Subdural hematoma

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Subdural hematoma
Classification and external resources

Subdural hematoma as marked by the arrow with significant midline shift
ICD-10I62.0, P10.0, S06.5
ICD-9852.2 - traumatic; 432.1 - nontraumatic
DiseasesDB12614
MedlinePlus000713
eMedicineneuro/575
MeSHD006408
 
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Subdural hematoma
Classification and external resources

Subdural hematoma as marked by the arrow with significant midline shift
ICD-10I62.0, P10.0, S06.5
ICD-9852.2 - traumatic; 432.1 - nontraumatic
DiseasesDB12614
MedlinePlus000713
eMedicineneuro/575
MeSHD006408

A subdural hematoma (American spelling) or subdural haematoma (British spelling), also known as a subdural haemorrhage (SDH), is a type of hematoma, a form of traumatic brain injury. Blood gathers within the outermost meningeal layer, between the dura mater, which adheres to the skull, and the arachnoid mater, which envelops the brain. Usually resulting from tears in bridging veins which cross the subdural space, subdural hemorrhages may cause an increase in intracranial pressure (ICP), which can cause compression of and damage to delicate brain tissue. Subdural hematomas are often life-threatening when acute. Chronic subdural hematomas, however, have better prognosis if properly managed.

In contrast, epidural hematomas are usually caused by tears in arteries, resulting in a build-up of blood between the dura mater and skull.

Contents

Classification

Subdural hematomas are divided into acute, subacute, and chronic, depending on the speed of their onset.[1] Acute subdural hematomas that are due to trauma are the most lethal of all head injuries and have a high mortality rate if they are not rapidly treated with surgical decompression.[2]

Acute bleeds often develop after high speed acceleration or deceleration injuries and are increasingly severe with larger hematomas. They are most severe if associated with cerebral contusions.[3] Though much faster than chronic subdural bleeds, acute subdural bleeding is usually venous and therefore slower than the usually arterial bleeding of an epidural hemorrhage. Acute subdural bleeds have a high mortality rate, higher even than epidural hematomas and diffuse brain injuries, because the force (acceleration/deceleration) required to cause them causes other severe injuries as well.[4] The mortality rate associated with acute subdural hematoma is around 60 to 80%.[5]

Chronic subdural bleeds develop over a period of days to weeks, often after minor head trauma, though such a cause is not identifiable in 50% of patients.[6] They may not be discovered until they present clinically months or years after a head injury.[7] The bleeding from a chronic bleed is slow, probably from repeated minor bleeds, and usually stops by itself.[8][9] Since these bleeds progress slowly, they present the chance of being stopped before they cause significant damage. Small chronic subdural hematomas, those less than a centimeter wide, have much better outcomes than acute subdural bleeds: in one study, only 22% of patients with chronic subdural bleeds had outcomes worse than "good" or "complete recovery".[3] Chronic subdural hematomas are common in the elderly.[7]

Signs and symptoms

Hematoma typeEpiduralSubdural      
LocationBetween the skull and the duraBetween the dura and the arachnoid
Involved vesselTemperoparietal locus (most likely) - Middle meningeal artery
Frontal locus - anterior ethmoidal artery
Occipital locus - transverse or sigmoid sinuses
Vertex locus - superior sagittal sinus
Bridging veins
SymptomsLucid interval followed by unconsciousnessGradually increasing headache and confusion
CT appearanceBiconvex lensCrescent-shaped








Symptoms of subdural hemorrhage have a slower onset than those of epidural hemorrhages because the lower pressure veins bleed more slowly than arteries. Therefore, signs and symptoms may show up in minutes, if not immediately[10] but can be delayed as much as 2 weeks.[11] If the bleeds are large enough to put pressure on the brain, signs of increased ICP or damage to part of the brain will be present.[3]

Other signs and symptoms of subdural hematoma can include any combination of the following:

Causes

Subdural hematomas are most often caused by head injury, when rapidly changing velocities within the skull may stretch and tear small bridging veins. Subdural hematomas due to head injury are described as traumatic. Much more common than epidural hemorrhages, subdural hemorrhages generally result from shearing injuries due to various rotational or linear forces.[3][8] Subdural hemorrhage is a classic finding in shaken baby syndrome, in which similar shearing forces classically cause intra- and pre-retinal hemorrhages. Subdural hematoma is also commonly seen in the elderly and in alcoholics, who have evidence of cerebral atrophy. Cerebral atrophy increases the length the bridging veins have to traverse between the two meningeal layers, hence increasing the likelihood of shearing forces causing a tear. It is also more common in patients on anticoagulants, especially aspirin and warfarin. Patients on these medications can have a subdural hematoma with a minor injury. A further cause can be a reduction in cerebal spinal fluid pressure which can create a low pressure in the dura and so cause rupture of the blood vessels

Risk factors

Factors increasing the risk of a subdural hematoma include very young or very old age. As the brain shrinks with age, the subdural space enlarges and the veins that traverse the space must travel over a wider distance, making them more vulnerable to tears. This and the fact that the elderly have more brittle veins make chronic subdural bleeds more common in older patients.[6] Infants, too, have larger subdural spaces and are more predisposed to subdural bleeds than are young adults.[3] For this reason, subdural hematoma is a common finding in shaken baby syndrome. In juveniles, an arachnoid cyst is a risk factor for a subdural hematoma.[12]

Other risk factors for subdural bleeds include taking blood thinners (anticoagulants), long-term alcohol abuse, and dementia.

Pathophysiology

Micrograph of a chronic subdural hematoma, as demonstrated by thin strands of collagen and neovascularization. HPS stain.

Collected blood from the subdural bleed may draw in water due to osmosis, causing it to expand, which may compress brain tissue and cause new bleeds by tearing other blood vessels.[6] The collected blood may even develop its own membrane.[13]

In some subdural bleeds, the arachnoid layer of the meninges is torn, and cerebrospinal fluid (CSF) and blood both expand in the intracranial space, increasing pressure.[8]

Substances that cause vasoconstriction may be released from the collected material in a subdural hematoma, causing further ischemia under the site by restricting blood flow to the brain.[9] When the brain is denied adequate blood flow, a biochemical cascade known as the ischemic cascade is unleashed, and may ultimately lead to brain cell death.

The body gradually reabsorbs the clot and replaces it with granulation tissue.

Diagnosis

A subdural hematoma demonstrated by CT.

Subdural hematomas occur most often around the tops and sides of the frontal and parietal lobes.[3][8] They also occur in the posterior cranial fossa, and near the falx cerebri and tentorium cerebelli.[3] Unlike epidural hematomas, which cannot expand past the sutures of the skull, subdural hematomas can expand along the inside of the skull, creating a concave shape that follows the curve of the brain, stopping only at the dural reflections like the tentorium cerebelli and falx cerebri.

On a CT scan, subdural hematomas are classically crescent-shaped, with a concave surface away from the skull. However, they can have a convex appearance, especially in the early stage of bleeding. This may cause difficulty in distinguishing between subdural and epidural hemorrhages. A more reliable indicator of subdural hemorrhage is its involvement of a larger portion of the cerebral hemisphere since it can cross suture lines, unlike an epidural hemorrhage. Subdural blood can also be seen as a layering density along the tentorium cerebelli. This can be a chronic, stable process, since the feeding system is low-pressure. In such cases, subtle signs of bleeding such as effacement of sulci or medial displacement of the junction between gray matter and white matter may be apparent. A chronic bleed can be the same density as brain tissue (called isodense to brain), meaning that it will show up on CT scan as the same shade as brain tissue, potentially obscuring the finding.

Treatment

It is important that a patient receive medical assessment, including a complete neurological examination, after any head trauma. A CT scan or MRI scan will usually detect significant subdural hematomas.

Treatment of a subdural hematoma depends on its size and rate of growth. Some small subdural hematomas can be managed by careful monitoring until the body heals itself. Other small subdural hematomas can be managed by inserting a temporary small catheter through a hole drilled through the skull and sucking out the hematoma; this procedure can be done at the bedside. Large or symptomatic hematomas require a craniotomy, the surgical opening of the skull. A surgeon then opens the dura, removes the blood clot with suction or irrigation, and identifies and controls sites of bleeding.[14][15] Postoperative complications include increased intracranial pressure, brain edema, new or recurrent bleeding, infection, and seizure. The injured vessels must be repaired.

Depending on the size and deterioration, age of the patient, and anaesthetic risk posed, some subdurals are inoperable; palliative management is the suitable treatment option in such cases.

See also

References

  1. ^ Herbert H Engelhard III, MD, PhD, FACS, Grant P Sinson, MD, George Timothy Reiter, MD, Paul L Penar, MD, FACS, Francisco Talavera, PharmD, PhD, Allen R Wyler, MD, Paolo Zamboni, MD, Allen R Wyler 2009. Subdural Hematoma Surgery . Medscape Reference, eMedicine.medscape.com retrieved on 7/21/2011.
  2. ^ UCLA Neurosurgery [1] retrieved on 7/21/2011.
  3. ^ a b c d e f g h Wagner AL. 2004. "Subdural hematoma." Emedicine.com. Retrieved on August 8, 2007.
  4. ^ Vinas F.C. and Pilitsis J. 2006. Penetrating Head Trauma. Emedicine.com.
  5. ^ Dawodu S. 2004. "Traumatic brain injury: Definition, epidemiology, pathophysiology" Emedicine.com. Retrieved on August 7, 2007.
  6. ^ a b c Downie A. 2001. "Tutorial: CT in head trauma". Retrieved on August 7, 2007.
  7. ^ a b Kushner D (1998). "Mild Traumatic Brain Injury: Toward Understanding Manifestations and Treatment". Archives of Internal Medicine 158 (15): 1617–1624. doi:10.1001/archinte.158.15.1617. PMID 9701095. http://archinte.highwire.org/cgi/content/full/158/15/1617.
  8. ^ a b c d University of Vermont College of Medicine. "Neuropathology: Trauma to the CNS." Accessed through web archive on August 8, 2007.
  9. ^ a b Graham DI and Gennareli TA. Chapter 5, "Pathology of brain damage after head injury" Cooper P and Golfinos G. 2000. Head Injury, 4th Ed. Morgan Hill, New York.
  10. ^ "Subdural hematoma : MedlinePlus Medical Encyclopedia". Nlm.nih.gov. 2012-06-28. http://www.nlm.nih.gov/medlineplus/ency/article/000713.htm. Retrieved 2012-07-27.
  11. ^ Sanders MJ and McKenna K. 2001. Mosby’s Paramedic Textbook, 2nd revised Ed. Chapter 22, "Head and facial trauma." Mosby.
  12. ^ Mori K, Yamamoto T, Horinaka N, Maeda M (2002). "Arachnoid cyst is a risk factor for chronic subdural hematoma in juveniles: twelve cases of chronic subdural hematoma associated with arachnoid cyst". J. Neurotrauma 19 (9): 1017–27. doi:10.1089/089771502760341938. PMID 12482115.
  13. ^ McCaffrey P. 2001. "The neuroscience on the web series: CMSD 336 neuropathologies of language and cognition." California State University, Chico. Retrieved on August 7, 2007.
  14. ^ Koivisto T, Jääskeläinen JE (2009). "Chronic subdural haematoma—to drain or not to drain?". Lancet 374 (9695): 1040–1041. doi:10.1016/S0140-6736(09)61682-2.
  15. ^ Santarius T, Kirkpatrick PJ, Dharmendra G, et al. (2009). "Use of drains versus no drains after burr-hole evacuation of chronic subdural haematoma: a randomised controlled trial". Lancet 374 (9695): 1067–1073. doi:10.1016/S0140-6736(09)61115-6.

External links