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Subdural hematoma

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: , Fahimeh Shojaei, M.D.

Synonyms and keywords: Subdural haematoma

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

A subdural hematoma (SDH) is a form of traumatic brain injury in which blood gathers between the dura (the outer protective covering of the brain) and the arachnoid (the middle layer of the meninges). Subdural hemorrhages may cause an increase in intracranial pressure (ICP), which can cause compression of and damage to delicate brain tissue (also known as a mass effect). Acute subdural hematoma (ASDH) has a high mortality rate and is a severe medical emergency.

Causes

Subdural hematomas are most often caused by head injury, when fast 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.[1][2] It is also commonly seen in the elderly and in alcoholics, who have evidence of brain 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.

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. Infants, too, have larger subdural spaces and are more predisposed to subdural bleeds than are young adults. 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.[3] Other risk factors for subdural bleeds include taking blood thinners (anticoagulants), long-term alcohol abuse, and dementia.

Treatment

Medical Therapy

Medicines used to treat a subdural hematoma depend on the type of subdural hematoma, the severity of symptoms, and how much brain damage has occurred. Diuretics and corticosteroids may be used to reduce swelling. Anticonvulsion medications, such as phenytoin, may be used to control or prevent seizures.

Surgery

Treatment of a subdural hematoma depends on its size and rate of growth. Small subdural hematomas can be managed by careful monitoring until the body heals itself. 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. Postoperative complications include increased intracranial pressure, brain edema, new or recurrent bleeding, infection, and seizure.

Primary Prevention

Always use safety equipment at work and play to reduce your risk of a head injury. For example, use hard hats, bicycle or motorcycle helmets, and seat belts. Older individuals should be particularly careful to avoid falls.

References

  1. University of Vermont College of Medicine. “Neuropathology: Trauma to the CNS.” Accessed through web archive on August 8, 2007.
  2. Wagner AL. 2004. “Subdural hematoma.” Emedicine.com. Retrieved on August 8, 2007.
  3. 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.

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Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

Overview

The first case of subdural hematoma was discovered by Johan J.Wpfer, in 1657. Trephination is the process of creating a hole in the skull. The evidence of these procedure is found all over the world starting from late paleolithic period also known as late stone age (50,000 years ago).

Historical Perspective

Discovery

  • The first case of subdural hematoma was discovered by Johan J.Wpfer, in 1657.[1][2][3][4][5]


 
 
 
 
 
 
 
 
1657
Johan J.Wepfer
Reported first case of subdural hematoma
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
1857
Virchow
Described pachymeningitis hemorrhage as a result of dura’s inflammation leading to fibrin and capillary prolifration
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
1925
Putnam and chushing
First described chronic subdural hematoma
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
1972
Watanabe et al.
First described animal models of chronic subdural hematoma
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
1974
Apfelbaumet al
Described the fact that CSF is not necessarily part of chrnoic subdural hematoma membrane formation
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
1975
Sato and suzuki
First described chronic subdural hematoma capsular structure
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
1976
Labadie and Glover
First decribed the effect of dexamethasone injection on inhibiting membrane formation
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

Landmark Events in the Development of Treatment Strategies

  • Trephination is the process of creating a hole in the skull. [6][7][8]
  • The evidence of these procedure is found all over the world starting from late paleolithic period also known as late stone age (50,000 years ago).
  • Until 19th century scientists used to think that these holes were made by accident or weapons, but further studies showed that they were actually surgical procedure.
  • The number of holes were different in every person and evidence of healing from edge of the holes was shown a 70% cure rate with limited infection or any complication.
  • In old stone age the old people with brain atrophy would developed chronic subdural hematoma.
  • One of the symptoms of subdural hematoma is ataxia.
  • These people were more susceptible to fall and heading their head into a sharp object (natural trephination).
  • Old stone age people observed a dark liquid comes out of the brain from puncture wound of these people, and the symptoms of the patients starts to go away.
  • It created the idea of “demonic brain” and established the trephination procedure.
Source:Image Courtesy by Kyeong-Seok Lee, MD
Source:Image Courtesy by Miguel A. Faria, Jr.
Source:Image Courtesy by Miguel A. Faria

Famous Cases

The following are a few famous cases of subdural hematoma:

  • Former fox news president Roger Ailes
  • Ann B. Davis’s the center square of the Brady Bunch tic-tac-toe grid
  • Alex Trebek the Canadian-American television personality

References

  1. D’Errico AP, German WJ (October 1930). “Chronic Subdural Hematoma”. Yale J Biol Med. 3 (1): 11–20. PMC 2606347. PMID 21433469.
  2. Putnam, Tracy Jackson (1925). “CHRONIC SUBDURAL HEMATOMA”. Archives of Surgery. 11 (3): 329. doi:10.1001/archsurg.1925.01120150002001. ISSN 0272-5533.
  3. Watanabe, Satoru; Shimada, Hironobu; Ishii, Shozo (1972). “Production of clinical form of chronic subdural hematoma in experimental animals”. Journal of Neurosurgery. 37 (5): 552–561. doi:10.3171/jns.1972.37.5.0552. ISSN 0022-3085.
  4. Apfelbaum, Ronald I.; Guthkelch, A. N.; Shulman, Kenneth (1974). “Experimental production of subdural hematomas”. Journal of Neurosurgery. 40 (3): 336–346. doi:10.3171/jns.1974.40.3.0336. ISSN 0022-3085.
  5. Sato, So; Suzuki, Jiro (1975). “Ultrastructural observations of the capsule of chronic subdural hematoma in various clinical stages”. Journal of Neurosurgery. 43 (5): 569–578. doi:10.3171/jns.1975.43.5.0569. ISSN 0022-3085.
  6. Campillo D (1984). “Neurosurgical pathology in prehistory”. Acta Neurochir (Wien). 70 (3–4): 275–90. PMID 6369893.
  7. Clower, William T.; Finger, Stanley (2001). “Discovering Trepanation: The Contribution of Paul Broca”. Neurosurgery. 49 (6): 1417–1426. doi:10.1097/00006123-200112000-00021. ISSN 0148-396X.
  8. Gross, Charles G. (2016). “A Hole in the Head”. The Neuroscientist. 5 (4): 263–269. doi:10.1177/107385849900500415. ISSN 1073-8584.

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Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

Overview

There are 3 classification system for subdural hematoma. Subdural hematoma may be classified according to symptom onset and duration into 3 subtypes including acute, subacute, and chronic, according to midline shift and thickness into 4 subtypes, and based on imaging findings into 6 subtypes.

Classification

There are 3 classification system for subdural hematoma:[1][2]

  • Subdural hematoma may be classified according to symptom onset and duration into 3 subtypes:
  • Subdural hematoma may be classified according to mid-line shift and thickness into 4 sub-types:
    • Type A: Thickness ≤ 1cm, midline shift ≤ 5 cm
    • Type B: Thickness > 1cm, midline shift ≤ 5 cm
    • Type C: Thickness > 1cm, midline shift > 5 cm
    • Type D: Thickness ≤ 1cm, midline shift > 5 cm
  • Subdural hematoma may be classified according to imaging findings into 6 subtypes:
    • Type 1: Hyperdense lesion, relatively homogeneous (describes acute subdural hemorrhages)
    • Type 2: Isodense lesion, relatively homogeneous (describes subacute hemorrhages)
    • Type 3: Hypodense, relatively homogeneous (describes chronic hemorrhages)
    • Type 4: Isodense to hypodense, relatively heterogeneous (describes recent rebleeding)
    • Type 5: Hypodense in its liquefied component, relatively heterogeneous; internal septations and loculations (higher risk for recurrence after surgical treatment)
    • Type 6: Calcified hyperdense, relatively homogeneous (describes subdural hemorrhage with calcified component)

References

  1. Alves JL, Santiago JG, Costa G, Mota Pinto A (September 2016). “A Standardized Classification for Subdural Hematomas- I”. Am J Forensic Med Pathol. 37 (3): 174–8. doi:10.1097/PAF.0000000000000255. PMID 27428027.
  2. Salahuddin T (February 1996). “Management of chronic subdural haematoma–a review of 23 cases”. J Pak Med Assoc. 46 (2): 32–3. PMID 8683845.


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Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: , Fahimeh Shojaei, M.D.

Overview

It is understood that subdural hematoma is the result of rupture in bridging veins (mostly due to head trauma) and hemorrhage between dura matter and arachnoid, leading to subdural hematoma, or rupture of small cortical atreries and hemorrhage into the space between dura matter and arachnoid, leading to subdural hematoma or intracranial hypotension (mostly due to lumbar punctue) and traction of bridging veins which leads to subdural hematoma. Genes involved in the pathogenesis of subdural hematoma include ADPKD, osteogenesis imperfecta, fabry’s disease, mucopolysaccharidosis IIIB, and type B Niemann–Pick disease. On gross pathology, crescentic shape blood in the subdural potential space are characteristic findings of subdural hematoma. On microscopic histopathological analysis, blood in subdural space is characteristic findings of subdural hematoma.

Pathophysiology

Physiology

The normal physiology of bridging veins can be understood as follows:[1]

  • In embryonic period, there is lots of anastomosis between brain and dura matter venous drainage.
  • After 12 weeks of gestation these anastomosis will disappear and what is left from them create bridging veins.
  • These vein s will drain venous blood from underlying brain tissue to the dural sinuses.
Bridging vein Source:Image Courtesy by Steven C. Gabaeff, MD


Pathogenesis

  • It is understood that subdural hematoma is the result of:
    • Rupture in bridging veins (mostly due to head trauma) and hemorrhage between dura matter and arachnoid, leading to subdural hematoma.
    • Rupture of small cortical atreries and hemorrhage into the space between dura matter and arachnoid, leading to subdural hematoma.
    • Intracranial hypotension (mostly due to lumbar punctue) and traction of bridging veins which leads to subdural hematoma
  • Subdural hematomas as a result of arterial rupture accounts for 20% of SDH cases and are mostly in temporoparietal region.
  • Since most of the SDH cases are due to vein rupture, the bleeding will stop on its own as a result of a clot formation or increased intracranial pressure.
https://commons.wikimedia.org/wiki/File:Types_of_Hematoma.jpg

Genetics

Genes involved in the pathogenesis of subdural hematoma include:

  • ADPKD[2][3][4][5][6]
  • Osteogenesis imperfecta
  • Fabry’s disease
  • Mucopolysaccharidosis IIIB
  • Type B Niemann–Pick disease

Associated Conditions

Conditions associated with subdural hematoma include:[7][8][9][10][11][12][13][14][15]

  • Elderly
  • Anticoagulant use
  • Alcoholics
  • Seizure
  • CSF shunt
  • Arachnoid cyst
  • Meningioma
  • Cocaine
  • Dural metastase
  • Roller coaster

Gross Pathology

On gross pathology, crescentic shape blood in the subdural potential space are characteristic findings of subdural hematoma.

Microscopic Pathology

On microscopic histopathological analysis, blood in subdural space is characteristic findings of subdural hematoma.

https://librepathology.org/wiki/File:Subdural_hematoma_-_very_low_mag.jpg
https://librepathology.org/wiki/File:Subdural_hematoma_-_intermed_low_mag.jpg


References

  1. Famaey, Nele; Ying Cui, Zhao; Umuhire Musigazi, Grace; Ivens, Jan; Depreitere, Bart; Verbeken, Erik; Vander Sloten, Jos (2015). “Structural and mechanical characterisation of bridging veins: A review”. Journal of the Mechanical Behavior of Biomedical Materials. 41: 222–240. doi:10.1016/j.jmbbm.2014.06.009. ISSN 1751-6161.
  2. McGovern, Margaret M.; Lippa, Natalie; Bagiella, Emilia; Schuchman, Edward H.; Desnick, Robert J.; Wasserstein, Melissa P. (2013). “Morbidity and mortality in type B Niemann–Pick disease”. Genetics in Medicine. 15 (8): 618–623. doi:10.1038/gim.2013.4. ISSN 1098-3600.
  3. Pirson, Yves (2010). “Extrarenal Manifestations of Autosomal Dominant Polycystic Kidney Disease”. Advances in Chronic Kidney Disease. 17 (2): 173–180. doi:10.1053/j.ackd.2010.01.003. ISSN 1548-5595.
  4. Mitsias, Panyiotis; Levine, Steven R. (1996). “Cerebrovascular complications of Fabry’s disease”. Annals of Neurology. 40 (1): 8–17. doi:10.1002/ana.410400105. ISSN 0364-5134.
  5. Groninger, Anja; Schaper, Jörg; Messing-Juenger, Martina; Mayatepek, Ertan; Rosenbaum, Thorsten (2005). “Subdural hematoma as clinical presentation of osteogenesis imperfecta”. Pediatric Neurology. 32 (2): 140–142. doi:10.1016/j.pediatrneurol.2004.07.011. ISSN 0887-8994.
  6. Aydin M, Akarsu S, Kabakus N, Akpolat N (May 2006). “Mucopolysaccharidosis IIIB, cerebral vasculopathy and recurrent subdural hematoma”. Indian Pediatr. 43 (5): 437–40. PMID 16735769.
  7. Okuno S, Touho H, Ohnishi H, Karasawa J (August 1999). “Falx meningioma presenting as acute subdural hematoma: case report”. Surg Neurol. 52 (2): 180–4. PMID 10447287.
  8. Koerbel A, Ernemann U, Freudenstein D (July 2005). “Acute subdural haematoma without subarachnoid haemorrhage caused by rupture of an internal carotid artery bifurcation aneurysm: case report and review of literature”. Br J Radiol. 78 (931): 646–50. doi:10.1259/bjr/60601877. PMID 15961850.
  9. Fukutake, T.; Mine, S.; Yamakami, I.; Yamaura, A.; Hattori, T. (2000). “Roller coaster headache and subdural hematoma”. Neurology. 54 (1): 264–264. doi:10.1212/WNL.54.1.264. ISSN 0028-3878.
  10. Keller, Thomas M.; Chappell, E.Thomas (1997). “Spontaneous acute subdural hematoma precipitated by cocaine abuse: Case report”. Surgical Neurology. 47 (1): 12–14. doi:10.1016/S0090-3019(96)00380-1. ISSN 0090-3019.
  11. Bergmann M, Puskas Z, Kuchelmeister K (1992). “Subdural hematoma due to dural metastasis: case report and review of the literature”. Clin Neurol Neurosurg. 94 (3): 235–40. PMID 1327614.
  12. Doherty DL (July 1988). “Posttraumatic cerebral atrophy as a risk factor for delayed acute subdural hemorrhage”. Arch Phys Med Rehabil. 69 (7): 542–4. PMID 3389997.
  13. Zwimpfer, Thomas J.; Brown, Jennifer; Sullivan, Irene; Moulton, Richard J. (1997). “Head injuries due to falls caused by seizures: a group at high risk for traumatic intracranial hematomas”. Journal of Neurosurgery. 86 (3): 433–437. doi:10.3171/jns.1997.86.3.0433. ISSN 0022-3085.
  14. Hylek, Elaine M. (1994). “Risk Factors for Intracranial Hemorrhage in Outpatients Taking Warfarin”. Annals of Internal Medicine. 120 (11): 897. doi:10.7326/0003-4819-120-11-199406010-00001. ISSN 0003-4819.
  15. Chen, Joseph C.T.; Levy, Michael L. (2000). “Causes, Epidemiology, and Risk Factors of Chronic Subdural Hematoma”. Neurosurgery Clinics of North America. 11 (3): 399–406. doi:10.1016/S1042-3680(18)30101-3. ISSN 1042-3680.

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Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

Overview

The most common causes of subdural hematoma include head trauma and neurosurgical procedures.

Causes

Life-threatening Causes

  • Head trauma
  • Aneurysmal rupture
  • Meningioma

Common Causes

  • Head trauma
  • Neurosurgical procedures

Less Common Causes

  • Cocaine
  • Dural metastase
  • Roller coaster

Genetic Causes

  • ADPKD
  • Osteogenesis imperfecta
  • Fabry’s disease
  • Mucopolysaccharidosis IIIB
  • Type B Niemann–Pick disease

Causes by Organ System

Cardiovascular No underlying causes
Chemical/Poisoning No underlying causes
Dental No underlying causes
Dermatologic No underlying causes
Drug Side Effect Anticoagulants
Ear Nose Throat No underlying causes
Endocrine No underlying causes
Environmental No underlying causes
Gastroenterologic No underlying causes
Genetic
  • ADPKD
  • Osteogenesis imperfecta
  • Fabry’s disease
  • Mucopolysaccharidosis IIIB
  • Type B Niemann–Pick disease
Hematologic No underlying causes
Iatrogenic
  • Lumbar puncture
  • Ventriculostomy
  • Lumboperitoneal shunt placement
Infectious Disease No underlying causes
Musculoskeletal/Orthopedic Osteogenesis imperfecta
Neurologic Brain aneurysm
Nutritional/Metabolic
  • Fabry’s disease
  • Mucopolysaccharidosis IIIB
  • Type B Niemann–Pick disease
Obstetric/Gynecologic No underlying causes
Oncologic
  • Meningioma
  • Dural metastasis
Ophthalmologic No underlying causes
Overdose/Toxicity Cocain
Psychiatric No underlying causes
Pulmonary No underlying causes
Renal/Electrolyte ADPKD
Rheumatology/Immunology/Allergy No underlying causes
Sexual No underlying causes
Trauma head trauma
Urologic No underlying causes
Miscellaneous No underlying causes

    References

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    Differentiating Subdural Hematoma from other Diseases

    Overview

    Subdural hematoma must be differentiated from other disease that causes headache,seizures and loss of consciousness such as Meningitis, encephalitis, brain tumor, hemorrhagic stroke, neurosyphilis, migrain, hypertensive encephalopathy, wernicke’s encephalopathy, brain abscess, drug toxicity, conversion disorders, metabolic disturbance, multiple sclerosis, and seizure.

    Differential diagnosis

    Subdural hematoma must be differentiated from other disease that causes headache,seizures and loss of consciousness such as Meningitis, encephalitis, brain tumor, hemorrhagic stroke, neurosyphilis, migrain, hypertensive encephalopathy, wernicke’s encephalopathy, brain abscess, drug toxicity, conversion disorders, metabolic disturbance, multiple sclerosis, and seizure.

    Differentiating subdural hematoma from other diseases on the basis of headache,seizures and loss of consciousness.

    Diseases Symptoms Physical Examination Past medical history Diagnostic tests Other Findings
    Headache LOC Motor weakness Abnormal sensory Motor Deficit Sensory deficit Speech difficulty Gait abnormality Cranial nerves CT /MRI CSF Findings Gold standard test
    Subdural hemorrhage + + + + + + Trauma, fall + Xanthochromia[1] CT scan without contrast[2][3] Confusion, dizziness, nausea, vomiting
    Meningitis + + + History of fever and malaise Leukocytes,

    Protein

    ↓ Glucose

    CSF analysis[4] Fever, neck

    rigidity

    Encephalitis + + +/- +/- + +/- + History of fever and malaise + Leukocytes, ↓ Glucose CSF PCR Fever, seizures, focal neurologic abnormalities
    Brain tumor[5] + + + + + Weight loss, fatigue + Cancer cells[6] MRI Cachexia, gradual progression of symptoms
    Hemorrhagic stroke + + + + + + + + Hypertension + CT scan without contrast[2][3] Neck stiffness
    Neurosyphilis[7][8] + + + + + + STIs + Leukocytes and protein CSF VDRL-specifc

    CSF FTA-Ab -sensitive[9]

    Blindness, confusion, depression,

    Abnormal gait

    Complex or atypical migraine + + + + Family history of migraine Clinical assesment Presence of aura, nausea, vomiting
    Hypertensive encephalopathy + + + + Hypertension + Clinical assesment Delirium, cortical blindness, cerebral edema, seizure
    Wernicke’s encephalopathy + + + + + History of alcohal abuse Clinical assesment and lab findings Ophthalmoplegia, confusion
    CNS abscess + + + + + History of drug abuse, endocarditis, immunosupression + leukocytes, glucose and protien MRI is more sensitive and specific High grade fever, fatigue,nausea, vomiting
    Drug toxicity + + + + + Drug screen test Lithium, Sedatives, phenytoin, carbamazepine
    Conversion disorder + + + + + + + + History of emotional stress Diagnosis of exclusion Tremors, blindness, difficulty swallowing
    Metabolic disturbances (electrolyte imbalance, hypoglycemia) + + + + + + Hypoglycemia, hypo and hypernatremia, hypo and hyperkalemia Depends on the cause Confusion, seizure, palpitations, sweating, dizziness, hypoglycemia
    Multiple sclerosis exacerbation + + + + + + History of relapses and remissions + CSF IgG levels

    (monoclonal bands)

    Clinical assesment and MRI [10] Blurry vision, urinary incontinence, fatigue
    Seizure + + + + + Previous history of seizures Mass lesion Clinical assesment and EEG [11] Confusion, apathy, irritability,

    References

    1. Lee MC, Heaney LM, Jacobson RL, Klassen AC (1975). “Cerebrospinal fluid in cerebral hemorrhage and infarction”. Stroke. 6 (6): 638–41. PMID 1198628.
    2. 2.0 2.1 Birenbaum D, Bancroft LW, Felsberg GJ (2011). “Imaging in acute stroke”. West J Emerg Med. 12 (1): 67–76. PMC 3088377. PMID 21694755.
    3. 3.0 3.1 DeLaPaz RL, Wippold FJ, Cornelius RS, Amin-Hanjani S, Angtuaco EJ, Broderick DF; et al. (2011). “ACR Appropriateness Criteria® on cerebrovascular disease”. J Am Coll Radiol. 8 (8): 532–8. doi:10.1016/j.jacr.2011.05.010. PMID 21807345.
    4. Carbonnelle E (2009). “[Laboratory diagnosis of bacterial meningitis: usefulness of various tests for the determination of the etiological agent]”. Med Mal Infect. 39 (7–8): 581–605. doi:10.1016/j.medmal.2009.02.017. PMID 19398286.
    5. Morgenstern LB, Frankowski RF (1999). “Brain tumor masquerading as stroke”. J Neurooncol. 44 (1): 47–52. PMID 10582668.
    6. Weston CL, Glantz MJ, Connor JR (2011). “Detection of cancer cells in the cerebrospinal fluid: current methods and future directions”. Fluids Barriers CNS. 8 (1): 14. doi:10.1186/2045-8118-8-14. PMC 3059292. PMID 21371327.
    7. Liu LL, Zheng WH, Tong ML, Liu GL, Zhang HL, Fu ZG; et al. (2012). “Ischemic stroke as a primary symptom of neurosyphilis among HIV-negative emergency patients”. J Neurol Sci. 317 (1–2): 35–9. doi:10.1016/j.jns.2012.03.003. PMID 22482824.
    8. Berger JR, Dean D (2014). “Neurosyphilis”. Handb Clin Neurol. 121: 1461–72. doi:10.1016/B978-0-7020-4088-7.00098-5. PMID 24365430.
    9. Ho EL, Marra CM (2012). “Treponemal tests for neurosyphilis–less accurate than what we thought?”. Sex Transm Dis. 39 (4): 298–9. doi:10.1097/OLQ.0b013e31824ee574. PMC 3746559. PMID 22421697.
    10. Giang DW, Grow VM, Mooney C, Mushlin AI, Goodman AD, Mattson DH; et al. (1994). “Clinical diagnosis of multiple sclerosis. The impact of magnetic resonance imaging and ancillary testing. Rochester-Toronto Magnetic Resonance Study Group”. Arch Neurol. 51 (1): 61–6. PMID 8274111.
    11. Manford M (2001). “Assessment and investigation of possible epileptic seizures”. J Neurol Neurosurg Psychiatry. 70 Suppl 2: II3–8. PMC 1765557. PMID 11385043.

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    Epidemiology and Demographics

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

    Overview

    The incidence of subdural hematoma is approximately 14.7 per 100,000 individuals in USA. The case mortality rate of traumatic subdural hematoma is approximately 14%. Patients of all age groups may develop subdural hematoma. The incidence of subdural hematoma increases with age. There is no racial predilection to subdural hematoma. Men are more commonly affected by chronic subdural hematoma than female.

    Epidemiology and Demographics

    Incidence

    • The incidence of subdural hematoma is approximately 14.7 per 100,000 individuals in USA.[1]

    Case Mortality rate

    • The case mortality rate of traumatic subdural hematoma is approximately 14%.

    Age

    • Patients of all age groups may develop subdural hematoma.
    • The incidence of subdural hematoma increases with age.

    Race

    • There is no racial predilection to subdural hematoma.

    Gender

    • Men are more commonly affected by chronic subdural hematoma than female.[2]

    References

    1. Kalanithi P, Schubert RD, Lad SP, Harris OA, Boakye M (November 2011). “Hospital costs, incidence, and inhospital mortality rates of traumatic subdural hematoma in the United States”. J. Neurosurg. 115 (5): 1013–8. doi:10.3171/2011.6.JNS101989. PMID 21819196.
    2. Kanat A, Kayaci S, Yazar U, Kazdal H, Terzi Y (September 2010). “Chronic subdural hematoma in adults: why does it occur more often in males than females? Influence of patient’s sexual gender on occurrence”. J Neurosurg Sci. 54 (3): 99–103. PMID 21423076.

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    Risk Factors

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

    Overview

    Common risk factors in the development of subdural hematoma include elderly, anticoagulant use, alcohol use, Seisure, and any other disease with gait and balance abnormality.

    Risk Factors

    Common Risk Factors

    • Common risk factors in the development of subdural hematoma include:[1][2][3][4]
      • Elderly
      • Anticoagulant use
      • Patients who are at risk of falling such as:
        • Alcoholics
        • Seizure
        • Any disease with gait and balance abnormality

    Less Common Risk Factors

    • Less common risk factors in the development of subdural hematoma include:[5][6][7]
      • CSF shunt
      • Arachnoid cyst

    References

    1. Doherty DL (July 1988). “Posttraumatic cerebral atrophy as a risk factor for delayed acute subdural hemorrhage”. Arch Phys Med Rehabil. 69 (7): 542–4. PMID 3389997.
    2. Zwimpfer, Thomas J.; Brown, Jennifer; Sullivan, Irene; Moulton, Richard J. (1997). “Head injuries due to falls caused by seizures: a group at high risk for traumatic intracranial hematomas”. Journal of Neurosurgery. 86 (3): 433–437. doi:10.3171/jns.1997.86.3.0433. ISSN 0022-3085.
    3. Hylek, Elaine M. (1994). “Risk Factors for Intracranial Hemorrhage in Outpatients Taking Warfarin”. Annals of Internal Medicine. 120 (11): 897. doi:10.7326/0003-4819-120-11-199406010-00001. ISSN 0003-4819.
    4. Chen, Joseph C.T.; Levy, Michael L. (2000). “Causes, Epidemiology, and Risk Factors of Chronic Subdural Hematoma”. Neurosurgery Clinics of North America. 11 (3): 399–406. doi:10.1016/S1042-3680(18)30101-3. ISSN 1042-3680.
    5. Mori, Kentaro; Yamamoto, Takuji; Horinaka, Naoaki; Maeda, Minoru (2002). “Arachnoid Cyst Is a Risk Factor for Chronic Subdural Hematoma in Juveniles: Twelve Cases of Chronic Subdural Hematoma Associated with Arachnoid Cyst”. Journal of Neurotrauma. 19 (9): 1017–1027. doi:10.1089/089771502760341938. ISSN 0897-7151.
    6. Blount, Jeffrey P.; Campbell, John A.; Haines, Stephen J. (1993). “Complications in Ventricular Cerebrospinal Fluid Shunting”. Neurosurgery Clinics of North America. 4 (4): 633–656. doi:10.1016/S1042-3680(18)30556-4. ISSN 1042-3680.
    7. McCullough, David C.; Fox, John L. (1974). “Negative intracranial pressure hydrocephalus in adults with shunts and its relationship to the production of subdural hematoma”. Journal of Neurosurgery. 40 (3): 372–375. doi:10.3171/jns.1974.40.3.0372. ISSN 0022-3085.

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    Natural History, Complications and Prognosis


    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: , Fahimeh Shojaei, M.D.

    Overview

    If left untreated, 14% of patients with subdural hematoma may progress to serious complications including death. Common complications of subdural hematoma include memory loss, dizziness, headache, anxiety, difficulty concentrating, seizures, temporary or permanent weakness, numbness, difficulty speaking, brain herniation, coma, death. Depending on the extent, type, and locationat of hematoma at the time of diagnosis, the prognosis may vary.

    Natural History, Complications, and Prognosis

    Natural History

    • The symptoms of chronic subdural hematoma usually develop in the sixth and seventh decade of life.[1][2]
    • In acute subdural hematoma, the symptoms of SDH typically develop 24 hours after head injury.
    • In subacute subdural hematoma, the symptoms os SDH typically develop between 1 to 10 days after head trauma.
    • In chronic subdural hematoma, the symptoms of SDH typically develop weeks or months after head trauma
    • If left untreated, 14% of patients with subdural hematoma may progress to serious complications including death.

    Complications

    Common complications of subdural hematoma include:

    • Memory loss
    • Dizziness
    • Headache
    • Anxiety
    • Difficulty concentrating
    • Seizures
    • Temporary or permanent weakness
    • Numbness
    • Difficulty speaking
    • Brain herniation
    • Coma
    • Death

    Prognosis

    • Acute subdural hematoma prognosis is generally poor, and the case mortality rate of traumatic subdural hematoma is approximately 14%.
    • Acute subdural hematomas has high rates of death and injury.
    • Depending on the extent, type, and locationat of hematoma at the time of diagnosis, the prognosis may vary.
    • However, the prognosis is generally regarded as poor in acute subdural hematoma and good in chronic subdural hematoma.
    • Subacute and chronic subdural hematomas have better outcomes in most cases, with symptoms often going away after the blood collection is drained.
    • There is a high frequency of seizures following a subdural hematoma, even after drainage.
    • These seizures are usually well controlled with medication.
    • Seizures may occur at the time the hematoma forms, or up to months or years afterward.
    • A period of rehabilitation is sometimes needed to assist the person back to his or her usual level of functioning.

    References

    1. Kalanithi P, Schubert RD, Lad SP, Harris OA, Boakye M (November 2011). “Hospital costs, incidence, and inhospital mortality rates of traumatic subdural hematoma in the United States”. J. Neurosurg. 115 (5): 1013–8. doi:10.3171/2011.6.JNS101989. PMID 21819196.
    2. Kanat A, Kayaci S, Yazar U, Kazdal H, Terzi Y (September 2010). “Chronic subdural hematoma in adults: why does it occur more often in males than females? Influence of patient’s sexual gender on occurrence”. J Neurosurg Sci. 54 (3): 99–103. PMID 21423076.

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    Diagnosis

    Diagnosis

    History and Symptoms | Physical Examination | Laboratory Findings | CT | MRI | Other Imaging Findings | Other Diagnostic Studies

    Treatment

    Treatment

    Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

    Case Studies

    Case Studies

    Case #1

    Related Chapters

    Template:Cerebral hemorrhage Template:Injuries, other than fractures, dislocations, sprains and strains

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