SUBDURAL HEMATOMA (SDH) is characterized by a collection of blood or fluid blood products in the space between the dura mater and arachnoid or pial layer in the brain. An SDH can occur spontaneously or result from a head injury or various other pathologies.
An SDH is classified as acute, chronic, or subacute based on the timing of occurrence and brain imaging. Morbidity and mortality associated with an SDH increases with age and exposure to anticoagulant and antiplatelet therapy.
Chronic SDH (cSDH) in adults, the focus of this article, typically develops 2 to 3 weeks after the inciting event and often has a poor prognosis. Because prompt diagnosis and treatment is essential to prevent disability or death, this article discusses nursing assessment and interventions that may improve patient outcomes in patients with cSDH.
SDH: Surprisingly common
Data collected from the United States census bureau show that the incidence of SDH almost doubles from ages 65 to 75, and continues to increase in people over age 80. The incidence of SDH is highest in the fifth through seventh decades of life.
The median age of patients with cSDH is 63, and 69% of them are over age 65. The incidence of cSDH is expected to increase as the population continues to age. (See cSDH: An expanding threat to older adults.)
Several causes and predisposing factors are associated with cSDH. These include cerebral atrophy, older age, male gender, head trauma, exposure to certain medications, alcohol use, and seizure activity (see Risk factors for cSDH).
Similar to an acute SDH, which is typically caused by trauma, cSDH is often associated with head injury. Falls are the most common cause of all traumatic brain injuries, including SDH. The incidence of falls peaks in both males and females between ages 75 and 79.
The incidence of mild head trauma has been reported in up to 80% of patients with cSDH, although many have little or no memory of the inciting event. Approximately 38% of patients with a cSDH have a history of only minor head trauma or can't recall any prior head trauma. Regardless of whether they're aware of a discrete traumatic event, most patients with cSDH experienced a mild trauma without loss of consciousness, suggesting that they may also have an intrinsic susceptibility to developing SDH.
Systemic effects of anticoagulation and antiplatelet therapy are well-known risk factors for cSDH. Approximately 75% of primary spontaneous or nontraumatic cases of cSDH are diagnosed in patients taking these medications. In population studies, patients on oral anticoagulation therapy are estimated to have a 4- to 15-fold increased risk for cSDH.
An SDH in the setting of anticoagulation can expand rapidly. Unless anticoagulation is quickly reversed, the expanding SDH can result in severe signs and symptoms and/or death.
Slow bleeding from the low-pressure venous system into the subdural space is the pathophysiologic mechanism leading to cSDH. A cSDH typically develops over 2 to 3 weeks to several months following an inciting event.
The relatively slow rate of bleeding enables a large collection of blood, blood degradation products, cerebrospinal fluid (CSF), and fluid drawn by osmosis from surrounding tissues to accumulate in the subdural space before clinical signs and symptoms appear. Over time, a cSDH may further enlarge due to continued or recurrent venous bleeding, leading to serious complications such as increased intracranial pressure (ICP).
Like other masses that enlarge within the rigid nonexpandable skull, an SDH may become lethal by increasing ICP. Compression of brain tissue results in cerebral ischemia, stroke, brain tissue shift, and brain herniation. Two common types of brain herniation associated with SDH are subfalcine (cingulate gyrus) herniation and transtentorial (uncal) herniation. (See Herniation syndromes.)
The presentation of cSDH can occasionally mimic stroke or rapidly progressive dementia. Many patients with cSDH present with multiple signs and symptoms, including headache (progressing in severity), gait disturbance, paresis, and acute confusion. Presentation can also include neurologic focal signs, aphasia, seizures, and significant alteration in level of consciousness, including coma. Patients with cSDH are at risk for additional intracerebral hemorrhage, seizure activity, and exacerbation of existing comorbidities, especially when the cSDH is associated with anticoagulant therapy. Up to 20% have poor neurologic outcomes resulting in permanent and significant disability.
Noncontrast brain computed tomography (CT) is the initial imaging study of choice. Because a cSDH develops over 2 to 3 weeks or longer, cSDHs appear as isodense or hypodense (lighter) crescent-shaped lesions that deform the brain's surface on CT scan. (See SDH on CT scan.)
Over time, a cSDH will develop encapsulating vascular membranes. Recurrent bleeding from small, friable vessels within these vascular membranes accounts for the expansion of some cSDHs, causing them to persist and enlarge over time.
Magnetic resonance imaging doesn't routinely have a role in diagnosis of cSDH, but it may be performed when SDH is suspected but not demonstrated on CT scan.
Because many older adults with cSDH also have chronic and often complex comorbidities, management requires collaboration among neurologists, neurosurgeons, neuroscience nurses, rehabilitation specialists, and others such as a social worker and case manager, based on the patient's clinical status.
As with any emergency situation, immediate interventions are initiated to support the ABCs—airway, breathing, and circulation—optimize BP and hemodynamics, and normalize coagulation status. Correction of existing coagulopathy is crucial to reduce the risk of continued or recurrent bleeding.
Besides immediate discontinuation of all anticoagulant and antiplatelet therapy, a specific anticoagulant reversal strategy will be initiated according to the specific agent's mechanism of action. Interventions may include infusion of prothrombin complex concentrate (PCC), fresh frozen plasma (FFP) or vitamin K.
Reversal of newer novel oral anticoagulants (NOACs) is necessary only in cases of life-threatening bleeding or emergency surgery. For patients taking any NOAC in the absence of life-threatening acute hematoma expansion, surgery should be delayed until 24 hours after the last dose if possible. This delay should be extended to 48 hours if the patient also has renal impairment. The dabigatran-specific humanized monoclonal antibody fragment idarucizumab was recently approved for dabigatran-treated patients when reversal of anticoagulant effects is needed for emergency surgery or urgent procedures, or in cases of life-threatening or uncontrolled bleeding.
For patients taking antiplatelet medications such as aspirin or clopidogrel, evidence is available to support a treatment delay of 7 to 10 days if possible to allow for the production of fully functional platelets. If treatment can't be delayed, the American Society of Hematology guidelines recommend preoperative platelet transfusion. Other sources of coagulation and platelet dysfunction that might exist in patients with SDH should be treated in consultation with hematologists. Surgical intervention may or may not be indicated and is determined on a case-by-case basis.
Surgical options for cSDH
The general consensus is that patients with signs and symptoms that can be attributed to radiologically confirmed cSDH should be treated surgically. While some reports describe successful nonsurgical management of cSDH, experts generally agree that most patients with a cSDH require surgical drainage because the hematoma's very existence suggests the failure or inability of physiologic mechanisms to naturally reabsorb it. Although no specific guidelines currently exist on the indications for surgery in cSDH, all symptomatic individuals should be considered potential surgical candidates.
Surgical evacuation is recommended in cases of any SDH confirmed by radiologic imaging with maximal thickness of greater than or equal to 1 cm, or greater than or equal to 0.5 cm of brain tissue midline shift. For an SDH not meeting those criteria, prompt surgical evacuation may be indicated if the patient has a Glasgow Coma Scale (GCS) score of 8 or less (severe brain injury) and meets one of the following criteria:
- a decrease in GCS score by 2 or more points from the time of injury to hospital presentation
- asymmetric or fixed and dilated pupils
- ICP greater than 20 mm Hg (normal, 0 to 15 mm Hg).
See Glasgow Coma Scale (GCS) scoring for details about GCS scoring.
ICP monitoring is indicated following successful emergent resuscitation and stabilization for patients with a traumatic brain injury, including SDH, who have a GCS score from 3 to 8 and an abnormal CT scan that reveals hematomas, contusions, swelling, herniation, or compressed basal cisterns. Increased ICP associated with reduced cerebral blood flow causes hypoperfusion of brain tissue, resulting in potentially lethal cerebral infarctions or strokes.
Once ICP monitoring is in place, treatment goals are to maintain ICP below 20 mm Hg and cerebral perfusion pressure between 50 and 70 mm Hg to achieve and sustain adequate cerebral perfusion and oxygenation.
Surgery to treat a symptomatic cSDH can result in both rapid improvement of signs and symptoms and a favorable outcome in over 80% of patients. Coupled with relatively low surgical risk, surgical evacuation is currently the mainstay of management for symptomatic patients. However, the optimal method of cSDH surgical management remains an area of continued research. The three primary surgical techniques are:
- twist drill craniostomy (TDC) involving small openings (<10 mm) using a handheld twist drill.
- burr hole craniostomy (BHC) involving openings of 10 to 30 mm.
- open craniotomy (OC) involving larger openings.
The TDC technique involves the creation of a small craniostomy using a handheld drill and closed system drainage. The advantage of this technique is that it can be performed under local anesthesia at the bedside, making it an attractive option for an older adult with multiple comorbidities.
BHC involves creation of two burr holes, usually drilled about 5 to 8 cm apart on the same side as the cSDH. This is done under general anesthesia. The cSDH is irrigated with saline until the effluent runs clear, and a soft silicone drain is inserted into the subdural space and connected to a passive closed drainage system that's removed after approximately 48 hours.
OC, which also requires general anesthesia, involves creation of a larger (>30 mm) free bone flap to allow direct irrigation and evacuation of the hematoma. Following irrigation and evacuation the bone flap is replaced and secured. If significant cerebral edema is associated with OC for cSDH management, the dural membrane can be left open or replaced with duraplasty, and the bone flap can be left off to allow for cerebral expansion. Known as a decompressive hemicraniectomy, this is done to control ICP, improve cerebral compliance, and maximize cerebral perfusion.
Between 11% and 19% of patients develop seizures following surgery to manage cSDH, but the use of antiepileptic drugs (AEDs) for seizure prophylaxis in cSDH patients remains controversial. Preoperative AED prophylaxis has been shown to lower the postoperative seizure rate but not to affect long-term development of posttraumatic epilepsy. The use of prophylactic AEDs in patients without a history of seizure isn't currently recommended.
Surgical complications can include focal brain injury, stroke, new acute subdural or intracranial hemorrhage, seizures, surgical site infection, subdural empyema, and pneumocephalus. Besides these, possible post-op complications include those related to general anesthesia, recurrent or residual hematoma, intracranial hypertension, wound infection, CSF leak, meningitis, cerebral abscess, residual neurologic deficits such as speech disturbances or motor deficit, bowel and bladder sphincter dysfunction, and behavioral changes. Several studies have shown a significant relationship between patient age and postoperative complications, meaning that complications increase with older age.
Although surgical outcomes in patients with cSDH are generally favorable, perioperative mortality ranges from 1.2% to 11%. One-year mortality in patients with cSDH can be as high as 32%, depending on such factors as comorbidities and GCS score. Data suggest that an admission GCS score of 9 or above in patients who undergo surgical treatment for cSDH is associated with good outcome at 6 months postoperatively. However, a recurrence within the same period is associated with poor outcomes.
Recurrence of SDH is a significant concern, with rates from 3.8% to 30% being reported. Predictive factors for recurrence include male gender, older age, hypertension, alcohol use, diabetes, cirrhosis, renal insufficiency, coagulopathy, and surgical treatment of the primary SDH. Exposure to medications including statins and anticoagulation and antiplatelet therapy also increase the risk of SDH recurrence. The cumulative risk for recurrence of an SDH is approximately 15%, usually occurring within the first year after the primary event.
Some patients with mild signs and symptoms and/or small hematomas may be treated medically. This approach includes observation and continued assessments and management of complications such as cerebral edema. Because of the known inflammatory nature of cSDH, steroids may be useful as adjunctive therapy as an alternative to surgical intervention, but their role remains ill-defined.
The decision on whether to manage cSDH surgically or nonsurgically is largely based on expert opinion, with only sparse evidence available to guide decisions. In a large, heterogeneous population of patients with nonsurgically managed cSDH, one study found that approximately one out of every eight patients was readmitted with new or worsening cSDH within 90 days. Approximately half of these readmissions resulted in surgical hematoma evacuation, and about 1 in 20 readmissions resulted in death. The risk of these outcomes was significantly higher after nontraumatic compared with traumatic cSDH because nontraumatic cSDHs are associated with older age and more comorbidities.
Nontraumatic cSDHs present in those who may be less able to tolerate the presence of an undrained cSDH and would benefit from surgical management. Current recommendations for surgical versus nonsurgical management are based on clinical symptomatology and radiographic size of the lesion. However, inclusion of the cSDH etiology as a factor when deciding surgical versus nonsurgical management of cSDH can be beneficial. Conclusions from one study suggest that in the context of current practice, patients with nontraumatic cSDH have worse outcomes when managed nonsurgically than do patients with traumatic cSDH.
When caring for patients with cSDH, the nurse must understand the risks of neurologic deterioration, such as SDH expansion or recurrence. This can result spontaneously or from factors such as uncontrolled hypertension, coughing, vomiting, or falls. Nursing care for these patients must be comprehensive because they're at risk for many complications including alteration in sleep-wake cycles, malnutrition, pain, confusion, delirium, falls, pressure injuries, dysphagia, impaired or loss of airway protective reflexes, infection, stroke, and venous thromboembolism.
Nurses must be prepared to perform admission and serial standardized neurologic assessments, including:
- mental status
- cranial nerve function
- motor system
- sensory system
- deep tendon, abdominal, and plantar reflexes.
Nurses must also maintain the integrity and accuracy of the ICP monitoring system and report pressure elevations beyond established parameters. These ongoing assessments are essential to both establish a baseline and to enable detection of changes that may represent neurologic deterioration. Because these changes may signal an impending neurologic catastrophe, they must be reported immediately, thoroughly investigated, and treated promptly. The neurologic assessment should include evaluation for a new headache or increased severity of an existing headache; dizziness; changes in level of consciousness or memory; and impaired ability to understand, speak clearly, and follow commands. The nurse should be vigilant for evidence of seizures in this population. Maintain seizure precautions, monitor serum levels of AEDs if prescribed, and be prepared to respond immediately should a seizure occur.
In collaboration with the healthcare provider, the nurse should maintain euvolemia by administering isotonic I.V. fluids to support cerebral perfusion without exacerbating cerebral edema. Avoid administering hypotonic I.V. fluids because they increase brain edema.
Keep the patient's head and neck aligned and free of constriction from devices such as cervical collars. Elevate the head of bed to approximately 45 degrees unless contraindicated. These strategies promote venous return from the brain, help control ICP, and facilitate reabsorption of the cSDH.
The nurse must assess the patient for the presence of pain using a standard validated pain intensity rating scale. The healthcare provider, pharmacist, and nurse collaborate on a pain management strategy with the goal of managing pain without excessive sedation, which could make the neurologic assessment difficult to perform and interpret.
For postoperative patients with a subdural drain, the nurse must assess the site for signs and symptoms of leaking or infection, ensure the patency of the drainage system, and monitor the dressing. The nurse must also secure and protect the drain from accidental dislodgement or removal, monitor the amount and characteristics of drainage, and report any abnormalities such as failure to drain or excessive drainage.
Patient and family education should include an explanation of the neurologic assessment and the treatment plan, and address questions and expectations of the patient and family.
It takes teamwork
cSDH is a common neurologic disorder in older adults, and its incidence is rising due to an aging population and increasing use of anticoagulant and antiplatelet medications. Patients with cSDH are increasingly being managed by multidisciplinary teams, including neurologists, neurosurgeons, neuroscience nurses, pharmacists, therapists, and rehabilitation specialists. All team members must be familiar with the presentation, diagnosis, and management of all types of SDH. More research is required to refine the management of cSDH, including exploration of minimally invasive techniques and adjuvant treatments that might reduce both recurrence and the need for surgery.
cSDH: An expanding threat to older adults
According to the CDC, the population of the United States in 2010 included 40 million people age 65 and over. The older population is projected to increase to 72 million by 2030, representing nearly 20% of the total U.S. population. The oldest-old population, defined as those age 85 and over, grew from just over 100,000 in 1900 to 5.5 million in 2010. The U.S. Census Bureau projects that the population age 85 and over could grow to 19 million by 2050.
As the population ages, the incidence of cSDH is expected to increase accordingly. Current trends in aging predict that once 20% to 25% of the population is over age 65, cSDH will surpass primary and metastatic brain tumors to become the most common neurosurgical condition. This is projected to occur in the United States by 2030.
Source: Pillitteri A. Maternal and Child Nursing. 4th ed. Philadelphia, PA: Lippincott, Williams & Wilkins; 2003.
Risk factors for cSDH
- vitamin K antagonists, such as warfarin
- novel oral anticoagulants, such as dabigatran
- antiplatelet medications, such as aspirin
- sympathomimetics, such as pseudoephedrine
Mechanism of injury
- motor vehicle crashes
- cerebral atrophy
- cerebral vascular disease
- older age
- CSF shunt
- seizure activity
- lumbar puncture
- alcohol use.
Herniation of the cingulate gyrus under the falx cerebri , central or transtentorial herniation , uncal herniation of the temporal lobe into the tentorial notch , and infratentorial herniation of the cerebellar tonsils .
Source: Porth CM. Essentials of Pathophysiology. 4th ed. Philadelphia, PA: Wolters Kluwer Health; 2014.
SDH on CT scan
Head CT reveals crescentic hyperdense lesions (see arrows) with edema/mass effect.
Source: Hickey JV. Clinical Practice of Neurological & Neurosurgical Nursing. 7th ed. Philadelphia, PA: Wolters Kluwer Health; 2013.
Bader MK, Littlejohns LR, Olson DM, eds. AANN Core Curriculum for Neuroscience Nursing. 6th ed. Chicago, IL: American Association of Neuroscience Nurses; 2016.
McBride W. Subdural hematoma in adults: prognosis and management. UpToDate. 2017. http://www.uptodate.com.
Hickey JV. The Clinical Practice of Neurological and Neurosurgical Nursing. 7th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins; 2009.
Meagher RJ. Subdural hematoma. Medscape. 2017. https://emedicine.medscape.com/article/1137207-overview.
5. Tabuchi S, Kadowaki M. Chronic subdural hematoma in patients over 90 years old in a super-aged society. J Clin Med Res. 2014;6(5):379–383.
6. Huang KT, Bi WL, Abd-El-Barr M, et al The neurocritical and neurosurgical care of subdural hematomas. Neurocrit Care. 2016;24(2):294–307.
7. Balser D, Rodgers SD, Johnson B, Shi C, Tabak E, Samadani U. Evolving management of symptomatic chronic subdural hematoma: experience of a single institution and review of the literature. Neurol Res. 2013;35(3):233–242.
8. Guha D, Coyne S, Macdonald RL. Timing of the resumption of antithrombotic agents following surgical evacuation of chronic subdural hematomas: a retrospective cohort study. J Neurosurg. 2016;124(3):750–759.
9. Iliescu IA. Current diagnosis and treatment of chronic subdural haematomas. J Med Life. 2015;8(3):278–284.
10. Ryan CG, Thompson RE, Temkin NR, Crane PK, Ellenbogen RG, Elmore JG. Acute traumatic subdural hematoma: current mortality and functional outcomes in adult patients at a Level I trauma center. J Trauma Acute Care Surg. 2012;73(5):1348–1354.
11. Kolias AG, Chari A, Santarius T, Hutchinson PJ. Chronic subdural haematoma: modern management and emerging therapies. Nat Rev Neurol. 2014;10(10):570–578.
12. de Araújo Silva DO, Matis GK, Costa LF, et al Chronic subdural hematomas and the elderly: surgical results from a series of 125 cases: old “horses” are not to be shot! Surg Neurol Int. 2012;3:150.
13. Connolly BJ, Pearce LA, Hart RG. Vitamin K antagonists and risk of subdural hematoma: meta-analysis of randomized clinical trials. Stroke. 2014;45(6):1672–1678.
14. Lucke-Wold BP, Turner RC, Josiah D, Knotts C, Bhatia S. Do age and anticoagulants affect the natural history of acute subdural hematomas. Arch Emerg Med Crit Care. 2016;1(2):1010.
McBride W. Subdural hematoma in adults: etiology, clinical features, and diagnosis. UpToDate. 2015. http://www.uptodate.com.
16. Brown KS, Zahir H, Grosso MA, Lanz HJ, Mercuri MF, Levy JH. Nonvitamin K antagonist oral anticoagulant activity: challenges in measurement and reversal. Crit Care. 2016;20(1):273.
Hemphill JC 3rd, Greenberg SM, Anderson CS, et al Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2015. http://stroke.ahajournals.org/content/46/7/2032.
Praxbind (idarucizumab) injection, for intravenous use. Prescribing information. http://www.praxbind.com.
19. Carney N, Totten AM, O'Reilly C. Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery. 2017;80(1):6–15.
20. Chesnut RM, Temkin N, Carney N, et al A trial of intracranial-pressure monitoring in traumatic brain injury. N Engl J Med. 2012;367(26):2471–2481.
Englehard HH III. Subdural hematoma surgery. Medscape. 2015. https://emedicine.medscape.com/article/247472-overview.
22. Crudele A, Shah SO, Bar B. Decompressive hemicraniectomy in acute neurological diseases. J Intensive Care Med. 2016;31(9):587–596.
23. Emich S, Richling B, McCoy MR, et al The efficacy of dexamethasone on reduction in the reoperation rate of chronic subdural hematoma—the DRESH study: straightforward study protocol for a randomized controlled trial. Trials. 2014;15(6):1–10.
24. Ghanem HM, El-khayat RAE-A. Chronic subdural hematoma: effect of developing and implementing postoperative nursing care standards on nurses performance for reduction or prevention postoperative complications. J Am Sci. 2012;8(2):686–697.
25. Schmidt L, Gørtz S, Wohlfahrt J, Melbye M, Munch TN. Recurrence of subdural haematoma in a population-based cohort—risks and predictive factors. PLoS One. 2015;10(10):e0140450.
26. Morris NA, Merkler AE, Parker WE, et al Adverse outcomes after initial non-surgical management of subdural hematoma: a population-based study. Neurocrit Care. 2016;24(2):226–232.
National Center for Health Statistics. Older Americans: Key Indicators of Well-Being. http://www.agingstats.gov.
28. Ortman JM, Velkoff VA, Hogan H. An aging nation: the older population in the United States. Population estimates and projections. United States Census Bureau. 2014.
Porth CM. Essentials of Pathophysiology. 4th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins;2015.
Akwaa F, Spyropoulos AC. Treatment of bleeding complications when using oral anticoagulants for prevention of strokes. Curr Treat Options Cardiovasc Med. 2013;15(3):288–298.
De Bonis P, Trevisi G, de Waure C, et al Antiplatelet/anticoagulant agents and chronic subdural hematoma in the elderly. PLoS One. 2013;8(7):e68732.
McClelland S, Mackey SJ, Kim SS. The dangerous gamble of heparinization within two weeks of nonoperative traumatic acute subdural hematoma in patients with increased stroke risk: a case series. J Postgrad Med. 2014;60(2):194–197.
Ross AG. Prudent care of head trauma in the elderly: a case report. J Med Case Rep. 2014;8:448.