eMedicine Specialties > Neurology > Critical Care Neurology

Subdural Hematoma

Richard J Meagher, MD, Attending Neurosurgeon, Neurosurgical Associates of Abington, Abington Memorial Hospital
William F Young, MD, Attending Neurosurgeon, Fort Wayne Neurological Center

Updated: Apr 23, 2009

Introduction

Background

Head injuries are the leading cause of death among accident victims younger than 45 years. They account for approximately 70% of traumatic deaths and most of the persisting disabilities in accident survivors in this age group. Many of these patients are comatose on admission. However, approximately 50% of patients with head injuries who require emergency neurosurgery present with head injuries that are classified as moderate or mild (Glasgow Coma Scale [GCS] scores 9-13 and 14-15, respectively). These patients may be more likely to benefit from medical and surgical intervention when instituted in a timely fashion (ie, before further neurological deterioration). See eMedicine's article Head Injury.

Many of these patients harbor intracranial mass lesions. In a large series of patients who developed intracranial hematomas requiring emergent decompression, more than half had lucid intervals and were able to make conversation between the time of their injury and subsequent deterioration. In a more comprehensive review of the literature on the surgical treatment of acute subdural hematomas, lucid intervals were noted in up to 38% of cases.

Intracranial hematoma plays an important role in the death and disability that are associated with head injury. Acute subdural hematoma is the most common type of traumatic intracranial hematoma, occurring in 24% of patients who present comatose. This type of head injury also is strongly associated with delayed brain damage, later demonstrated on CT scan. Such patients portend devastating outcomes, and overall mortality rates are usually quoted at around 60%. Significant trauma is not the only cause of subdural hematoma. Chronic subdural hematoma can occur in the elderly after apparently insignificant head trauma. Often, the antecedent event is never recognized.

Much less common causes of subdural hematoma involve coagulopathies and ruptured intracranial aneurysms. Subdural hematomas have even been reported to be caused by intracranial tumors. This article focuses on the acute traumatic subdural hematoma (ATSDH) and chronic subdural hematoma (CSDH), each separately discussed. Conditions comorbid with acute traumatic subdural hematoma and a brief discussion of atraumatic subdural hematoma also are included.

Pathophysiology

Acute subdural bleeding usually develops by 1 of 3 mechanisms: bleeding by a damaged cortical artery (including epidural hematoma), bleeding from underlying parenchymal injury, and tearing of bridging veins from the cortex to one of the draining venous sinuses. Acute traumatic subdural hematoma is often associated with significant parenchymal injury and contusion, prompting some authorities to speculate that the associated mortality rate is unlikely to change despite new treatment plans for acute traumatic subdural hematoma.

The contention is that the primary brain injury associated with subdural hematomas plays a major role in the patient's death. However, most subdural hematomas are thought to result from torn bridging veins, as judged by surgery or autopsy. Furthermore, not all subdural hematomas are associated with diffuse parenchymal injury. As mentioned earlier, many patients who sustain these lesions are able to speak before their condition deteriorates—an unlikely scenario in patients who sustain diffuse damage.

Using a primate model, Gennarelli and Thibault demonstrated that the rate of acceleration-deceleration of the head was the major determinant of bridging vein failure. By using an apparatus that controlled head movement and minimized impact or contact phenomena, they were able to produce acute subdural hematoma in rhesus monkeys. In all cases, the sagittal movement of the head produced by an angular acceleration caused rupture of parasagittal bridging veins and an overlying subdural hematoma. They reported that their results were consistent with the clinical causes of subdural hematoma, in that 72% were associated with falls and assaults and only 24% were associated with vehicular trauma. The acceleration (or deceleration) rates caused by falls and assaults are greater than those caused by the energy-absorbing mechanisms in cars, such as dashboard padding, deformable steering wheels, and laminated windshields.¹

Chronic subdural hematoma is commonly associated with cerebral atrophy. Cortical bridging veins are thought to be under greater tension as the brain gradually shrinks from the skull; even minor trauma may cause one of these veins to tear. Slow bleeding from the low-pressure venous system often enables large hematomas to form before clinical signs appear. Small subdural hematomas often spontaneously resorb. Larger collections of subdural blood usually organize and form vascular membranes that encapsulate the subdural hematoma. Repeated bleeding from small, friable vessels within these membranes may account for the expansion of some chronic subdural hematomas.

As a subdural hematoma expands in the subdural space, it raises the intracranial pressure and deforms the brain. The rise in intracranial pressure is initially compensated by efflux of cerebrospinal fluid (CSF) toward the spinal axis and compression of the venous system, expediting venous drainage through the jugular veins. During this stage, the rise in intracranial pressure is relatively slow, because the intracranial compliance is relatively high; in other words, the initial changes in intracranial volume are associated with small changes in intracranial pressure.

However, as the hematoma (and edema from associated parenchymal injury) expands, a limit is reached beyond which compensatory mechanisms fail. The intracranial compliance begins to decrease; small increases in intracranial volume are associated with larger increases in intracranial pressure. Intracranial pressure exponentially rises, leading to decreased cerebral perfusion and global cerebral ischemia. In a rapidly expanding hematoma, this whole process can happen in minutes.

In addition to increasing the intracranial pressure, the hematoma deforms and displaces the brain. Eventually, transtentorial or subfalcine herniation can develop as the brain is pushed past the dural folds of the tentorial incisura or falx, respectively. Tonsillar herniation through the foramen magnum may develop if the whole brain stem is forced down through the tentorial incisura by elevated supratentorial pressure. Although much less common than supratentorial subdural hematoma, infratentorial subdural hematoma can develop and cause tonsillar herniation and brainstem compression.

Characteristic herniation syndromes may develop as the brain shifts. As the medial temporal lobe, or uncus, herniates past the tentorium, it can compress the ipsilateral posterior cerebral artery, oculomotor nerve, and cerebral peduncle. Clinically, the consequent oculomotor nerve palsy and cerebral peduncle compression are often manifested by an ipsilaterally dilated pupil and a contralateral hemiparesis.

The patient also may develop a stroke of the posterior cerebral artery distribution. In approximately 5% of cases, the hemiparesis may be ipsilateral to the dilated pupil. This phenomenon is called the Kernohan notch syndrome and results when uncal herniation forces the midbrain to shift so that the contralateral cerebral peduncle is forced against the contralateral tentorial incisura. Subfalcine herniation caused by midline brain shift may result in compression of anterior cerebral artery branches against the fixed falx cerebri, leading to infarcts in an anterior cerebral artery distribution.

Investigation of brain physiological and biochemical parameters in patients with acute traumatic subdural hematoma has suggested variables that might be associated with secondary injury to the brain. Hlatky et al used brain oxygen tension monitoring and microdialysis techniques to evaluate brain biochemical patterns after acute subdural hematoma evacuation. They found that postsurgical patients who succumbed to their injury exhibited lower values of brain tissue oxygen tension and higher dialysate values of lactate and pyruvate in the brain underlying the hematoma. They suggested that identification of this brain biochemistry pattern after surgery might signify an evolving brain injury that warrants further evaluation or treatment.²

Cerebral blood flow (CBF) can become markedly reduced. Schroder et al used a stable xenon-CT method for measuring CBF in 2 patients with acute subdural hematoma requiring emergent craniotomy. CBF and cerebral blood volume (CBV) were measured before and after surgery. In both cases, the hemisphere ipsilateral to the subdural hematoma demonstrated lower CBF than the contralateral hemisphere. Furthermore, both hemispheres revealed decreased CBF compared to normal values. Impressive increases in CBF and CBV that could not be attributed to pCO₂ or blood pressure changes were noted immediately after surgery. The authors speculated that the decreased CBV caused by the subdural hematoma was a result of a compressed microcirculation, which was caused by increased intracranial pressure.³

In patients with chronic subdural hematoma, blood flow to the thalamus and basal ganglia regions appears to be particularly affected compared to that to the rest of the brain. Tanaka et al suggested that impaired thalamic function can lead to a spreading depression that impairs various cortical regions, thereby producing various clinical deficits. They found that a 7% decrease of CBF was commonly associated with headache, whereas a 35% decrease of CBF was associated with neurological deficit such as hemiparesis.⁴

Given that the pathophysiology of chronic subdural hematoma is often directly associated with cerebral atrophy, the fact that subdural hematomas are associated with conditions that cause cerebral atrophy (eg, alcoholism, dementia) is not surprising. In a series reported by Foelholm and Waltimo, alcoholics constituted over half of the patient population. Most chronic subdural hematomas are probably caused by head injury; other causes and predisposing factors include coagulopathy (including patients on warfarin and aspirin), seizure disorders, and CSF shunts.⁵

Spontaneous subdural hematoma is rare. The literature is limited to sporadic case reports. These cases often have an arterial source, because they are usually associated with the same pathology as that involved in subarachnoid or intracerebral hemorrhage. The blood from a ruptured aneurysm may dissect through the brain parenchyma or subarachnoid space into the subdural space. Likewise, the blood released from a "hypertensive" intracerebral hemorrhage can dissect into the subdural space. In fact, a case has been reported of an acute spontaneous subdural hematoma precipitated by cocaine abuse.

Coagulopathy, occasionally associated with malignancy, also has been associated with spontaneous subdural hematoma. Subdural hematoma also can be caused by bleeding from intracranial tumors. The treatment of spontaneous subdural hematoma is similar to that of subdural hematoma caused by trauma, but the underlying cause must be sought and treated.

Frequency

United States

The incidence of chronic subdural hematoma appears to be highest in the fifth through seventh decades of life. One retrospective study reported that 56% of cases were in patients in their fifth and sixth decades; another study noted that more than half of all cases were seen in patients older than 60 years. The highest incidence of 7.35 cases per 100,000 persons occurs in adults aged 70-79 years.

Mortality/Morbidity

• Mortality rates for patients with acute subdural hematoma are reported from 30-90%, but around 60% is typical.
• The morbidity and mortality rates associated with surgical treatment of chronic subdural hematoma have been estimated at 11% and 5%, respectively.

Clinical

History

• Acute traumatic subdural hematoma often results from falls, violence, or motor vehicle accidents. The clinical presentation depends on the location of the lesion and the rate at which it develops. Often, patients are rendered comatose at the time of the injury. A subset of patients remain conscious; others deteriorate in a delayed fashion as the hematoma expands.
• Chronic subdural hematomas are arbitrarily defined as those hematomas presenting 21 days or more after injury. Subacute subdural hematomas are defined arbitrarily as those that present between 4 and 21 days after injury.
• These numbers are not absolute, and a more accurate classification of a subdural hematoma usually is based on imaging characteristics.
  • Acute blood appears hyperdense on CT scan; it progresses to isodense and then to hypodense during the timeframe of a few weeks. Although the distinction between subacute and chronic is an arbitrary one, it can be important.
  • Chronic subdural hematomas have a liquid consistency, typically resembling crank case oil. They can be drained through burr holes. The consistency of subacute subdural hematomas might be too thick for burr-hole drainage and might require craniotomy.
• In the pre-CT era, chronic subdural hematoma earned the label "great imitator" because of its variable course and presentation. A history of head injury was lacking in 25-50% of patients in most series. Without the diagnostic capability of CT scan, chronic subdural hematoma was commonly misdiagnosed (as many as 72% of cases).
  • Misdiagnosis of chronic subdural hematoma often is aided by its insidious course. In patients who have sustained head injury, 25% have an interval of 1-4 weeks before symptoms develop. Another 25% experience symptoms from 5 weeks to 3 months before their hospital admission. Only one third of patients have no asymptomatic period.
  • Headache and confusion appear to be the most common presenting features, occurring in as many as 90% and 56% of cases, respectively. In 75% of cases, the headache had at least one of the following characteristics: sudden onset, severe pain, nausea and vomiting, and exacerbation by coughing, straining, or exercise. Other common symptoms include weakness, seizures, and incontinence.
  • Hemiparesis and decreased level of consciousness appear to be the most common signs, occurring in approximately 58% and 40%, respectively. Hemiparesis was ipsilateral to the hematoma in 40% of cases in one series.
  • Luxon and Harrison reported these signs (in decreasing order of frequency): papilledema, reflex asymmetry, extensor plantar response, dysphasia, neck stiffness, hemianopia, hemisensory change, and dysarthria. They also noted third nerve palsies caused by transtentorial herniation in 10% of patients, and sixth nerve palsies, presumably caused by increased intracranial pressure, in 7% of patients.⁶
  • Gait dysfunction is another common finding. When signs of chronic subdural hematoma in different age groups are compared, somnolence, confusion, and memory loss are significantly more common in elderly patients (aged 60-79 y). Signs of increased intracranial pressure, such as headache and vomiting, are more likely to be seen in younger patients.
  • Fluctuating signs or symptoms occur in as many as 24% of cases. Prior to the availability of CT, common misdiagnoses included dementia, stroke, transient ischemic attack, tumor, subarachnoid hemorrhage, meningitis, and encephalitis.

Physical

The initial neurologic examination provides an important baseline that should be used to follow the patient's clinical course. When recorded in the form of the GCS score, it also provides important prognostic information.

• Patients with serious head injuries often are intubated quickly and given trauma-oriented care. However, because of its prognostic significance, a brief neurologic examination quantified by using the GCS is an essential component of the secondary assessment and takes less than 2 minutes to complete.
  • The GCS focuses on the patient's ability to produce intelligible speech, open his eyes, and follow commands. During the initial evaluation, the patient should be assessed for the ability to open his eyes spontaneously, to voice or to pain.
  • The patient's speech and mentation should be characterized as oriented, confused, inappropriate, incomprehensible, or none.
  • The patient's motor function is determined by the patient's ability to follow commands on both the left and right sides. If the patient is unable to follow commands, note his ability to localize painful stimuli or to exhibit normal flexion on either side in response to the pain.
  • Decorticate and decerebrate posturing or lack of any motor function should also be recorded.
  • Assess the size and reactivity of both pupils.
  • Look for signs of a basilar skull fracture. These include bilateral periorbital ecchymoses (raccoon's eyes) and retroauricular ecchymoses (Battle sign).
  • Note the presence or absence of CSF rhinorrhea or otorrhea.
  • Areas surrounding lacerations should be shaved and inspected. Patients with severe head injuries should be assumed to have a cervical spine (C-spine) injury; immobilize the patient until clinical and radiographic studies can prove otherwise.

Causes

The differential diagnosis of an acute traumatic subdural hematoma is the same as that for any traumatic, intracranial mass lesion. This includes intracerebral hematoma and contusion.

Differential Diagnoses

Epidural Hematoma
Subarachnoid Hemorrhage

Workup

Laboratory Studies

• The prevalence of coagulation abnormalities has long been recognized as unusually high in patients with head injuries. These abnormalities are believed to result from the release of thromboplastic materials by damaged brain tissue.
• Stein et al showed that the presence of coagulopathy and the development of delayed brain injury are associated strongly. In a review of 253 patients with head injury who required serial CT scans, the risk of developing a delayed brain insult as seen on CT scan increased from 31% in patients with coagulation study findings within reference range to almost 85% in patients with abnormal findings on prothrombin time (PT), activated partial thromboplastin time (aPTT), or platelet count.⁷
  • Subdural hematomas themselves were associated with disease progression; 26 of 35 patients with subdural hematoma had expansion of their hematoma or a delayed brain injury seen on a follow-up CT scan. Therefore, all patients with head injury should have at least a basic coagulation panel (PT, aPTT, and platelet count). Fresh frozen plasma or platelets should be given as needed. Awaiting the results of these studies should not delay emergency surgery.
  • Blood products can be given intraoperatively to improve clotting parameters. All patients with subdural hematoma should have a baseline CBC and basic metabolic panel. Electrolyte abnormalities can exacerbate brain injury and should be corrected in a timely manner. For example, hyponatremia (5-12% estimated incidence in patients with head injury) can potentiate brain edema and cause seizures.

Imaging Studies

• The trauma team and neurosurgeon must determine quickly which lesions warrant immediate evacuation. The imaging modality of choice to facilitate this decision is a CT scan of the head. Modern CTs can produce appropriate images in about 5 minutes and are highly sensitive to acute blood.
  • Acute subdural hematoma appears hyperdense, concave toward the brain, and unlimited by suture lines, as opposed to epidural hematomas, which are convex toward the brain and restricted by suture lines (see Media file 1).
    
    

    

    Acute right-sided subdural hematoma associated with significant midline shift (ie, subfalcine herniation) shown on CT scan.

    
    
  • Surgery for emergent decompression has been advocated if the acute subdural hematoma is associated with a midline shift greater than or equal to 5 mm. Surgery also has been recommended for acute subdural hematomas exceeding 1 cm in thickness. These indications have been incorporated into the Guidelines for the Surgical Management of Acute Subdural Hematomas proposed by a joint venture between the Brain Trauma Foundation and the Congress of Neurological Surgeons released in 2006.⁸
  • These guidelines also call for emergent decompression in a comatose patient with an acute subdural hematoma less than 1 cm in thickness causing a midline shift of less than 5 mm if any one of the following criteria are met: if the GCS decreases by 2 or more points between the time of injury and hospital evaluation, the patient presents with fixed and dilated pupils, and/or the intracranial pressure exceeds 20 mm Hg.
  • In a series of patients with acute traumatic subdural hematoma initially treated conservatively, Wong found that if patients presented with a GCS score less than or equal to 15 and a midline shift greater than 5 mm, their condition usually would deteriorate and they would require surgery.⁹ In another series reported by Matthew et al, all patients initially treated nonoperatively that subsequently required surgery presented with subdural hematomas that were at least 10 mm thick on their initial CT scan.
  • Surgery has been advocated when a subdural hematoma is associated with compressed or effaced basilar cisterns. In one large series of patients with severe head injuries, the mortality rates were 77%, 39%, and 22% for patients with effaced, compressed, or normal cisterns, respectively.¹⁰
• CT scanning is the initial imaging modality of choice for chronic subdural hematoma. However, as a subdural hematoma becomes isodense to the brain (usually 2-3 weeks after injury), it may go undetected.
  • Chronic subdural hematomas are bilateral about 20% of the time and may prevent midline shift, thereby making the subdural hematoma harder to detect (see Media file 2).
    
    

    

    Bilateral chronic subdural hematomas shown on CT scan. Midline shift is absent because of bilateral mass effect. Subdural hematoma is bilateral in 20% of patients with chronic subdural hematoma.

    
    
  • Despite this caveat, CT scan still supersedes MRI because of its reliability, shorter study time, and lower cost.
• MRI is a viable alternative that can clearly delineate chronic subdural hematoma.
• C-spine radiograph series are important in evaluating the possibility of concomitant C-spine fracture.

Treatment

Medical Care

Although significant acute traumatic subdural hematoma requires surgical treatment, temporizing medical maneuvers can be preoperatively used to decrease intracranial pressure. These measures are germane for any acute mass lesion and have been standardized by the neurosurgical community. They are discussed only briefly.

• As with any trauma patient, resuscitation begins with the ABCs (airway, breathing, circulation).
  • All patients with a GCS score of less than 8 should be intubated for airway protection.
  • After stabilizing respiratory function, perform a brief neurologic examination. Adequate respiration should be initially addressed and maintained to avoid hypoxia. Hyperventilation can be used if a herniation syndrome is present.
  • The patient's blood pressure should be maintained at normal or high levels using isotonic saline, pressors, or both. Hypoxia and hypotension, which are particularly detrimental in patients with head injury, are independent predictors of poor outcome.¹¹
• Short-acting sedatives and paralytics should be used only when needed to facilitate adequate ventilation or when elevated intracranial pressure is suspected. If the patient exhibits signs of a herniation syndrome, administer mannitol 1 g/kg rapidly by intravenous (IV) push.
• The patient should also be mildly hyperventilated (pCO₂ ~30-35 mm Hg).
• Administer anticonvulsants to prevent seizure-induced ischemia and subsequent surges in intracranial pressure.
• Do not give steroids, as they have been found to be ineffective in patients with head injury.

Surgical Care

The indications for emergent decompression of an acute subdural hematoma have been previously addressed, and operative management is discussed here briefly.

• The standard reverse question mark incision provides wide access to the frontal, temporal, and parietal regions.
  • The patient is positioned supine with the head turned to the appropriate side. A shoulder roll is placed to help prevent jugular vein kinking. A 3-point head fixation device should be used in patients with an unstable C-spine fracture.
  • The whole head is shaved to facilitate placement of an intracranial pressure monitor on the contralateral side, if desired. Infiltrating the scalp with 1% lidocaine (with 1:100,000 epinephrine) is unnecessary, but the short time taken to do this may hasten hemostasis.
  • A reverse question mark incision is started at the level of the zygoma within 1 cm anterior to the tragus. This allows for full temporal access and minimizes the possibility of injuring the anterior branch of the facial nerve. The incision is carried down to the bone and through the temporalis muscle; Raney clips are used to maintain hemostasis.
  • The periosteum and temporalis are then reflected with a periosteal elevator. The initial burr hole is made over the zygoma.
  • The dura is opened and the clot is removed with gentle suction and irrigation. The initial burr hole allows for early subtemporal decompression to forestall or ameliorate uncal herniation; it may be made before opening the entire incision. Additional burr holes are placed at the perimeter of the exposure, as needed, to facilitate turning the bone flap with a craniotome.
  • The dura is opened in a cruciate fashion with a flap based on the sagittal sinus (see Media file 3). The remainder of the clot is removed with biopsy forceps, irrigation, and suction.
    
    

    

    An acute subdural hematoma is shown in this intraoperative photograph. Note the frontotemporoparietal flap used. The hematoma is currant jelly–like in appearance.

    
    
  • Bipolar electrocautery, gel foam, and absorbable cellulose (eg, Surgicel) are used to achieve hemostasis.
  • If substantial brain swelling develops, a dural augmentation patch graft is placed and the bone flap and overlying temporalis fascia are closed loosely.
  • Subdural drains, subgaleal drains, or both may be placed, if needed, and the wound is closed.
• This standard trauma craniotomy flap, which was developed in the pre/early CT era, exposes most acute traumatic subdural hematomas. However, today's rapid CT scanners almost always elucidate the subdural hematoma's location preoperatively. Therefore, linear incisions have become effective surgical options in trauma cases.
• Linear incisions may offer advantages over the standard reverse question mark incision. Because they are shorter for a given size bone flap and less time is spent controlling bleeding, linear incisions reduce surgical time. They may be extended easily across the midline to control bleeding from a distant, intraoperatively identified source. Linear incisions also eliminate issues regarding a vascular pedicle. If the cerebellar retractors used to keep the incision open are placed in a crossed axis configuration (ie, to maintain a hexagonal opening), Raney clips may be unnecessary.
• Exploratory burr holes are rarely indicated but sometimes may be used as life-saving measures. Patients with head injury can be rapidly triaged and evacuated to trauma centers with CT scanners, making exploratory burr holes a thing of the past. However, burr holes can be used for emergent decompression in patients who show signs of rapid herniation if circumstances prevent access to radiographic studies.
• Acute traumatic subdural hematomas are often associated with acute brain swelling. Ironically, rapid decompression of acute traumatic subdural hematomas via craniotomy in these patients may potentiate damage to the brain by allowing it to herniate through the craniotomy defect. A novel method of decompression was devised to prevent the brain from extruding through the craniotomy defect. This entails proceeding with the standard trauma craniotomy exposure but fenestrating the dura in a meshlike fashion rather than opening it. The clot can then be removed through the small dural openings. In a series of 31 patients operated on in this manner more than 80% of the clot was removed in 29 patients as demonstrated by CT. Eighty seven percent of patients had presented with a GCS of 8 or less, and the mortality rate for that series of patients was 52%.¹² Symptomatic chronic subdural hematoma is surgically treated. Craniotomy is a valid option; however, burr hole drainage and twist drill craniotomy are less invasive and appear to be equally effective. They also can be performed using local anesthesia.
  • One or 2 burr holes are placed over the thickest aspects of the hematoma. Many surgeons place frontal and parietal burr holes that later can be incorporated into a frontotemporoparietal craniotomy, if needed. The dura is opened in a cruciate fashion, and the dural leaves are coagulated. A thin rubber catheter, often a ventriculostomy catheter, is carefully placed in the subdural space. Residual subdural hematoma is gently irrigated with saline solution until the irrigant is clear. The rubber catheter is redirected to different areas of the subdural space to irrigate the hematoma. Often, the brain does not re-expand right away. In these circumstances, the rubber catheter may be tunneled under the skin and left as a subdural drain. It is then connected to a closed drainage system placed at the level of the ear or slightly lower.
  • When a twist drill is used, a hole is drilled at a 45° angle to the skull over the thickest part of the hematoma (unless this lies over the motor strip). The twist drill is used to perforate the dura and to release the subdural hematoma. A thin rubber catheter is gently guided into the subdural space, tunneled under the scalp, and brought out through a stab incision. It is connected to a closed drainage system that is set at the level of the ear or slightly below the craniotomy.
  • Hwang et al evaluated external carotid angiograms and skull radiographs to develop an optimal entry point for twist drill craniostomy. After finding that all branches of the middle meningeal artery and vascular grooves were located posterior to the coronal suture, they determined that the optimal entry point should be 1 cm anterior to the coronal suture at the level of the superior temporal line.¹³
  • Laying the patient flat postoperatively was previously believed to promote brain re-expansion. However, Miele et al found that hematoma recurrence and complication rate appeared to be unaffected by keeping a patient flat in bed or raising the head of the bed to 30º.¹⁴  Postoperative CT scans often show a residual subdural fluid collection that usually should be left alone unless it continues to exert significant mass effect.
  • Evacuating chronic subdural hematoma via burr holes or twist drill craniotomy is a simple task for the neurosurgeon, but complications are not uncommon. The most common complications include reaccumulation of the hematoma, intracerebral hemorrhage caused by sudden brain shift or misguided irrigation and drainage tubes, tension pneumocephalus, seizures, and subdural empyemas. However, success rates are high; 86-95% of patients are adequately treated after one procedure.¹⁵

Follow-up

Prognosis

• When deciding whether to operate, consider the patient's prognosis. The ideal is to maximize the likelihood of appropriate resource allocation and, more importantly, allow for appropriate family counseling; keep in mind that no method of assessing the prognosis is 100% accurate.
• In a retrospective review of 109 consecutive patients with head injury with a CT scan diagnosis of acute traumatic subdural hematoma, Phuenpathom et al found that poor outcome was strongly correlated with the best sum GCS score within the first 24 hours of head injury and pupillary inequality. Age and pupillary reaction to light also correlated well with the outcome. The mortality rate in the whole series was 50%. The mortality rate for all 37 patients with a GCS score of 3 was 100%, and this rate decreased as the GCS increased. The mortality rate for those with unequal pupils was 64%, compared to 40% for those with equal pupils. The mortality rate associated with one nonreactive pupil was 48% and 88% with bilateral nonreactive pupils. Interestingly, the survival rate for patients with bilateral nonreactive pupils was 12%, although their outcome status was not noted.¹⁶
• Wilberger et al also found an 88% mortality rate associated with fixed, dilated pupils and noted a 7% functional recovery associated with this finding. This study found that neurological presentation and postoperative intracranial pressure (not evaluated by Phenpatham et al) were strong predictors of outcome. Wilberger et al also found a trend of increasing mortality rate with age, although it was not statistically significant.¹⁷
• Sakas et al examined 1-year outcomes following craniotomy for traumatic hematomas in patients with fixed, dilated pupils. Their results suggested that the presence of an acute subdural hematoma was the single most important predictor of a negative outcome in patients with fixed and dilated pupils. Patients with subdural hematomas had a mortality rate of 64% compared with a mortality rate of 18% in patients with extradural hematomas.¹⁸
• Seelig et al also showed that neurologic examination and postoperative intracranial pressure were important prognostic factors. The peak intracranial pressure was less than 20 mm Hg in 53% of patients with acute traumatic subdural hematoma (similar to 59% of patients with other types of head injuries), but this group accounted for 79% of the patients with functional recoveries. All patients with uncontrollably elevated intracranial pressure (>60 mm Hg) died. These authors claimed a 25% functional recovery rate (defined by the Glasgow Outcome Scale) in patients presenting with fixed, dilated pupils.¹⁹
• Although rare, acute subdural hematomas that would otherwise be considered operative by imaging criteria may possibly resolve on their own. A series of 4 such patients was reported by Kapsalaki et al.²⁰
• No clear prognostic factors are associated with chronic subdural hematoma. While some authors have found an association with preoperative level of neurological function and outcome, others have not.
• Between 86% and 90% of patients with chronic subdural hematoma are adequately treated after one surgical procedure.

Patient Education

For excellent patient education resources, visit eMedicine's Headache Center. Also, see eMedicine's patient education article Aneurysm, Brain.

Miscellaneous

Medicolegal Pitfalls

Inadequate discharge instructions for patients discharged from the hospital after sustaining a very small acute traumatic subdural hematoma may not prompt a patient to return to the emergency department in a timely manner if symptoms progress or develop. Inadequate assessment and surveillance of patients admitted to the hospital might lead to missed opportunities for care in patients who are still at risk for delayed neurologic deterioration. This can result in morbidity or death as subsequent herniation occurs.

• The legal liability in such a situation is unavoidable. The patient returning home from the emergency department needs to be able to solicit help from another person who is competent to provide assistance and lives with the patient. A surveillance plan ("head injury check list"), designed to show clear signs of potential herniation, needs to be given to the patient and caregiver with clear indications of when to return to the emergency department.
• Likewise, a patient with head trauma admitted to the hospital needs to have explicit nursing orders for neurologic examinations ("neuro checks") to be followed at frequent (30-60 min) intervals with instructions to call the clinician with any significant changes in neurological status. Such follow-up care should eliminate any ambiguity that later compromises the practitioner's position in a litigation response and, most of all, establishes a required pattern of immediate follow-up care.

Acute traumatic subdural hematomas have been observed to develop in a delayed fashion. Itshayek et al presented 4 patients that developed acute traumatic subdural hematoma after sustaining mild traumatic brain injury and having a normal initial CT scan of the head. All 4 patients had been on anticoagulant or antiaggregation therapy. Three of the 4 required craniotomy for evacuation of their hematomas. Elderly anticoagulated patients with mild traumatic brain injury might warrant a longer period of clinical observation.²¹

Multimedia

Media file 1: Acute right-sided subdural hematoma associated with significant midline shift (ie, subfalcine herniation) shown on CT scan.

Media file 2: Bilateral chronic subdural hematomas shown on CT scan. Midline shift is absent because of bilateral mass effect. Subdural hematoma is bilateral in 20% of patients with chronic subdural hematoma.

Media file 3: An acute subdural hematoma is shown in this intraoperative photograph. Note the frontotemporoparietal flap used. The hematoma is currant jelly–like in appearance.

References

1. Gennarelli TA, Thibault LE. Biomechanics of acute subdural hematoma. J Trauma. Aug 1982;22(8):680-6. [Medline].

2. Hlatky R, Valadka AB, Goodman JC, Robertson CS. Evolution of brain tissue injury after evacuation of acute traumatic subdural hematomas. Neurosurgery. Jul 2007;61(1 suppl):249-254. [Medline].

3. Schroder ML, Muizelaar JP, Kuta AJ. Documented reversal of global ischemia immediately after removal of an acute subdural hematoma. Report of two cases. J Neurosurg. Feb 1994;80(2):324-7. [Medline].

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Keywords

head injury, subdural hematoma, epidural hematoma, extraaxial hematoma, intracranial mass lesions, head injuries, intracranial hematomas, traumatic intracranial hematomas, chronic subdural hematoma, CSDH, coagulopathies and ruptured intracranial aneurysms, acute traumatic subdural hematoma, ATSDH, atraumatic subdural hematoma, acute subdural bleeding, brain injury, cerebral atrophy, herniation syndromes, stroke of the posterior cerebral artery distribution, spontaneous subdural hematoma

Contributor Information and Disclosures

Author

Richard J Meagher, MD, Attending Neurosurgeon, Neurosurgical Associates of Abington, Abington Memorial Hospital
Richard J Meagher, MD is a member of the following medical societies: American Association of Neurological Surgeons, Congress of Neurological Surgeons, and North American Spine Society
Disclosure: Nothing to disclose.

Coauthor(s)

William F Young, MD, Attending Neurosurgeon, Fort Wayne Neurological Center
William F Young, MD is a member of the following medical societies: Congress of Neurological Surgeons
Disclosure: Nothing to disclose.

Medical Editor

Norman C Reynolds Jr, MD, Neurologist, Veterans Affairs Medical Center of Milwaukee
Norman C Reynolds Jr, MD is a member of the following medical societies: American Academy of Neurology, Association of Military Surgeons of the US, Movement Disorders Society, Sigma Xi, and Society for Neuroscience
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center
Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association
Disclosure: Boehringer Ingelheim Honoraria Speaking and teaching; BMS/Sanofi Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health & Science University; Associate Director, Oregon Stroke Center
Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association
Disclosure: Co-Axia Consulting fee Review panel membership; Talecris Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Boehringer Ingelheim Honoraria Speaking and teaching; Concentric Medical Consulting fee Review panel membership; Abbott Consulting fee Consulting; Sanofi  Consulting

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