Critical Care Medicine
Subdural hematoma, subdural hemorrhage
- 1. Description of the problem
- 2. Emergency Management
- 3. Diagnosis
4. Specific Treatment
- 5. Disease monitoring, follow-up and disposition
Special considerations for nursing and allied health professionals.
What's the evidence?
Also known as: Subdural Hemorrhage
Related conditions: Epidural Hematoma, Subarachnoid Hematoma, Intracerebral Hemorrhage
1. Description of the problem
What every clinician needs to know
Subdural hematoma (SDH) is defined as an intracranial accumulation of blood within the subdural space that typically occurs due to traumatic brain injury. There are two main types of SDH distinguished both on the basis of radiography and time. Acute SDH is diagnosed within 3 days of trauma (usually within 48 hours) and is seen on CT scan as a hyperdense crescentic accumulation of blood between the brain parenchyma and inner table of the calvarium. Chronic SDH follows the same crescentic pattern as acute SDH but is hypodense in appearance on CT and is diagnosed ≥14 days after the initial trauma. A third category, subacute SDH, is isodense on CT and may be seen anywhere from 2 to 14 days after trauma. The radiographic appearance of SDH corresponds to the evolution of blood products over time.
Acute SDH usually presents with altered mental status (AMS), and/or focal neurological deficits including cranial nerve palsies (ie, pupillary dilatation due to oculomotor nerve compression) or hemiplegia. Acute SDH may be a neurosurgical emergency depending on the size and characteristics of the bleed as well as the patient's clinical presentation.
Chronic SDH may also present with AMS, but also can be found on evaluation of chronic headaches, dizziness, memory loss, anxiety, or difficulty with concentration. Unlike acute SDH, chronic SDH is most often not a neurosurgical emergency and can be dealt with on a more elective (non-urgent) basis. However, neurological and/or neurosurgical consultation is still warranted in newly diagnosed chronic SDH.
Symptoms of SDH may include:
Confusion and/or slurred speech
Weakness or numbness
Nausea and/or vomiting
Loss of consciousness
Visual changes (blurry or double vision)
Specifically in infants, symptoms of SDH may include:
Feeding problems, including relentless vomiting
Full or bulging fontanelles
Increasing head circumference
Splayed cranial sutures
Key management points
General Emergency Department 'safety net' measures should be initiated for patients suspected of having SDH, including but not limited to: oxygen therapy, intravenous access, blood pressure and cardiac rhythm monitoring, pulse oximetry, etc.
Preoperative lab measurements (ie, complete blood count, blood chemistry, coagulations studies, type/screen, and urinalysis) should be ascertained in case imminent surgery is mandated.
NPO status should be maintained until surgical intervention has been determined to be unnecessary by appropriate consultants.
In patients presenting with AMS with high suspicion for intracranial pathology (ie, GCS < 13) or those with focal neurological deficits, a noncontrast head CT should be obtained. The Canadian CT Head rule provides a good general guideline for deciding whether to order a head CT in patients with minor head injuries (GCS 13-15).
Canadian CT Head Rule: Applies to patients with minor headinjuries with any one of the following:
High risk (for neurological intervention):
GCS score <15 at 2 h after injury
Suspected open or depressed skull fracture
Any sign of basal skull fracture (hemotympanum, “raccoon” eyes, cerebrospinal fluid otorrhea/rhinorrhea, Battle's sign)
Vomiting ≥2 episodes
Age ≥65 years
Medium risk (for brain injury on CT):
Amnesia before impact >30 min
Dangerous mechanism (pedestrian struck by motor vehicle, occupant ejected from motor vehicle, fall from height >3 feet or five stairs)
Minor head injury is defined as witnessed loss of consciousness, definite amnesia, or witnessed disorientation in a patients with a GCS score of 13-15
-From the Canadian CT Head Rule paper, Lancet 2001.
2. Emergency Management
Emergency 'safety net' measures: nursing staff to initiate these.
oxygen therapy and pulse oximetry
intravenous access (generally 2 large-bore catheters)
blood pressure and cardiac rhythm monitoring
Glasgow Coma Score: what is the patient's level of consciousness?
Eyes: Open spontaneously (4), Open to voice (3), Open to pain (2), or No eye opening (1)
Verbal: Oriented/appropriate (5), Disoriented (4), Incomprehensible speech (3), Moaning (2), None (1)
Motor: Follows commands (6), Localizes/purposeful (5), Withdraws (4), Abnormal flexion (3), Abnormal extension (2), None (1)
GCS 13-15: minor head injury, GCS 9-12: moderate head injury, GCS ≤8: severe head injury
Primary Trauma survey: are there other life-threatening injuries suggestive of major trauma?
Neurological exam (Disability): what is the patient's mental status and are there any focal cranial nerve or motor deficits?
Based on primary and secondary evaluation, is any diagnostic imaging warranted?
Is GCS ≤12?
If so, then get noncontrast CT head
Is GCS >12?
Refer to Canadian CT Head rule for diagnostic imaging in patients with minor head trauma
Foley catheter and arterial line placement may be instrumental in managing patients with elevated intracranial pressure.
Noncontrast CT head: is there any evidence of intracranial pathology (ie, subdural hematoma)?
If evidence of intracranial pathology, neurological and/or neurosurgical consultations are likely warranted.
Key management points
If the patient has signs of brain herniation (ie, oculomotor palsy and/or Cushing's reflex ), do not delay immediate neurosurgical consultation and hyperosmolar therapy (ie, mannitol) once the patient has been resuscitated (i.e., normalization of lactate, base deficit, cardiac index, etc.) as described below.
Do not delay diagnostic imaging (noncontrast head CT) in those with suspected SDH and declining neurological exam, unless the patient is hemodynamically labile and therefore unstable.
Diagnostic criteria and tests
Noncontrast head CT should be obtained promptly in patients with suspected SDH. Absence of subdural fluid accumulation of any density on noncontrast head CT rules out the diagnosis of SDH, in which case alternative causes of AMS should be considered.
Normal lab values
The main types of SDH are distinguished both on the basis of radiography and time.
Acute SDHis diagnosed within 3 days of trauma (usually within 48 hours) and is seen on CT scan as a hyperdense crescentic accumulation of blood between the brain parenchyma and inner table of the calvarium. Subacute SDHis isodense on CT and may be seen anywhere from 2-14 days after trauma. Chronic SDHfollows the same crescentic pattern as acute SDH but is hypodense in appearance on CT and is diagnosed ≥14 days after the initial trauma. Acute on Chronic SDHmay be seen in patients with a history of chronic SDH but with new head trauma causing new bleeding into the subdural space. This is typically seen on non-contrast head CT as focal areas of hyperdensity within a background of hypodense subdural fluid collection.
The radiographic appearance of SDH corresponds to the evolution of blood products over time.
Not all extra-axial fluid on non-contrast head CT is SDH. Epidural hematoma, which is also hyperdense and extra-axial on head CT, has a more lenticular appearance due to its limitation by dural-cranial suture line adhesions but also represents a neurosurgical emergency. Extra-axial isodense fluid may represent subacute SDH, subdural hygroma, or subdural empyema.
Non-contrast head CT is key in making the diagnosis of SDH. MRI may help differentiate subacute or chronic SDH from subdural hygroma or subdural empyema.
4. Specific Treatment
SDH warrants urgent neurological and/or neurosurgical consultation. Acute SDH >1 cm in thickness on CT and/or with >5 mm of midline shift should be considered for emergent surgical evacuation. Patients with GCS<9 generally require intubation for airway protection and an intracranial pressure monitor if surgical evacuation of the SDH is delayed.
Acute SDH can cause elevated intracranial pressure (ICP) due to local compression of brain tissue. Therefore, optimal medical management of elevated ICP should be initiated as soon as clinical suspicion of such arises (see below).
If SDH is causing brain herniation, as evidenced by oculomotor palsy or Cushing's reflex (bradycardia, hypertension, and irregular respirations), hyperosmolar therapy with mannitol (an osmotic diuretic) should be considered. Mannitol general dosing is 0.25 to 1 gm/kg i.v. bolus given as quickly as possible. In emergency situations where the patient's exact weight is not known, a 100-grams i.v. bolus can be given to average-size adults. (Please refer to the manufacturer's product information for exact dosing and use of this product.) Hyperosmolar therapy can lower ICP by causing brain parenchyma tissue diuresis. Caution must be exercised in the hypovolemic, under-resuscitated patient, however. Brisk diuresis in these patients can compromise blood flow to the brain itself, which may cause secondary brain injury due to malperfusion.
Anti-epileptic drugs (AEDs) are also generally given to patients with acute SDH as extravasation of blood intracranially can irritate the brain's cortical surface and trigger seizures. Levetiracetem (Keppra) is one such agent often chosen due to its route of administration (both oral and intravenous forms are available) and lack of need to titrate the medication based on blood levels of the drug. A typical emergency loading dose of levetiracetem is 1000 mg i.v. x 1, then anywhere from 500 mg to 1500 mg i.v. every 12 hours. There are several other AEDs that can be used (ie, phenytoin) but will not be discussed here. (Please refer to the manufacturer's product information for exact dosing and use of all aforementioned drugs.)
If the patient is intubated and on a ventilator, adjustments should be made to keep the pCO2 ≤ 35 mmHg (but ≥25 mmHg). Doing so decreases intracranial vasodilation and can temporarily lower ICP. This may be used for emergent temporization of intracranial hypertension. Prolonged hyperventilation has shown to be detrimental to brain perfusion with poorer outcomes due to malperfusion. In addition, the body compensates within about 24 hours and renders this maneuver relatively useless and potentially harmful.
Tight blood pressure control may help prevent further bleeding and/or secondary brain injury. Arterial line placement for invasive blood pressure monitoring and use of a titratable antihypertensive infusion to keep systolic blood pressure (SBP) < 160 mmHg is generally indicated in acute SDH.
Correction of blood clotting deficiency should not be delayed in patients with acute SDH. Elevated prothrombin time/INR and/or activated partial thromboplastin time should be treated with fresh frozen plasma, vitamin K, and/or recombinant Factor VIIa as necessary to normalize values and keep INR ≤ 1.3. If the patient is on a continuous heparin infusion and has an elevated activated partial thromboplastin time, protamine should be administered and the infusion stopped. Patients who take aspirin or other platelet inhibitors should refrain from further use of said agents and be given at least 1 unit of platelets. If thrombocytopenic, platelets should be administered in attempts to keep a measured value >100k. In some circles these practices remains controversial, however.
Optimal medical management of elevated ICP in SDH includes:
'Safety net' measures (cardiac monitoring, pulse oximetry, etc.)
Keep SpO2 > 90% and pCO2 ≤ 35 mmHg
Foley catheter and arterial line placement
Tight blood pressure control (SBP < 160 mmHg)
Use a titratable antihypertensive such as nicardipine infusion
Correct any blood clotting deficiency with appropriate agents
If the patient takes aspirin or other platelet inhibitor, administer at least 1 unit of platelets
If the patient has elevated prothrombin time/INR or activated partial thromboplastin time, normalize these values with appropriate intervention (ie, fresh frozenplasma, vitamin K and recombinant Factor VIIa).
If the patient has an elevated activated partial thromboplastin time due to heparin infusion, stop the infusion and use protamine to reverse the therapeutic effects of heparin.
There should not be a delay in operative intervention for SDH causing brainstem herniation in most cases. While awaiting transfer to a facility offering neurosurgical consultation, optimize the management of the patient's ICP as noted above.
Steroids (ie, glucocorticoids) are contraindicated in head trauma.
5. Disease monitoring, follow-up and disposition
Expected response to treatment
After diagnosing SDH, neurological and/or neurosurgical consultation should be immediately sought. Disposition of the patient will occur after evaluation by the appropriate consulting service (ie, surgical versus medical management of SDH). In some situations, surgical evacuation of acute SDH not causing significant neurological deterioration may be delayed until the SDH becomes chronic. For example, a small acute SDH in an elderly individual with significant comorbidities who would likely not tolerate a massive craniotomy for surgical evacuation may be treated with a less morbid surgical drainage through small burr holes once the SDH has become chronic.
Alternative diagnoses should be sought if non-contrast head CT does not demonstrate a subdural fluid collection in patients suspected of having SDH. Also, as mentioned above, not all iso- or hypodense fluid collections are SDH, and MRI may help differentiate these.
Patients with SDH should be followed by neurological and/or neurosurgical services per their discretion.
SDH usually arise from one of the following mechanisms: 1) Trauma causing primary brain injury with parenchymal laceration and subsequent accumulation of blood in the subdural space, 2) Traumatic brain injury causing shearing of surface or bridging vessels (which join the cerebrum to the venous sinuses), 3) Spontaneous.
Acute SDH is generally due to serious head injury and can be very dangerous as blood can quickly fill the subdural space and elevate ICP (Monro-Kellie Doctrine) and damage underlying brain parenchyma.
Chronic SDH is often seen in the elderly or alcoholics and typically occurs after minor head injury, which may go unnoticed for days to months. The elderly and alcoholics are prone to developing chronic SDH because they often have cerebral atrophy, which causes stretching of the bridging veins between the cortical surface and the dura. Also, these two populations are prone to frequent falls, which can cause tearing of these veins.
Risk factors for SDH:
Extremes of age (very young or very old)
Anticoagulant medications (aspirin, warfarin, etc.)
Multiple head injuries
In adults, cerebral atrophy (which may be due to age or alcoholism) can lead to stretching of the bridging veins that span between the cerebrum and venous sinuses, making them more prone to shear injury. It is important to remember that patients, especially the elderly, may be taking warfarin and/or other blood thinners for diseases such as atrial fibrillation, deep venous thrombosis, pulmonary embolus, or other cardiac/vascular disease states. Specifically, warfarin may be associated with increased morbidity and mortality in patients with minor head trauma, and these are risk factors for chronic SDH and for intracerebral hemorrhage.
In children, particularly those <3 years old, SDH is most commonly due to major trauma (tripping, assault, road accidents, serious falls) or non-accidental trauma. In fact, in infants <1 year of age, non-accidental trauma is the most common cause of subdural bleeding found at autopsy.
In some cases, patients may present with SDH without identifiable trauma. Spontaneous SDH may be due to any of the following : alcoholism, hypertension, aneurysm, arteriovenous malformation, neoplasm, coagulopathies, hypovitaminosis, infection (ie, meningitis, tuberculosis), etc.
The frequency of SDH is directly tied to the incidence of blunt head trauma in the United States. SDH occurs in approximately one third of those presenting with severe head injuries. SDH not associated with underlying parenchymal injury is associated with a mortality rate of around 20%. When underlying brain is injured, mortality rates rise to about 50%. In recent literature, the incidence of acute SDH in patients with severe traumatic brain injury is between 12% and 29%. In regards to prevalence, SDH was incidentally found in <0.1% in a study of brain MRI of 2,000 persons older than 45 in the Netherlands.
See the chapter on Traumatic Brain Injury for further information on incidence/prevalence of head injury.
Prognosis for patients sustaining SDH varies tremendously based on the type and location of head injury, the size of the SDH, and time from injury to definitive treatment. Acute SDHs have the highest rates of death and injury due to their acuity, association with serious head injury, and sometimes delay in getting to a facility capable of surgical intervention. Better outcomes can typically be expected from subacute and chronic SDHs as symptoms often resolve after drainage of the SDH. Often, neurological rehabilitation may be required to help an individual deal with long-term neurologic deficits or to regain his/her baseline level of functioning.
Even after drainage of a SDH, the frequency of seizures can be quite high, necessitating AEDs for months to years after the initial diagnosis/injury.
Complications of SDH include (but are not limited to):
Brain herniation causing coma and/or death
Weakness, numbness, speech difficulty
As with most injuries, prevention is key. Reduce your risk of head injury by implementing appropriate safety equipment at both work and play (ie, hard hats, seat belts, helmets). Falls in the elderly should be especially anticipated and, if possible, avoided.
Special considerations for nursing and allied health professionals.
Adjuncts to care of the SDH patient include the following:
1) Frequent turns to avoid decubitous ulcer formation. Nurses must keep in mind to protect the patient with a craniectomy who may be missing a portion of the calvarium.
2) Aggressive pulmonary toilet and oral care with a chlorhexidine solution
3) Accurate measurement and documentation of fluids, extraventricular drainage devices and monitors as well as hemodynamics
4) Facilitating discussion among team members and family
5) Elevation of head of bed whenever possible
6) Monitor for abdominal compartment syndrome, a key and often-overlooked etiology in intracranial hypertension
1) Frequent ventilator checks and optimization of settings and support
2) Educating caregivers in tolerance and understanding of dysynchronous breathing patterns
3) Prevention of pneumonia by keeping circuits clean and preventing backwash, especially when traveling throughout the hospital
1) Providing much-needed calories, as these patients specifically have extraordinarily high metabolic demands
2) Providing essential branched chain amino acids
Physical and occupational therapy:
1) Prevention of contractures and skin breakdown
2) Education for patient and families
a. movement and mobilization
b. life at home
3. constant evaluation for patient's safety and reintegration into home life
1) Frequently reviewing medications as a barrier from progression of care (i.e., H2 antagonists as a cause of confusion and agitation)
2) Monitoring and facilitation of bowel and bladder programs
3) Weaning of chronic medications or stopping medications that are no longer required
What's the evidence?
Description of the problem
Stiell, IG. "The Canadian CT Head Rule for patients with minor head injury". Lancet. vol. 357. 2001 May 5. pp. 1391-6.A validated criteria for when to order a non-contrast head CT in minor head injury patients.
"Subdural hematoma". DynaMed [database online]. EBSCO Publishing. June 17, 2010.This online review was used as a reference throughout this chapter but most importantly for association with warfarin as a risk factor, incidence/prevalence, and diagnosis.
Biros, MH, Heegaard, WG, Marx, JA. "Head injury". Rosen’s Emergency Medicine: Concepts and Clinical Practice. Mosby Elsevier. 2009.A guide for the presentation and emergency management of head injury from the Emergency Medicine perspective. This reference was used throughout most all sections of this chapter.
Rockswold, GL, Tintinalli, JE. "Head Injury". Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill. 1996. pp. 1142.A guide for the presentation and emergency management of head injury from the Emergency Medicine perspective. This reference was used throughout most all sections of this chapter.
Greenberg, MS. "Handbook of Neurosurgery". Thieme. 2006. pp. 672-677.This handbook provides a sound base of information regarding acute and chronic subdural hematomas including radiographic presentation (Table 24-25), Morbidity and Mortality, Surgical Considerations, etc. This reference was used throughout most all sections of the paper.
Bullock, MR, Chesnut, R, Ghajar, J, Gordon, D, Hartl, R, Newell, DW. "Surgical management of acute subdural hematomas". Neurosurgery. vol. 58. Mar 2006. pp. S16-24; discussion Si-iv.This article gives guidelines for surgical management of acute SDH.
Nishijima, DK, Dager, WE, Schrot, RJ, Holmes, JF. "The Efficacy of FactorVIIa in Emergency Department Patients With Warfarin Use and Traumatic Intracranial Hemorrhage". Acad Emerg Med. vol. 17. Mar 2010. pp. 244-251.Recombinant factor VIIa was associated with decreased time to correction of INR in patients with intracranial hemorrhage who were taking warfarin.
Bell, RS, Neal, CJ, Lettieri, CJ, Armonda, RA. "Severe Traumatic Brain Injury: Evolution and Current Surgical Management". Medscape. June 12, 2011. http://www.medscape.org/viewarticle/575753.General guidelines and management for dealing with traumatic brain injury and elevated ICP.
Cohen, M, Scheimberg, I. "Subdural haemorrhage and child maltreatment". Lancet. vol. 373. Apr 4 2009. pp. 1173-4.The presentation, incidence, etc. of SDH in children.
Tandon, PN. "Acute subdural haematoma : a reappraisal". Neurol India [serial online]. vol. 49. 2011 Jun 12. pp. 3-10.This article addresses some of the updated thoughts on pathophysiology of acute SDH.
Wilberger, JE, Harris, M, Diamond, DL. "Acute subdural hematoma: Morbidity, mortality, and operative timing". J Neurosurg. vol. 74. 1991. pp. 212-8.A study of 101 patients with acute SDH found overall mortality 66% and functional recovery 19%.
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