Intracranial hematoma (ICH) occurs when a blood vessel ruptures within a person’s brain or between the skull and the brain, causing increased intracranial pressure (ICP) as the collection of blood compresses brain tissue. This can occur when an external force causes the brain to slide forcefully against the inner wall of the skull and become injured. ICH can be categorized according to which layer of the brain the rupture occurs. Diagnosing ICH can be difficult as symptoms can vary in type and severity from milder symptoms such as headaches, vomiting, and dizziness, to more severe symptoms such as loss of consciousness, seizures, and weakness in the limbs on one side of the body. Diagnosis can further be complicated by a complete absence of symptoms in the period immediately following the trauma, termed the lucid interval, with symptoms appearing several weeks later. Imaging techniques such as CT scans and MRI scans are commonly used to define the position and size of the hematoma. Depending on the size of the hematoma, surgery may be required in the acute response to remove the pooled blood. The prolonged chronic stage of treatment may require anticonvulsant medications to control post-traumatic seizures. If ICH is left untreated, possible medical complications can result including herniation, cerebral edema, cerebral ischemia, and cerebral infarction.[1] The mortality rate of patients with ICH is high and as a result, ICH has been the focus of growing medical research into the short-term and long-term implications of increased ICP on the structures and functions of the brain.


1. Etiology and Classification

Intracranial hematoma occurs when trauma to the head causes a blood vessel within the brain to rupture (also called a brain hemorrhage) and blood to accumulate. This can occur when the brain's cerebrospinal fluid (CSF) is unable to absorb the force of a traumatic blow. Intracranial hematoma is classified compartmentally according to the anatomical location within the brain the hemorrhage occurs. Subdural hematoma occurs between the arachnoid and the dura matter caused by bleeding from the bridging veins which cross the subdural space.[2] Epidural hematoma occurs between the outermost surface of the dura matter and the skull caused by bleeding from an artery or large vein, often when a skull fracture tears the blood vessel.[3] And intraparenchymal hematoma occurs when blood pools within the brain itself resulting from cerebral contusion from a severe head injury. Intraparenchymal hematoma can also result from non-traumatic causes such as blood vessel disorders, long-term hypertension, and central nervous system infections.[4] Subdural hematoma is further categorized into acute (symptoms appearing immediately), subacute (symptoms take days or weeks to appear), and chronic (slowest progression of symptoms, usually weeks to appear)[5] . Multi compartmental hemtomas are not uncommon (see Figure 1).[6] Subdural hematoma is the most frequently treated intracranial hematoma.

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Figure 1: Multicompartmental hematoma. The white and black arrows show the different hematoma locations.

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Figure 2: Cross section showing epidural and subdural hematoma. (Taken from: http://www.merckmanuals.com/home/injuries_and_poisoning/head_injuries/intracranial_hematomas.html)

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Figure 3: CT scan of intraparenchymal hematoma indicated by the arrow. (Taken from: Naidech, A. Concise Clinical Review: Intracranial Hemorrhage. American Journal of Respiratory and Critical Care Medicine. 184, 998-1006 (2011).)


2. Clinical Assessment and Diagnosis

Diagnostic investigation seeks to 1) confirm clinical suspicion of an intracranial abnormality such as hematoma, 2) define the type, size, location, and severity of the hematoma, 3) consider evidenced based etiology and clinical differential diagnosis for the hematoma, 4) consider possible surgical and non-surgical treatments to reduce intracranial pressure and removal of hematoma, and 5) consider plans for long-term follow up.[7]

2.1 Clinical Features

Symptoms of ICH are variable and may appear immediately following a trauma or several weeks later following the lucid interval. Over time the accumulation of blood increases pressure on the brain resulting in some or all of the following symptoms: dizziness, confusion, vomiting, increased headache, unequal pupil size, increased blood pressure, weak limbs on one side of the body, drowsiness, and progressive loss of consciousness. At higher levels of intracranial pressure, other signs and symptoms become apparent such as: lethargy, seizures, and unconsciousness[8] . Headaches of variable intensity are the most prevalent clinical feature to occur. Studies have shown seizures to occur in approximately 10% of all patients.[9] Seizures will likely occur at onset of hemorrhaging or within the first 24 hours. Patients with large hematomas may present in coma resulting from elevated intracranial pressure and decreased cerebral perfusion (blood flow to brain), or due to distortion of diencephalic or brainstem structures. The severity and occurrence of these symptoms will depend on the size and location of the hematoma.

2.2 Severity

Assessing severity of neurological trauma is significant for guiding diagnostic studies, guiding resuscitation, and planning surigical and non-surgical intervention. Examinations are generally performed off sedation.[10]

2.2.1 Scoring System

Glasgow Coma Scale: The Glasgow Coma Scale (GCS) is the standard scale for assessing level of consciousness. There are 3 axes: eye opening, motor response, and verbal response. The best possible score on the GCS is a 15 (eyes open spontaneously, oriented, and follows commands) and the worst possible score is a 3 (no eye opening, no motor response, and no verbal response).[11]

2.3 Imaging Techniques

Imaging technologies are required to define the size and location of the hematoma within the skull. Only once the qualitative (type) and quantitative (volume, density, location) features of the hemotoma are determined can a plan for treatment be pursued. Liao et al, suggest an ideal system for diagnosing intracranial hematoma should be capable of using minimally processed initial diagnostic images to produce qualitative and quantitative information of the hematoma readily available for clinical use. Such a system should provide decision support without increasing the burden on physicians by keeping human assistance to a minimum. In this way, errors caused by inexperienced users will be reduced.[12]

2.3.1Traditional Neuro-imaging Techniques

Computerized tomography (CT) scan is the most commonly used imaging scan to diagnose intracranial hematoma and is used to determine if emergency surgery is required. CT scans use X-rays to determine tissue density. Acute intracranial hematoma is readily diagnosed on CT images appearing as hyperdense regions or regions with gray levels higher than normal brain tissue.[13] Magnetic resonance imaging (MRI) scans are less commonly used than CT scans as the procedure is longer and the technology is not as widely available. MRI scans rely on magnets and radio waves to produce a computerized image of the hematoma. MRI is capable of detecting hyperacute intracerebral hemorrhage and microhemorrhages (see Figure 4).[14] MRI as well as cerebral angiography can be used to detect secondary causes of ICH such as aneurisms, arteriovenous malformations, dural venous thromboses, and vasculitis. Cranial ultrasound is used as the first imaging modality for newborns suspected of hematoma resulting from head injury due to its instrument transportability, low cost of operation, and absence of exposure to radiation.[15]
Screen_shot_2012-04-02_at_3.50.18_AM.png
Figure 4: Microhemorrhage is shown in the MRI scan (left) but not in the CT scan (right).

2.3.2 Novel Neuro-imaging Techniques

Liao et al, describe a novel method for detecting ICH that can measure midline shift, hematoma shape, and size in a more robust and automated fashion than diagnoses only involving CT scans. The procedure begins using single brain CT slices to differentiate the skull from soft tissue regions such as the brain. Intracranial regions are then determined using a method involving connectivity across CT slices, starting with the vertex of the skull (see Figure 5). Adaptive threshold density rules are used to pinpoint hematoma locations. For example, large hematomas that cause brain deformations can be pinpointed since they are always larger than 1 cm in thickness. Threshold densities are used to differentiate hematoma types, between subdural, epidural, and intraparenchymal. Similar thresholding procedures have been used to differentiate cerebral spinal fluid (CSF) from white and grey matter. The final step involves applying a multiresolutionary binary set method onto the candidate hematoma voxels (Volumetric Picture Element) until the original resolution is achieved with the results quantitatively evaluated by a human expert.[16]
Screen_shot_2012-04-02_at_3.56.02_AM.png
Figure 5: An example of connecting consecutive hematoma regions from the CT data set in a case of subdural hematoma (SDH). The hematoma regions are shown in black. The key hematoma slice is labeled with a thick square and other hematoma slices are labeled with thin squares. The type of the hematoma is labeled at the left upper part of each slice, and the final diagnosis derived from the voting process is displayed after the last slice.


3. Treatment

Initial evaluation begins with obtaining a thorough patient history of proceeding or initiating events and a thorough general physical and neurologic examination. Previous or current drug use, hemorrhages, or known structural lesions can provide important information about a potential source of hemorrhage.[17] Diringer et al, suggest that aggressive medical management and specialist care show statistical significance in improving the overall outcome in patients with ICH. Trials addressing a single severity factor for positive clinical outcome have been unsuccessful, suggesting that a single treatment approach might accomplish its physiological goal but be insufficient to produce clinical benefit, thus calling for a multimodal therapy addressing several different severity factors.[18]

3.1 Intracranial Pressure (ICP) Monitoring

ICP is affected by cranial size, volume of blood and CSF in the head, and the constriction or dilation of blood vessels in the brain. Patients with elevated ICP are at risk of developing cerebral edema and subsequent neurological dysfunction and deterioration. The placement of a device into the skull to monitor intracranial pressure will depend on the nature, severity, and location of the injury. ICP can be monitored using ICP bolts, also called a subdural screw. The device is inserted through a hole drilled in the skull and uses a fiber-optic wire placed directly on the dura matter to measure changes in brain tension. This occurs under consistent neurological examination in the intensive care unit. Monitoring of brain temperature and brain oxygen also accompany ICP monitoring.[19]
Screen_shot_2012-04-02_at_4.30.45_AM.png
Figure 6: Cerebral Compliance Curve. Initially, volume added to the cranial vault results in no increase in intracranial pressure (ICP) due to compensatory mechanisms. However, once these mechanisms are exhausted, ICP increases rapidly as volume is added. (Taken from: Vanderheyden, B., Buck, B. Management of Elevated Intracranial Pressue. Journal of Pharmacy Practice. 15 (2), 167-185 (2002).)

3.2 Surgical Evacuation

Physicians determined whether to surgically remove an intracranial hematoma depending on the type, volume, and thickness of hematoma, as well as the degree of compression on the brain. There is a general consensus that surgical evacuation is required for hematomas 3 cm in diameter and larger. An epidural hematoma larger than 30 cm cubed will require surgical evacuation regardless of other clinical features of the patient.[20] Surgical evacuation is generally required to prevent expansion of the hematoma and increases in local ICP, decrease harmful mass-effects on brain structures, and block the release of neurotoxic products from the pooled fluid, and thus prevent harmful pathological processes from occuring.[21]

3.2.1 Craniotomy

Craniotomy is a surgical procedure that involves making a surgical cut through the scalp in the location of the hematoma to remove the bone flap. This is performed using a high-speed drill to create a pattern of holes through the cranium and a fine wire saw to connect the holes until a segment of bone can be removed, thus giving the surgeon access to the inside of the skull to remove or suction out the hematoma (see Video 1).[22] Despite being a common surgical procedure to treat ICH, craniotomy can result in certain complications such as neural damage and recurrence of bleeding in deep lesions. A trial involving 1033 patients randomly assigned to either early surgery or non-invasive treatment showed early surgery carried no significant benefit compared with initial conservative treatment: 24% versus 26% showed good recovery or moderate disability after treatment.[23]


( Video 1: Surgical procedure for removal of epidural hematoma. The hematoma is seen being removed after gaining access to inside the skull.)

3.2.2 Minimally Invasive ICH Surgical Treatments

Although not widely accepted as standard forms of therapy, minimally invasive procedures are increasingly used to reduce neural damage and risk of recurrent bleeding associated with open craniotomy. Stereotactic and endoscopic evacuation use precisely positioned instruments within the brain during surgery and require only a small incision be made and a hole less than half an inch be drilled into the skull.[24] The use of thrombolytic drugs is another form of therapy also used to minimize invasive intervention. Such drugs are used to break up or dissolve blood clots within the pooled intracranial blood.[25]
One study has shown that stereotactic evacuation was associated with lower mortality and better functional recovery than surgical procedures in patients with neurological Grade 3 hemorrhage (mildly reduced consciousness).[26] The ASA Stroke Council 88 and EUSI Guidelines do not recommend surgical evacuation of ICH by craniotomy within 96 hours of the initial trauma. These guidelines state that removal within 12 hours with minimally-invasive methods has the most evidence for beneficial effect and could even be considered for deep hemorrhages.[27]

3.3 Anticonvulsant Medications

Anticonvulsant medications are prescribed to prevent or control post-traumatic seizures. They are taken up to a year after the trauma. 8% of patients with untreated ICH have clinical seizures within 1 month of the initial trauma, associated with hematoma enlargement.[28] Seizures are associated with neurological worsening, an increase in midline shift, and poorer outcomes. Observational studies advise a 30-day course of prophylactic anticonvulsants is recommended in patients with lobar hemorrhage and those who develop seizures.[29] Patients who have a seizure more than 2 weeks after ICH onset are at greater risk of recurrent seizures than those who do not, and may require long-term prophylactic treatment with anticonvulsants.[30]

4. Possible Complications

If left untreated, certain complications can result from increased intracranial pressure. These include brain herniation (movement of brain structures, CSF, and blood vessels from their usual position in the skull), cerebral edema (accumulation of water in the intracellular and extracellular spaces of the brain), cerebral ischemia (inadequate oxygen and blood flow to brain tissue) and subsequent cerebral infarction (neurological deterioration).
Studies have shown that areas surrounding an ICH have decreased blood flow close to ischemic levels.[31] Patients with large hematomas showed increased cerebral oxygen extraction, suggestive of early ischemia.[32] This is further supported by numerous cerebral blood flow (CBF) studies showing decreased perfusion in the areas surrounding a cerebral hemorrhage.[33]
Observational studies have shown that a large percentage of patients will develop hematoma expansion. 26% of patients evaluated within the first 3 hours after the initial trauma showed ICH expansion.[34] ICH volume can increase by as much as 40% and is likely to result in increased ICP and low cerebral perfusion pressure and subsequent neurologic deterioration.[35] One study has suggested that poorly controlled diabetes mellitus and systolic blood pressure greater than 200 mm Hg are major predictors of hematoma volume expansion.[36]
Neurological deterioration can also result from cerebral edema, supported by evidence in which patients with a larger amount of cerebral edema show worse clinical outcomes.[37] Peak edema generally occurs 3 to 7 days after the initial hemorrhage and correlates with lysis of red blood cells. Hemoglobin and its degradation products have been implicated in direct and indirect neural toxicity.[38]

See Also

Epo & TBI
Diffure Axonal Injury
Shaken Baby Syndrome
Concussions
Cerebral Aneurysm
Rupture
Pathogenesis and Treatment
Spinal Cord Injury (SCI)

External Links

NYTimes: Intracerebral Hemorrhage
Medscape: Intracranial Hemorrhage

References

1.Vanderheyden, B. Management of elevated intracranial pressure. Journal of Pharmacy Practice, (2002) 15, 167-185
2. Maiese, Kenneth. "Intracranial Hematomas." The Merck Manual, Jan. 2011. Web. http://www.merckmanuals.com/home/injuries_and_poisoning/head_injuries/intracranial_hematomas.html
3. See above.
4. See above.
5. See above
6. Naidech, A. Concise Clinical Review: Intracranial Hemorrhage. American Journal of Respiratory and Critical Care Medicine. 184, 998-1006 (2011).
7. Gupta, N. Surya, Kechli, Amer. Intracranial Hemorrhage in Term Newborns: Management and Outcomes. Pediatric Neurology. 40 (1), 1-12 (2009)
8. Mayo Clinic Staff. "Intracranial Hematoma." Mayo Clinic, 25 June. 2011. Web. http://www.mayoclinic.com/health/intracranial-hematoma/DS00330
9. Faught, E. Seizures after primary intracerebral hemorrhage Neurology. 39, 1089 (1989).
10. Naidech, A. Concise Clinical Review: Intracranial Hemorrhage. American Journal of Respiratory and Critical Care Medicine. 184, 998-1006 (2011).
11. Wijdicks, E., Bamlet, R., Maramattom V., Manno, E., McClelland, L. Validation of a new coma scale: the FOUR score. Ann Neurol. 58, 585–593 (2005).
12. 
Liao, C., Furen, X., Jau-Min, W., I-Jen, C. Computer-aided diagnosis of intracranial hematoma with brain deformation on computed tomography. Computerized Medical Imaging and Graphics. 34 (7), 563-571 (2010).
13. See above
14. Goldstein, J. Contrast extravasation on CT angiography predicts hematoma expansion in intracerebral hemorrhage. Neurology. 68, 889 (2007).
15. Gupta, N. Surya, Kechli, Amer. Intracranial Hemorrhage in Term Newborns: Management and Outcomes. Pediatric Neurology. 40 (1), 1-12 (2009)
16. Liao, C., Furen, X., Jau-Min, W., I-Jen, C. Computer-aided diagnosis of intracranial hematoma with brain deformation on computed tomography. Computerized Medical Imaging and Graphics. 34 (7), 563-571 (2010).
17. Manno, E., Atkinson, J., Fulgham, J., Wijdicks, E. Emerging Medical and Surgical Management Strategies in the Evaluation and Treatment of Intracerebral Hemorrhage. Mayo Clinic Proceedings. 80 (3), 420-433 (2005).
18. Diringer, M. Admission to a neurologic/neurosurgical intensive care unit is associated with reduced mortality rate after intracerebral hemorrhage Crit Care Med. 29, 635 (2011)
19. Lang E., Chesnut R. Intracranial pressure and cerebral perfusion pressure in severe head injury. New Horizons. 3, 400-409, (1995)


20. Rabinstein, A. Emergency craniotomy in patients worsening due to expanded cerebral hematoma: to what purpose? Neurology. 58, 1367 (2002)
21. Barnett, H., Livingstone, C. Intracerebral hemorrhage: surgical considerations, Stroke: Pathophysiology, Diagnosis, and Management. (1998)
22. Warnick, R.. "Craniotomy." Mayfield Clinic, Feb. 2010. Web. http://www.mayfieldclinic.com/PE-Craniotomy.htm
23. Mendelow, A. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH): a randomised trial. Lancet. 365, 387 (2010)
24. Broderick, J. The STICH trial: what does it tell us and where do we go from here? Stroke. 36, 1619 (2010)
25. Yamamoto, T. Endoscopic hematoma evacuation for hypertensive cerebellar hemorrhage. Minim Invasive Neurosurg. 49, 173 (2006)
26. See above.
27. Steiner, T. Recommendations for the management of intracranial haemorrhage—part I: spontaneous intracerebral haemorrhage. Cerebrovasc Dis. 22, 294 (2006)
28. Passero, S. Seizures after spontaneous supratentorial intracerebral hemorrhage. Epilepsia. 43, 1175 (2002)
29. See above.
30. See above.
31. Bullock, R. Intracerebral hemorrhage in a primate model: effect on regional cerebral blood flow. Surg Neurol. 29, 101 (1988)
32. Helden, A. Monitoring of jugular venous oxygen saturation in comatose patients with subarachnoid haemorrhage and intracerebral haematomas. Acta Neurochir Suppl (Wien). 59, 102 (1993)
33. See above.
34. Brott, T. Early hemorrhage growth in patients with intracerebral hemorrhage. Stroke. 28, 1 (1997)
35. See above.
36. See above.
37. Kamel H, Navi B, Nakagawa K, Hemphill JC III, Ko NU. Hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: a meta-analysis of randomized clinical trials. Crit Care Med. 39, 554–559 (2011).
38. See above.
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