NOTE! This site uses cookies and similar technologies.

If you not change browser settings, you agree to it. Learn more

I understand

In order to make our website more comfortable and intuitive, we use cookies: they are small files of information needed to understand how users navigate in our website and make your browsing experience more enjoyable and more efficient in the future. Cookies do not store any personal information, and will not be stored any identifiable data. If you want to disable the use of cookies you have to customize the settings of your internet browser by removing all existing cookies and disabling their storage. To proceed without modifying the application of the cookies just continue the surfing.

Please visit AboutCookies.org for more information about cookies and how they affect your browsing experience.

Types of cookies used:

Technical cookie 
These cookies are essential for the website navigation; without some of these, technical issues could not work.

Performance cookie
These cookies collect informations about how visitors use the website: for example, which pages are most popular, and which pages have reported warnings or error messages. These cookies do not collect any personal information about the visitor, and they are used only to improve the website operation. By using our website, you agree that these cookies may be installed on your device.

Functionality Cookie
Cookies allow the website to remember the choices made by the user (for example, to remember the language choice) and provide custom functionality. These cookies can also be used to remember changes to the text size and other features of web pages that you can customize. They can also be used to provide services such as watching a video or sharing on social networks. The information gathered from these types of cookies can be anonymous and can't track your browsing activity on other websites. By using our website, you agree that these cookies may be installed on your device.

Google Analytics
This website uses Google Analytics, a web analytics service provided by Google Inc.
The information generated by the cookie about your use of the website (including your anonymous IP address) will be transmitted and stored in Google's servers in the United States. Google will use this information with the purpose of evaluating your use of the website, compiling reports on website activity for the operators and providing other services relating to website activity and internet usage. Google may also transfer this information to third parties, unless required by law, or where such third parties process the information on Google's behalf. Google will not associate your IP address with any other data held by Google. By using this website, you allow Google to process the data about you in the manner and purposes set out above.

Facebook 
This website uses plugins from the social network facebook.com, which is operated by Facebook Inc., 1601 S. California Ave, Palo Alto, CA 94304, USA (subsequently called "Facebook"). When opening a website that contains such a plugin, your browser will establish a direct connection to the Facebook servers. Facebook will transfer the content of the plugin directly to your browser, the latter of which will embed it in the website. This website hence does not have any influence on the amount of data that Facebook collects through this plugin and informs you according to its best knowledge. Through embedding the plugins Facebook receives the information that you have opened the respective website. If you are logged in to Facebook, Facebook can link this information to your Facebook account. If you interact with the plugins, for example by clicking the Like-button or commenting, your browser will submit this information directly to Facebook, which will save it. If you are not a member of Facebook, Facebook nonetheless might identify and save your IP address. Purpose and scope of the data collection as well as its distribution and usage of the data by Facebook as well as respective rights and preferences regarding privacy can be found in Facebook's privacy policy http://www.facebook.com/policy.php. If you are a member of Facebook and do not want Facebook to collect data through this website and connect it to your Facebook profile, you have to log out from Facebook prior to visiting this site.

Etiology

  • Head trauma: motor vehicle accident, falls, assaults
  • Brain atrophy is a risk factor that is characteristic of:
    • Elderly
    • Chronic alcoholists
    • People with previous traumatic brain injury
  • Antithrombotic therapy
  • Spontaneous SDH: rare (2,6%)

Unusual etiologies

  • Aneurysmal SAH associated with SDH
  • Aneurysmal rupture in absence of SAH
  • Vascular malformations
  • Meningiomas
  • Dural metastasis
  • Coagulopathy
  • Complication of systemic thrombolysis during myocardial infarction
  • CSF leak during: lumbar puncture, ventriculostomy, lumboperitoneal shunt placement. The risk is higher in patients with thrombocytopenia.
  • Cocaine abuse

 

Phatophysiology

A high-speed head injury produced by a lateral acceleration along the diameter of the skull can produce injury to vessels or brain parenchyma resulting in both a SDH, epidural hematoma or contusion.

 

Acute Subdural Hematoma

Acute SDH could be produced by several mechanisms: 

Vessel rupture

The acute SDH caused by traumatic injury is the result of the rupture of the bridging veins (the veins that drain from the brain to the venous sinuses) that transverse the subdural space. The bleeding is usually stopped by high intracranial pressure (ICP) or by the formation of a blood clot.

SDH can also be caused by arterial rupture (20-30% of cases): the arteries involved are the small cortical arteries with a diameter < 1mm. 

Intracranial hypotension

Another form of SDH is caused by a intracranial hypotension due to spontaneous or iatrogenic CSF leak (for example after a lumbar puncture). The result of this leak is a reduction of the suspensibility in the CSF of the brain that cause a stretch of the bridging vein: if this injury is severe there is a bleeding.

Brain atrophy

In the elderly people, the brain atrophy may already stretch the bridging veins so a less powerful head injury can cause a SDH.

Common sites

Note that SDHs caused by arterial rupture are usually located in the temporoparietal region and SDHs caused by bridging veins rupture are usually located in the frontoparietal region.

 

Chronic Subdural Hematoma

Chronic SDH could be produced by several mechanisms: 

Brain atrophy

Generally, chronic SDH is associated with brain atrophy that increase bridging veins tension.

Hygromas

Some chronic SDHs derive from subdural hygromas. Some conditions that lead to brain atrophy (alcoholism, stroke, etc.) may increase the space between the dura and the brain: in addition to that, a CSF flow in this space results in a stretch of the bridging veins. Note that the hygromas can be a results of a head injury, too.

Other mechanisms

A chronic SDH can develop also from:

  • a liquefaction of an acute SDH after 1-3 weeks
  • an osmotic gradient that move more fluid in the subdural space.

 

Natural history 

When a subdural hematoma expands, the ICP raise and consequently the brain is compressed.

The first phase is a high intracranial compliance phase so the ICP raise very slowly. In fact the ICP raising is compensated both by a higher CSF flow in the spinal compartment and by a compression of venous structures with the result of a higher venous flow through the internal jugular vein. When these mechanism of compensation fall, small increase of a SDH is associated with exponential increase in ICP: this lead to decreased cerebral perfusion and cerebral ischemia.

Note that this process can occur in minutes.

Acute-on-chronic SDH

Small SDHs can reabsorb themselves and large SDHs usually develop a thin vascular membrane that encapsulate the bleeding area: the rupture of the vessels of this membrane lead to an expansion of this hematoma

 

Complications

As the hematoma expands, the ICP raise and the brain is compressed. So, herniation syndromes can develop.

Transfalcine and transtetorial herniation

They develop if the brain is pushed past the falx cerebri and the tentorium, respectively.

Tonsillar herniation

Both a infratentorial and supratentorial (less frequently) hematomas can push the brainstem downward and cause this herniation

Uncal herniation

If the medial temporal lobe (uncus) is pushed medially, it herniates past the tentorium. This result in the compression of the ipsilateral PCA, III CN and cerebral peduncle leading to:

  • III nerve palsy
  • ipsilateral dilated pupil
  • contralateral hemiparesis

Subfalcine herniation

A midline brain shift can compress the ACA branches near the falx resulting in a infarction of the areas vascularized by this arteries.

Kernohan notch syndrome

The contralateral cerebral peduncle can be pushed against the contralateral tentorial incisura leading to a ipsilateral hemiparesis (5% of cases)

 

Clinical Presentation

As far as the time of onset, SDH is classified in:

  • Acute SDH: presents after 1 to 2 days after onset
  • Subacute SDH: presents after 3 o 14 days after onset
  • Chronic SDH: presents 15 or more days after onset

Note that for onset is intended the traumatic event but this classification is not useful if there is no history of trauma.

Acute SDH

  • Coma: in 50% of cases from the time of injury
  • Lucid interval: in 12-38% of cases, after the injury there is a period followed by a progressive neurological deterioration to coma.
  • ICP symptoms (especially if SDH is in the posterior fossa): headache, anisocoria, vomiting, dysphagia, cranial nerve palsy, ataxia, nuchal rigidity.
  • Cerebral infarction especially if SDH is in the posterior fossa due to a ICP.

Chronic SDH

Insidious onset of

  • Global deficits
  • Headaches
  • Light-headedness
  • Apathy
  • Somnolence
  • Cognitive impairment
  • Seizure (occasionally)
  • Focal deficits (less frequent): either ipsilateral or contralateral to SDH
  • Controlateral hemparesis: due to brain compression under the hematoma
  • Ipsilateral hemiparesis: due to cortical brain shift caused by the mass effect of the hematoma
  • Intermittent paraparesis (proximal and painless) if a bitemporal chronic SDH develops 

 

Diagnosis

In the setting of a traumatic brain injury a variety of lesions (fractures, contusions, hemorrages, etc.) could happen. It’s important to recognize and treat those that are life-threatening.


Note that lumbar puncture is contraindicated if there is a suspect oh SDH because the decrease in intracranial pressure can produce a cerebral herniation.


Head CT

Acute SDH: hyperdense crescentic collection across the hemispheric convexity

Subacute and chronic SDH: isodense or hypodense crescent-shaped collection. The membranes are enhanced by the intravenous contrast.

Head MRI

It is used if there is a suspicion of SDH without evidence on CT scan

Acute SDH: hypointense on T2 due to the presence of deoxyhemoglobin

During weeks: hyperintense on T1 and T2 because of the presence of methemoglobin

After months: hypointense on T1 because of hemosiderin

Differential diagnosis

Note that SDH can cross the sutural margins but is limited by dural attachments. Instead, epidural hematomas are limited by sutural margins but can cross dural attachments so it has a lens-shape appearance.

 

References

Lee KS. The pathogenesis and clinical significance of traumatic subdural hygroma. Brain Inj 1998; 12:595.

Yadav YR, et.al. Chronic subdural hematoma. Asian J Neurosurg. 2016 Oct-Dec;11(4):330-342.

Lee KS. History of Chronic Subdural Hematoma. Korean J Neurotrauma. 2015 Oct;11(2):27-34. doi: 10.13004/kjnt.2015.11.2.27. Epub 2015 Oct 31.

Iliescu IA, Constantinescu AI. Clinical evolutional aspects of chronic subdural haematomas - literature review. J Med Life. 2015;8 Spec Issue:26-33.

Miller JD1, Nader R. Acute subdural hematoma from bridging vein rupture: a potential mechanism for growth. J Neurosurg 2014 Jun;120(6):1378-84.

Gennarelli TA, Thibault LE. Biomechanics of acute subdural hematoma. J Trauma 1982; 22:680.

Besenski N. Traumatic injuries: imaging of head injuries. Eur Radiol 2002; 12:1237.

Lee KS, et.al. Origin of chronic subdural haematoma and relation to traumatic subdural lesions. Brain Inj. 1998 Nov;12(11):901-10.

Lee KS. Chronic Subdural Hematoma in the Aged, Trauma or Degeneration?. J Korean Neurosurg Soc. 2016 Jan;59(1):1-5. 

Kaminski HJ, et.al. Transient neurologic deficit caused by chronic subdural hematoma. Am J Med 1992; 92:698.

Mark S. Greenberg. Handbook of neurosurgery. Thieme

 

Authors

 

Giorgio Saraceno, MS

University of Brescia (Italy) 
Scientific Team UpSurgeOn

 

Antonio D'Ammando, MD

University of Milan (Italy)
"Spedali Civili" Hospital Brescia (Italy)
Scientific Team UpSurgeOn