of critical importance and consequence; "an acute (or critical) lack of research funds"
having or demonstrating ability to recognize or draw fine distinctions; "an acute observer of politics and politicians"; "incisive comments"; "icy knifelike reasoning"; "as sharp and incisive as the stroke of a fang"; "penetrating insight"; "frequent penetrative observations" (同)discriminating, incisive, keen, knifelike, penetrating, penetrative, piercing, sharp
extremely sharp or intense; "acute pain"; "felt acute annoyance"; "intense itching and burning" (同)intense
having or experiencing a rapid onset and short but severe course; "acute appendicitis"; "the acute phase of the illness"; "acute patients"
of an angle; less than 90 degrees
below the dura mater but above the arachnoid membrane of the meninges
a localized swelling filled with blood (同)haematoma
Subdural hematoma as marked by the arrow with significant midline shift
Specialty
Neurosurgery
A subdural hematoma (SDH), is a type of hematoma, usually associated with traumatic brain injury. Blood gathers between the inner layer of the dura mater and the arachnoid mater.
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 a 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. Subarachnoid hemorrhage, the third type of brain hemorrhages, is bleeding into the subarachnoid space — the area between the arachnoid membrane and the pia mater surrounding the brain.
Contents
1Signs and symptoms
2Causes
2.1Risk factors
3Pathophysiology
4Diagnosis
4.1Classification
5Treatment
6See also
7References
8External links
Signs and symptoms
Hematoma type
Epidural
Subdural
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Location
Between the skull and the outer endosteal layer of the dura mater
Between dura mater and arachnoid mater.[1]
Involved vessel
Temperoparietal locus (most likely) - Middle meningeal artery Frontal locus - anterior ethmoidal artery Occipital locus - transverse or sigmoid sinuses Vertex locus - superior sagittal sinus
Bridging veins
Symptoms (depend on severity)[2]
Lucid interval followed by unconsciousness
Gradually increasing headache and confusion
CT appearance
Biconvex lens
Crescent-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[3] but can be delayed as much as 2 weeks.[4] If the bleeds are large enough to put pressure on the brain, signs of increased ICP (intracranial pressure) or damage to part of the brain will be present.[5]
Other signs and symptoms of subdural hematoma can include any combination of the following:
A history of recent head injury
Loss of consciousness or fluctuating levels of consciousness
Irritability
Seizures
Pain
Numbness
Headache (either constant or fluctuating)
Dizziness
Disorientation
Amnesia
Weakness or lethargy
Nausea or vomiting
Loss of appetite
Personality changes
Inability to speak or slurred speech
Ataxia, or difficulty walking
Loss of muscle control
Altered breathing patterns
Hearing loss or hearing ringing (tinnitus)
Blurred Vision
Deviated gaze, or abnormal movement of the eyes.[5]
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.[5][6] Subdural hemorrhage may be seen in shaken baby syndrome, in which similar shearing forces may cause 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 or antiplatelet drugs, such as warfarin and aspirin. Patients on these medications can have a subdural hematoma after a relatively minor traumatic event.
A further cause can be a reduction in cerebral spinal fluid pressure which can create a low pressure in the subarachnoid space, pulling the arachnoid away from the dura mater and leading to a 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.[7] Infants, too, have larger subdural spaces and are more predisposed to subdural bleeds than are young adults.[5] 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.[8]
Other risk factors for subdural bleeds include taking blood thinners (anticoagulants), long-term alcohol abuse, dementia, and the presence of a cerebrospinal fluid leak.[9]
Pathophysiology
Micrograph of a chronic subdural hematoma, as demonstrated by thin strands of collagen and neovascularization. HPS stain.
Acute subdural haematoma is usually caused external trauma that creates tension in the wall of a bridging vein as it passes between the arachnoid and dural layers, i.e. the subdural space, of the brain's lining. This is because in the short course of the vein in the subdural space, circumferential arrangement of collagen surrounding the vein causes it to be susceptible to tear by this tension. However, intracerebral hemorrhage and rupture of cortical vessels (vessels running on the surface of the brain) can also cause subdural haematoma. Such haematoma usually accumulates in between the two layers of the dura membrane. Such haematoma can cause ischemic brain damage by two mechanisms: pressure effect on the cortical blood vessels,[10] and vasoconstriction due to the substances may be released from the collected material in a subdural hematoma, causing further ischemia under the site by restricting blood flow to the brain.[11] 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.[12] This condition lead to higher risk of death for the patient.[10]
Subdural haematoma may continually grow in size by the pressure effect of the haematoma on the brain. This causes the intracranial pressure of the brain to rise, squeezing the intracranial blood into the dural venous sinuses, raising the dural venous pressure, and resulting in more bleeding from the ruptured bridging veins. Subdural haematoma only stopped to enlarge when the pressure of the haematoma equalises with the intracranial pressure of the brain, as the space for haematoma expansion getting smaller and smaller.[10]
Chronic subdural haematoma is usually asymptomatic until four to seven weeks later. In this case, accumulation of blood in the dural space is caused by inflammation. Trauma causes damage to the dural border cells (e.g. separation of dura membrane bilayer), resulting in inflammatory reaction.[13] Post craniotomy for unruptured intracranial aneurysm is another risk factor for the development of chronic subdural haematoma. The incision of arachnoid membrane during the operation causes leakage of CSF into the subdural space, leading to inflammation. This post-operative complication would usually resolved spontaneously.[14] Inflammation causes the new membrane formation through fibrosis. The inflammatory process also produces new fragile and leaky blood vessels through angiogenesis, permitting the leakage of red blood cells, white blood cells, and plasma into the haematoma cavity and easily causes mirco bleeds. Besides, tearing of arachnoid mater during trauma causes leakage of cerebrospinal fluid (CSF) into the haematoma cavity, causing increase in haematoma size over time. Excessive fibrinolysis is another factor that causes continuous bleeding. Examples of pro-inflammatory mediators acted in the haematoma expansion process are: Interleukin 1α (IL1A), Interleukin 6, Interleukin 8; while the anti-inflammatory mediator is Interleukin 10. Mediators that promote angiogenesis are: angiopoietin and vascular endothelial growth factor (VEGF). Meanwhile, prostaglandin E2 promotes the expression of VEGF. Matrix metalloproteinases remove surrounding collagen, thus providing space for new blood vessels to grow.[13]
Diagnosis
A subdural hematoma demonstrated by CT.
It is important that a person receive medical assessment, including a complete neurological examination, after any head trauma. A CT scan or MRI scan will usually detect significant subdural hematomas.
Subdural hematomas occur most often around the tops and sides of the frontal and parietal lobes.[5][6] They also occur in the posterior cranial fossa, and near the falx cerebri and tentorium cerebelli.[5] 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.
Age
Attenuation (HU)
First hours
+75 to +100[15]
After 3 days
+65 to +85[15]
After 10-14 days
+35 to +40[16]
Fresh subdural bleeding is hyperdense, but becomes more hypodense over time due to dissolution of cellular elements. After somewhere between 3–14 days, the bleeding becomes isodense with brain tissue and may therefore be missed.[17] Subsequently, it will become more hypodense than brain tissue.
Classification
Subdural hematomas are divided into acute, subacute, and chronic, depending on the speed of their onset.[18] 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.[19]
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.[5] Though much faster than chronic subdural bleeds, acute subdural bleeding is usually venous and therefore slower than the typically 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.[20] The mortality rate associated with acute subdural hematoma is around 60 to 80%.[21]
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.[7] They may not be discovered until they present clinically months or years after a head injury.[22] The bleeding from a chronic bleed is slow, probably from repeated minor bleeds, and usually stops by itself.[6][11] 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".[5] Chronic subdural hematomas are common in the elderly.[22]
Treatment
Treatment of a subdural hematoma depends on its size and rate of growth. Some small subdural hematomas can be managed by careful monitoring as the clot is eventually resorbed naturally. 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.[23][24] 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, subdural hematomas occasionally require craniotomy for evacuation; most frequently, simple burr holes for drainage; often conservative treatment; and rarely, palliative treatment in patients of extreme age or with no chance of recovery.[25]
In those with a chronic subdural hematoma, but without a history of seizures, the evidence is unclear if using anticonvulsants is harmful or beneficial.[26]
See also
Concussion
Diffuse axonal injury
Epidural hematoma
Extra-axial hemorrhage
Intra-axial hemorrhage
Head injury
Subarachnoid hemorrhage
Traumatic brain injury
References
^"Subdural Haematoma". Patient. Patient Platform Ltd. Retrieved 30 January 2017.
^Gillet, Jane. "What's the Difference Between a Subdural and Epidural Hematoma?" (PDF). brainline.org. Archived from the original (PDF) on 4 March 2016. Retrieved 30 January 2017.
^"Subdural hematoma : MedlinePlus Medical Encyclopedia". Nlm.nih.gov. 2012-06-28. Retrieved 2012-07-27.
^Sanders MJ and McKenna K. 2001. Mosby’s Paramedic Textbook, 2nd revised Ed. Chapter 22, "Head and facial trauma." Mosby.
^ abcdefghImaging in Subdural Hematoma at eMedicine
^ abcUniversity of Vermont College of Medicine. "Neuropathology: Trauma to the CNS." Accessed through web archive on August 8, 2007.
^ abDownie A. 2001. "Tutorial: CT in head trauma" Archived 2005-11-06 at the Wayback Machine.. Retrieved on August 7, 2007.
^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.
^Beck J; Gralla J; Fung C; Ulrich C; Schuct P; Fichtner J; ... Raabe A (December 2014). "Spinal cerebrospinal fluid leak as the cause of chronic subdural hematomas in nongeriatric patients". Journal of Neurosurgery. 121 (6): 1380–1387. doi:10.3171/2014.6.JNS14550. PMID 25036203.
^ abcMiller, Jimmy D; Nader, Remi (June 2014). "Acute subdural hematoma from bridging vein rupture: a potential mechanism for growth". Journal of Neurosurgery. 120 (6): 1378–1384. doi:10.3171/2013.10.JNS13272. PMID 24313607.
^ abGraham 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.
^Tandon, PN (2001). "Acute subdural haematoma : a reappraisal". Neurology India. 49 (1): 3–10. PMID 11303234. Retrieved 26 November 2017. . The possibility of direct effect of some vasoactive substances released by the blood clot, being responsible for the ischaemia, seems attractive.
^ abEdlmann, Ellie; Giorgi-Coll, Susan; Whitfield, Peter C. (30 May 2017). "Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy". Journal if Neuroinflammation. 14 (1): 108. doi:10.1186/s12974-017-0881-y. PMC 5450087. PMID 28558815.
^Tanaka, Y; Ohno, K (1 June 2013). "Chronic subdural hematoma - an up-to-date concept" (PDF). Journal of Medical and Dental Sciences. 60 (2): 55–61. PMID 23918031. Retrieved 26 November 2017.
^ abFig 3 in: Rao, Murali Gundu (2016). "Dating of Early Subdural Haematoma: A Correlative Clinico-Radiological Study". Journal of Clinical and Diagnostic Research. 10 (4): HC01–5. doi:10.7860/JCDR/2016/17207.7644. ISSN 2249-782X. PMC 4866129. PMID 27190831.
^Dr Rohit Sharma and A.Prof Frank Gaillard. "Subdural haemorrhage". Radiopaedia. Retrieved 2018-08-14.
^"Acute Subdural Hematomas". UCLA Health. Retrieved 21 July 2011.
^Penetrating Head Trauma at eMedicine
^Traumatic Brain Injury (TBI) - Definition, Epidemiology, Pathophysiology at eMedicine
^ ab
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.
^Koivisto T, Jääskeläinen JE (2009). "Chronic subdural haematoma–to drain or not to drain?". Lancet. 374 (9695): 1040&ndash, 1041. doi:10.1016/S0140-6736(09)61682-2. PMID 19782854.
^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&ndash, 1073. doi:10.1016/S0140-6736(09)61115-6. PMID 19782872.
^de Araújo Silva, DaniloOtávio; Matis, GeorgiosK; Kitamura, MatheusAugusto Pinto; de Carvalho Junior, EduardoVieira; Silva, Monalisade Moura; Pereira, CarlosUmberto; da Silva, JoacilCarlos; de Azevedo Filho, HildoRocha Cirne; Costa, LeonardoFerraz; Barbosa, Breno JoséA. P.; Birbilis, TheodossiosA (2012). "Chronic subdural hematomas and the elderly: Surgical results from a series of 125 cases: Old "horses" are not to be shot!". Surgical Neurology International. 3 (1): 150. doi:10.4103/2152-7806.104744. ISSN 2152-7806. PMC 3551521. PMID 23372967.
^Ratilal, BO; Pappamikail, L; Costa, J; Sampaio, C (Jun 6, 2013). "Anticonvulsants for preventing seizures in patients with chronic subdural haematoma". The Cochrane Database of Systematic Reviews. 6 (6): CD004893. doi:10.1002/14651858.CD004893.pub3. PMID 23744552.
External links
Classification
D
ICD-10: I62.0, P10.0, S06.5
ICD-9-CM: 852.2 - traumatic; 432.1 - nontraumatic
MeSH: D006408
DiseasesDB: 12614
External resources
MedlinePlus: 000713
eMedicine: neuro/575
Wikimedia Commons has media related to Subdural hematoma.
Subdural Hematoma at eMedicine
Imaging and Mechanism of Subdural Hematoma - MedPix
v
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Cardiovascular disease (heart) (I00–I52, 390–429)
Ischaemic
Coronary disease
Coronary artery disease (CAD)
Coronary artery aneurysm
Spontaneous coronary artery dissection (SCAD)
Coronary thrombosis
Coronary vasospasm
Myocardial bridge
Active ischemia
Angina pectoris
Prinzmetal's angina
Stable angina
Acute coronary syndrome
Myocardial infarction
Unstable angina
Sequelae
hours
Hibernating myocardium
Myocardial stunning
days
Myocardial rupture
weeks
Aneurysm of heart / Ventricular aneurysm
Dressler syndrome
Layers
Pericardium
Pericarditis
Acute
Chronic / Constrictive
Pericardial effusion
Cardiac tamponade
Hemopericardium
Myocardium
Myocarditis
Chagas disease
Cardiomyopathy
Dilated
Alcoholic
Hypertrophic
Restrictive
Loeffler endocarditis
Cardiac amyloidosis
Endocardial fibroelastosis
Arrhythmogenic right ventricular dysplasia
Endocardium / valves
Endocarditis
infective endocarditis
Subacute bacterial endocarditis
non-infective endocarditis
Libman–Sacks endocarditis
Nonbacterial thrombotic endocarditis
Valves
mitral
regurgitation
prolapse
stenosis
aortic
stenosis
insufficiency
tricuspid
stenosis
insufficiency
pulmonary
stenosis
insufficiency
Conduction / arrhythmia
Bradycardia
Sinus bradycardia
Sick sinus syndrome
Heart block: Sinoatrial
AV
1°
2°
3°
Intraventricular
Bundle branch block
Right
Left
Left anterior fascicle
Left posterior fascicle
Bifascicular
Trifascicular
Adams–Stokes syndrome
Tachycardia (paroxysmal and sinus)
Supraventricular
Atrial
Multifocal
Junctional
AV nodal reentrant
Junctional ectopic
Ventricular
Accelerated idioventricular rhythm
Catecholaminergic polymorphic
Torsades de pointes
Premature contraction
Atrial
Junctional
Ventricular
Pre-excitation syndrome
Lown–Ganong–Levine
Wolff–Parkinson–White
Flutter / fibrillation
Atrial flutter
Ventricular flutter
Atrial fibrillation
Familial
Ventricular fibrillation
Pacemaker
Ectopic pacemaker / Ectopic beat
Multifocal atrial tachycardia
Pacemaker syndrome
Parasystole
Wandering pacemaker
Long QT syndrome
Andersen–Tawil
Jervell and Lange-Nielsen
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Cardiac arrest
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Asystole
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Other / ungrouped
hexaxial reference system
Right axis deviation
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QT
Short QT syndrome
T
T wave alternans
ST
Osborn wave
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Left
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Left
Right
Other
Cardiac fibrosis
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v
t
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Nonmusculoskeletal injuries of head (head injury) and neck (S00–S19, 850–854)
Intracranial
see neurotrauma
Extracranial/ facial trauma
eye:
Black eye
Eye injury
Corneal abrasion
ear:
Perforated eardrum
Either/both
Penetrating head injury
v
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Cerebrovascular diseases (G45–G46 and I60–I69, 430–438)
5. 急性外傷性脳損傷患者への麻酔 anesthesia for patients with acute traumatic brain injury
English Journal
The biomechanical behaviour of the bridging vein-superior sagittal sinus complex with implications for the mechanopathology of acute subdural haematoma.
Monea AG1, Baeck K2, Verbeken E3, Verpoest I4, Sloten JV5, Goffin J6, Depreitere B7.Author information 1Division of Experimental Neurosurgery and Neuroanatomy, Katholieke Universiteit Leuven, UZ Herestraat 49 - box 7003, 3000 Leuven, Belgium; Biomechanics Section, K.U. Leuven, Celestijnenlaan 300 - box 2419, 3001 Heverlee, Belgium. Electronic address: moneaaida@yahoo.com.2Biomechanics Section, K.U. Leuven, Celestijnenlaan 300 - box 2419, 3001 Heverlee, Belgium. Electronic address: katrien.baeck@mech.kuleuven.be.3Translational Cell and Tissue Research, K.U. Leuven, Minderbroedersstraat 12 blok q - box 1032, 3000 Leuven, Belgium. Electronic address: erik.verbeken@med.kuleuven.be.4Department of Metallurgy and Materials Engineering (MTM), K.U. Leuven, Kasteelpark Arenberg 44 - box 2450, 3001 Heverlee, Belgium. Electronic address: ignaas.verpoest@mtm.kuleuven.be.5Biomechanics Section, K.U. Leuven, Celestijnenlaan 300 - box 2419, 3001 Heverlee, Belgium. Electronic address: jos.vandersloten@mech.kuleuven.be.6Division of Experimental Neurosurgery and Neuroanatomy, Katholieke Universiteit Leuven, UZ Herestraat 49 - box 7003, 3000 Leuven, Belgium. Electronic address: jan.goffin@med.kuleuven.be.7Division of Experimental Neurosurgery and Neuroanatomy, Katholieke Universiteit Leuven, UZ Herestraat 49 - box 7003, 3000 Leuven, Belgium. Electronic address: bart.depreitere@med.kuleuven.be.AbstractBACKGROUND: Traumatic brain injury is expected to become the major cause of death and disability for children and young adults by the year 2020. One of the most frequent and most morbid pathologies resulted from a head trauma is acute subdural haematoma (ASDH). For nearly one third of the ASDH cases the etiopathology directly relates to a bridging vein (BV) rupture.
Journal of the mechanical behavior of biomedical materials.J Mech Behav Biomed Mater.2014 Apr;32:155-65. doi: 10.1016/j.jmbbm.2013.12.007. Epub 2014 Jan 4.
BACKGROUND: Traumatic brain injury is expected to become the major cause of death and disability for children and young adults by the year 2020. One of the most frequent and most morbid pathologies resulted from a head trauma is acute subdural haematoma (ASDH). For nearly one third of the ASDH cases
Spontaneous resolution of large acute subdural hematoma and the value of neurological exam in conservative management of high risk patients.
Towers WS1, Kurtom KH2.Author information 1University of Maryland Shore Regional Health, 219 S Washington Street, Easton 21601, USA. Electronic address: Wendy.towers@yahoo.com.2University of Maryland Shore Regional Health, Department of Neurosurgery, University of Maryland School of Medicine, 219 S Washington Street, Easton 21601, USA.KEYWORDS: Acute subdural hematoma, Conservative management, Neurological examination, Spontaneous resolution
Clinical neurology and neurosurgery.Clin Neurol Neurosurg.2014 Mar;118:98-100. doi: 10.1016/j.clineuro.2013.12.014. Epub 2014 Jan 7.
Predictors of rapid spontaneous resolution of acute subdural hematoma.
Fujimoto K1, Otsuka T2, Yoshizato K2, Kuratsu J3.Author information 1Department of Neurosurgery, National Hospital Organization Kumamoto Medical Center, 1-5, Ninomaru, Chuo-ku, Kumamoto 860-0008, Japan; Department of Neurosurgery, Faculty of Life Sciences, Kumamoto University School of Medicine, 1-1-1, Honjo, Kumamoto, Kumamoto 861-8556, Japan. Electronic address: schwarz_k1216@yahoo.co.jp.2Department of Neurosurgery, National Hospital Organization Kumamoto Medical Center, 1-5, Ninomaru, Chuo-ku, Kumamoto 860-0008, Japan.3Department of Neurosurgery, Faculty of Life Sciences, Kumamoto University School of Medicine, 1-1-1, Honjo, Kumamoto, Kumamoto 861-8556, Japan.AbstractOBJECTIVE: Acute subdural hematoma (ASDH) usually requires emergency surgical decompression, but rare cases exhibit rapid spontaneous resolution. The aim of this retrospective study was to identify factors predictive of spontaneous ASDH resolution.
Clinical neurology and neurosurgery.Clin Neurol Neurosurg.2014 Mar;118:94-7. doi: 10.1016/j.clineuro.2013.11.030. Epub 2013 Dec 7.
OBJECTIVE: Acute subdural hematoma (ASDH) usually requires emergency surgical decompression, but rare cases exhibit rapid spontaneous resolution. The aim of this retrospective study was to identify factors predictive of spontaneous ASDH resolution.METHODS: A total of 366 consecutive patients with AS
