do not recommend routine neuroimaging, expert groups have identified prediction rules for neuroimaging.12 These prediction rules include the following clinical variables in addition to dementia: rapid unexplained decline in cognitive function, focal neurologic signs, gait disorder or ataxia, subdural hematomas from other causes of mental status changes and focal neurologic deficits.13 Alzheimers dementia. Chronic subdural hematomas can be differentiated from Alzheimers dementia based on the onset and progression of memory deficits. Memory impairment in Alzheimers disease develops over several months to years, whereas in chronic subdural hematomas, changes in cognitive function develop over several (approximately 2 to 6) weeks. Some patients with chronic subdural hematomas will show focal neurologic signs whereas patients with Alzheimers dementia will not. Cerebrovascular insults. Cerebrovascular insults can lead to cognitive impairment and focal neurologic signs. However, patients with cerebrovascular insults are more likely to show acute focal neurologic signs and acute mental status impairment (ie, within hours or days) whereas in patients with chronic subdural hematomas focal neurological signs and mental status impairment develop progressively over weeks. Neoplasms. Intracranial neoplasms are difficult to differentiate from chronic subdural hematomas without neuroimaging. Patients with intracranial neoplasms often present with signs of increased intracranial pressure that include headaches, altered mental status, and focal neurologic signs, a similar presentation to chronic subdural hematoma. Neuroimaging would be diagnostic. (Whereas MRI would be the study of choice, it does take longer to obtain and is less readily available than CT scanning.) Normal-pressure hydrocephalus. Symptoms of normal pressure hydrocephalus are similar to those of chronic subdural hematoma with the exception of urinary incontinence. The clinical triad of gait ataxia, altered mental status, and urinary incontinence is considered classic for normal pressure hydrocephalus or other subcortical dementia.14 Whereas urinary incontinence is a late manifestation of normal-pressure hy-

Figure 2. Subdural hematoma causing midline shift.

Source: Illustration supplied by author

39% (17/44) with confusion, 32% (14/44) with ataxia, and 30% (13/44) with hemiparesis. Two neurologic grading systems (table 1) have been proposed to assess the severity of neurological deficits.4,7,8
Diagnosis

The diagnosis of subdural hematoma is definitively established with neuroimaging of the braineither with computed tomography (CT) or magnetic resonance imaging (MRI).Chronic subdural hematomas appear as hypodense (ie, similar density as brain) areas on CT images of the brain after three weeks duration.2 (Tissue density as seen on CT scan is described in Hounsfield unitswith air being the least dense and bone being the most dense. Density of blood in the subdural hematoma varies with the age of the hematoma.) Subdural hematomas are hyperdense in the acute phase (ie, 1 week), isodense in the subacute phase (ie, 2 to 3 weeks), and hypodense in the chronic phase (ie, 3 to 4 weeks).9 According to one study, the density of subdural hematomas may vary after one month.10 Isodense hematomas are difficult to detect on CT scanning and can be detected by evidence of mass effect either by midline shift or blunting of sulci. MRI is a better imaging study for detecting isodense hematomas. MRI would show the isodense hematoma as a hyperintense lesion.11 MRI has the disadvantage of be20

In chronic subdural hematomas, changes in focal neurologic signs and mental status progressively develop over weeks
recent head trauma, anticoagulation, bleeding disorder, new onset headache, and seizures. The presence of any one of these clinical variables might increase the likelihood of finding a subdural hematoma.
Differential diagnosis

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The symptoms associated with chronic subdural hematomas can mimic other disorders such as Alzheimers dementia, stroke, transient ischemic attacks, normal pressure hydrocephalus, and intracranial neoplasm. A careful clinical history is mandatory, as the pattern of onset and time course of symptoms will help to differentiate chronic

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drocephalus, it is usually not encountered in chronic subdural hematomas. Differentiating normal-pressure hydrocephalus from chronic subdural hematoma based on clinical exam alone can be difficult; neuroimaging would be diagnostic.
Management
Surgical. Smely and colleagues found

Table 1 Neurologic grading systems for subdural hematomas

Bender
Group 1 Normal mental function; no focal signs

Markwalder
Grade 0 Grade 1 No neurologic signs Headache; reflex asymmetry Altered mental status hemiparesis Stupor but responsive; hemiplegia Coma; decerebrate or decorticate posturing

Group 2 Group 3

Lethargic; focal neurologic signs Stuporous; marked focal neurologic signs Coma; signs of hibernation (pupillary dilation, decerebrate or decorticate posturing, respiratory arrest)

Grade 2 Grade 3

twist-drill trephination (TDT) with a CORDIS catheter to be a superior treatment to burr-hole craniotomy (BHC) with closed-system drainage.15 In their study, 18% (6/33) of patients who underwent TDT required repeat surgical intervention as compared with 33% (11/33) of patients who underwent BHC; another 6% of these BHC patients had to operated on a third time. Total mortality rate was 6% for patient undergoing TDT versus 9% for patients undergoing BHC. Craniotomy is reserved for patients with re-accumulating hematoma or residual hematoma membrane that prevents re-expansion of the brain. Medical. Medical management is an option for patients with minimal neurologic signs, ie, headache only with no other neurologic signs, no focal neurologic deficits or memory impairment. Conservative therapy consists of inpatient observation, a trial of steroids or mannitol and serial CT scans. Inpatient medical management of chronic subdural hematomas can result in a hospital stay of 4 to 22 weeks.16 Medical management has not been widely used because patients generally do well after surgical treatment and require considerably shorter hospital stays (eg, 4 weeks). Inzelberg and colleagues reported successful non-surgical treatment of a subdural hematoma in a hemodialysis patient in whom surgery was contraindicated.17 The patient, who was on maintenance anticoagulation treatment because of recurrent clotting of her hemodialysis access, presented with hemiparesis and aphasia.CT scan of the brain revealed a subdural hematoma without midline shift. This patient was
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Group 4

Grade 4

Source: Created for Geriatrics by Bernard Karnath, MD, with information from references 8 and 9.

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Prognosis

started on 16 mg/d of dexamethasone parenterally for two weeks. The steroid treatment was tapered over the subsequent month and a follow-up CT scan revealed no evidence of subdural fluid. Observation. A subset of patients with acute subdural hematomas will resolve spontaneously. Factors favoring spontaneous resolution of hematomas are low-density fluid on CT scan, chronic subdural hematomas of small size, and ventricular dilation as opposed to compression. Asymptomatic patients with small chronic subdural hematomas can be followed with serial CT scans. Parlato and colleagues reported a series of 5 patients who were diagnosed with chronic subdural hematomas and were observed with serial CT scans.18 All patients had spontaneous resolution of their hematomas without medical or surgical intervention.These patients,average age 73, presented with headache and mild cognitive impairment. CT scans showed subdural hematoma without a midline brain shift. All 5 patients had hematoma resolution within a 6week follow-up period.

pital mortality in older patients with subdural hematoma include presenting level of consciousness with Glasgow coma scale <7 (table 2), age >80, acute duration of hematoma formation, and craniotomy.19 The presence of focal neurologic signs and a midline shift on neuroimaging is not associated with increased hospital mortality. Isodensity of the subdural hematoma on CT scan is considered a positive prognostic factor whereas hypodensity of the subdural hematoma on CT scan is considered a negative prognostic factor.20 Isodensity indicates that the subdural hematoma is of short duration. Therefore the brain should re-expand more readily upon drainage of the hematoma.
Chronic Anticoagulation

Mortality rates for subdural hematomas can approach 30%.19 Predictors for hos-

The risks and benefits of chronic anticoagulation, especially in chronic atrial fibrillation, must be considered. Intracranial hemorrhage is the most concerning of complications. The two most common conditions requiring chronic anticoagulation are prosthetic heart valves and chronic atrial fibrillation (AF). Adjusted-dose warfarin has been shown to reduce stroke incidence by 62% in patients with
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Subdural hematoma
Table 2 Glasgow coma scale
Eye opening spontaneous to speech to pain no response Best motor response To verbal command obeys To painful stimulus localizes pain flexion-withdrawal flexion-abnormal extension no response Best verbal response Oriented and converses disoriented and converses inappropriate words incomprehensible sounds no response E 4 3 2 1 M 6 5 4 3 2 1 V 5 4 3 2 1

Scores must be broken down into components, ie, E3V3M5 = GCS 11

* 90% 8 are in coma * 8 at 6 hours, 50% die * 9 note in coma * 9-11 = moderate severity * 8 is critical score * 12 = minor injury
Source: Created for Geriatrics by Bernard Karnath, MD.

chronic AF.20 This benefit was not offset by the occurrence of major hemorrhage. The rate of intracranial hemorrhage is approximately 0.3% per year for patients receiving warfarin with a maintained INR of 2.0 to 3.0. The rate of stroke among patients with chronic AF who are not receiving anticoagulation ranges from 5% to 12% per year.21,22 There is a dramatic increase in the risk for intracranial hemorrhage with increasing INR, especially with INRs greater than 4.0.19 Should the risk of falling influence the decision to place a patient with chronic AF on anticoagulation? A metaanalysis of studies involving older patients with chronic AF who received no therapy, aspirin, or warfarin, found that warfarin provided a 68% relative risk reduction of stroke.23 Patients on chronic
22

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Discussion
Case #1. The patient in case # 1 presents

warfarin who were at risk for falls had a relative risk of 1.4 for developing a subdural hematoma (ie, patients on warfarin with risk for falls are 40% more likely to develop a subdural hematoma). This increased risk of developing a subdural hematoma was overshadowed by the 68% relative risk reduction in stroke for patients on chronic warfarin. Anticoagulation should be reversed with fresh frozen plasma and vitamin K in patients who develop a subdural hematoma. Evidence supports the safety of temporary interruption of anticoagulation therapy in patients with intracranial hemorrhage and mechanical heart valves or AF.24,25 The estimated risk of having an ischemic stroke after discontinuation of warfarin therapy within 30 days was 3% for patients with metallic valves or AF. Phan and colleagues found no recurrences of intracranial hemorrhage in patients who resumed anticoagulation therapy.24 Anticoagulation therapy can be restarted 1 to 2 weeks after evacuation of a subdural hematoma.23-25 Three separate studies involving 83 cases of subdural hematomas in patients receiving chronic anticoagulation reported only one recurrence of hematoma after recommencing warfarin after a mean duration of 7 to10 days of discontinuation.24-26 Some authors recommend CT before and after surgical drain removal to evaluate the possibility of bleeding caused by drain removal.27 No study has evaluated the optimal time to recommence anticoagulation therapy in a patient with a subdural hematoma who was medically managed, ie, no evacuation performed. If evacuation is not performed then a repeat CT should be performed in 1 to 2 weeks. Serial CT scans should be performed during a 4- to 6-week period to confirm resolution of hematoma, at which time anticoagulation can be restarted.

tually consistent with the classic triad of normal pressure hydrocephalus. This case underscores the importance of neuroimaging in making the correct diagnosis. Urinary incontinence is an unlikely finding in chronic subdural hematoma. The patients main risk fac-

Evidence supports safety of temporary interruption of anticoagulation in patients with intracranial hemorrhage
tor for developing a subdural hematoma was alcohol abuse.Alcoholism has been reported to be a predisposing factor in the development of chronic subdural hematoma in up to 35% of patients.20 The chronic use of alcohol leads to liver disease with secondary coagulopathy and thrombocytopenia. Alcoholism is also a risk factor for all categories of trauma. Neuroimaging revealed a large right subdural hematoma with midline shift.The patient had altered mental status with focal neurologic signs (grade 2 Markwalder signs or group 2 Bender signs) and a midline shift was seen on CT scan, providing clear indications for surgical intervention. The patient underwent burr-hole evacuation with closed-system drainage without complications. Conservative management is acceptable in cases where there are minimal signs and symptoms. For example, in a patient who presents with a headache and without focal neurologic signs and the CT scan does not reveal a midline shift, conservative management is appropriate. Case #2. This patient represents a common dilemma for the physician treating a patient with chronic AF.

with signs and symptoms that were ac-

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Older patients with chronic AF are at risk for embolic stroke. The annual stroke incidence in patients with chronic AF is 6% if they are not on chronic anticoagulation. However, an older patient on chronic anticoagulation is at risk for intracranial bleeds. This patient presented with headache (grade 1 Markwalder signs) and was placed under inpatient observation and received serial neuroimaging with CT scanning. Her warfarin was discontinued. The subdural hematoma resolved in 6 weeks. Considering the risk-tobenefit ratio of chronic anticoagulation in patients with chronic AF, warfarin should be restarted once the hematoma has resolved. The risk of developing another subdural hematoma is overshadowed by the risk reduction in stroke prevention.
Conclusion

1990; 83(10):1182-9. 4. Ernestus RI, Beldzinski P , Lanfermann H, Klug N. Chronic subdural hematoma: Surgical treatment and outcome in 104 patients. Surg Neurol 1997; 48(3):220-5. 5. Sambasivan M. An overview of chronic subdural hematoma: Experience with 2300 cases. Surg Neurol 1997; 47(5):418-22. 6. OBrien DF, Basu S, ODonnell JR, Roberts GA, Phillips J. The impact of aspirin therapy and anticoagulation on the prevalence of spontaneous subdural haematoma. Ir Med J 2000; 93(8):244-6. 7. Bender MB, Christoff N. Nonsurgical treatment of subdural hematomas. Arch Neurol 1974; 31(2):73-9. 8. Markwalder TM. Chronic subdural hematomas: A review. J Neurosurg 1981; 54(5):637-45. 9. Scotti G, Terbrugge K, Melancon D, Belanger G. Evaluation of the age of subdural hematomas by computerized tomography. J Neurosurg 1977; 47(3):311-5. 10. Lee KS, Bae WK, Bae HG, Doh JW, Yun IG. The computed tomographic attenuation and the age of subdural hematomas. J Korean Med Sci 1997; 12(4):353-9. 11. de Almeida GM, Laumer R, Fahlbusch R, Sambasivan M, Fuakui M, Wissinger JP . Subdural hematoma. Surg Neurol 1997; 47(1):2-5. 12. Gifford DR, Holloway RG, Vickrey BG. Systematic review of clinical prediction rules for neuroimaging in the evaluation of dementia. Arch Intern Med 2000; 160(18):2855-62.

18. Parlato C, Guarracino A, Moraci A. Spontaneous resolution of chronic subdural hematoma. Surg Neurol 2000; 53(4):312-7. 19. Rozzelle CJ, Wofford JL, Branch CL. Predictors of hospital mortality in older patients with subdural hematoma. J Am Geriatr Soc 1995; 43(3):240-4. 20. El-Kadi H, Miele VJ, Kaufman HH. Prognosis of chronic subdural hematomas. Neurosurg Clin N Am 2000; 11(3):553-67. 21. Hart RG, Benavente O, McBride R, Pearce LA. Antithrombotic therapy to prevent stroke in patients with atrial fibrillation: A meta-analysis. Ann Intern Med 1999; 131(7):492-501. 22. Hylek EM, Singer DE. Risk factors for intracranial hemorrhage in outpatients taking warfarin. Ann Intern Med 1994; 120(11):897-902. 23. Man-Son-Hing M, Nichol G, Lau A, Laupacis A. Choosing antithrombotic therapy for elderly patients with atrial fibrillation who are at risk for falls. Arch Intern Med 1999; 159(7):677-85. 24. Phan TG, Koh M, Wijdicks EFM. Safety of discontinuation of anticoagulation in patients with intracranial hemorrhage at high thromboembolic risk. Arch Neurol 2000; 57(12):1710-3. 25. Wijdicks EFM, Schievink WI, Brown RD, Mullany CJ. The dilemma of discontinuation of anticoagulation therapy for patients with intracranial hemorrhage and mechanical heart valves. Neurosurgery 1998; 42(4):76973. 26. Butler AC, Tait RC. Restarting

Chronic subdural hematoma is one of the reversible causes of dementia. Presenting symptoms can be subtle and subdural hematomas are often overlooked. Whereas current clinical practice guidelines for dementia do not recommend routine neuroimaging, the presence of clinical variables, such as focal neurologic signs in the presence of dementia of brief duration, should prompt the use of neuroimaging. Surgical intervention should be used in cases where there are signs of increased intracranial pressure. G
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anticoagulation in prosthetic heart valve For Client Review Only. All Rights Reserved. Advanstar Communications Inc. 2003 patients after intracranial haemorrhage: 13. Machulda MM, Haut MW. Clinical features of chronic subdural hematoma. Neuropsychiatric and neurophysiologic changes in patients with chronic subdural hematoma. Neurosurg Clin N Am 2000; 11(3):473-7. 14. Vanneste JA. Diagnosis and management of normal-pressure hydrocephalus. J Neurol 2000; 247(1):5-14. 15. Smely C, Madlinger A, Scheremet R. Chronic subdural haematoma a comparison of two different treatment modalities. Acta Neurochir 1997; 139(9):818-26. 16. Voelker JL. Nonoperative treatment of chronic subdural hematoma. Neurosurg Clin N Am 2000; 11(3):507-13. 17. Inzelberg R, Neufeld MY, Reider I, Gari P . Non surgical treatment of subdural hematoma in a hemodialysis patient. Clin Neurol Neurosurg 1989; 91(1):85-9. A 2-year follow-up. Br J Haematol 1998; 103(4):1064-6. 27. Zingale A, Chibbaro S, Florio A, Distefano G, Porcaro S. Management of chronic subdural hematoma in patients treated with anticoagulation. J Neurosurg Sci 1999; 43(4):277-84.

References
1. Traynelis VC. Chronic subdural hematoma in the elderly. Clin Geriatr Med 1991; 7(3):583-98. 2. Chen JCT, Levy ML. Causes, epidemiology, and risk factors of chronic subdural hematoma. Neurosurg Clin N Am 2000; 11(3):399-406. 3. Pary R, Tobias CR, Lipmann S. Dementia: What to do. South Med J

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