U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination

Subdural hemorrhage

MedGen UID:
6775
Concept ID:
C0018946
Pathologic Function
Synonyms: Hematoma, Subdural; Hematomas, Subdural; Hemorrhage, Subdural; Hemorrhages, Subdural; Subdural Hematoma; Subdural Hematomas; Subdural Hemorrhage; Subdural Hemorrhages
SNOMED CT: SDH - Subdural hematoma (95453001); Subdural hematoma (95453001); Subdural intracranial hemorrhage (35486000); Subdural intracranial hematoma (95453001); Subdural hemorrhage (35486000)
 
HPO: HP:0100309

Definition

Hemorrhage occurring between the dura mater and the arachnoid mater. [from HPO]

Conditions with this feature

Glanzmann thrombasthenia
MedGen UID:
52736
Concept ID:
C0040015
Disease or Syndrome
Glanzmann thrombasthenia is a bleeding disorder that is characterized by prolonged or spontaneous bleeding starting from birth. People with Glanzmann thrombasthenia tend to bruise easily, have frequent nosebleeds (epistaxis), and may bleed from the gums. They may also develop red or purple spots on the skin caused by bleeding underneath the skin (petechiae) or swelling caused by bleeding within tissues (hematoma). Glanzmann thrombasthenia can also cause prolonged bleeding following injury, trauma, or surgery (including dental work). Women with this condition can have prolonged and sometimes abnormally heavy menstrual bleeding. Affected women also have an increased risk of excessive blood loss during pregnancy and childbirth.\n\nAbout a quarter of individuals with Glanzmann thrombasthenia have bleeding in the gastrointestinal tract, which often occurs later in life. Rarely, affected individuals have bleeding inside the skull (intracranial hemorrhage) or joints (hemarthrosis).\n\nThe severity and frequency of the bleeding episodes in Glanzmann thrombasthenia can vary greatly among affected individuals, even in the same family. Spontaneous bleeding tends to become less frequent with age.
Glutaric aciduria, type 1
MedGen UID:
124337
Concept ID:
C0268595
Disease or Syndrome
The phenotypic spectrum of untreated glutaric acidemia type 1 (GA-1) ranges from the more common form (infantile-onset disease) to the less common form (later-onset disease – i.e., after age 6 years). Of note, the GA-1 phenotype can vary widely between untreated family members with the same genotype, primarily as a function of the age at which the first acute encephalopathic crisis occurred: three months to six years in infantile-onset GA-1 and after age six years in later-onset GA-1. Characteristically these crises result in acute bilateral striatal injury and subsequent complex movement disorders. In the era of newborn screening (NBS), the prompt initiation of treatment of asymptomatic infants detected by NBS means that most individuals who would have developed manifestations of either infantile-onset or later-onset GA-1 remain asymptomatic; however, they may be at increased risk for other manifestations (e.g., renal disease) that are becoming apparent as the understanding of the natural history of treated GA-1 continues to evolve.
TARP syndrome
MedGen UID:
333324
Concept ID:
C1839463
Disease or Syndrome
The classic features of TARP syndrome are talipes equinovarus, atrial septal defect, Robin sequence (micrognathia, cleft palate, and glossoptosis), and persistent left superior vena cava. Not all patients have all classic features. Some patients have the additional features of central nervous system dysfunction, renal abnormalities, variable cardiac anomalies including hypertrophic obstructive cardiomyopathy, and variable distal limb defects including syndactyly. Most patients die in late prenatal or early postnatal stages (summary by Kaeppler et al., 2018).
Congenital afibrinogenemia
MedGen UID:
749036
Concept ID:
C2584774
Disease or Syndrome
Inherited disorders of fibrinogen affect either the quantity (afibrinogenemia and hypofibrinogenemia; 202400) or the quality (dysfibrinogenemia; 616004) of the circulating fibrinogen or both (hypodysfibrinogenemia; see 616004). Afibrinogenemia is characterized by the complete absence of immunoreactive fibrinogen. Bleeding due to afibrinogenemia usually manifests in the neonatal period, with 85% of cases presenting umbilical cord bleeding, but a later age of onst is not unusual. Bleeding may occur in the skin, gastrointestinal tract, genitourinary tract, or the central nervous system, with intracranial hemorrhage being reported as the major cause of death. Patients are susceptible to spontaneous rupture of the spleen. Menstruating women may experience menometrorrhagia. First-trimester abortion is common. Both arterial and venous thromboembolic complications have been reported (summary by de Moerloose and Neerman-Arbez, 2009). Hypofibrinogenemia is characterized by reduced amounts of immunoreactive fibrinogen. Patients are often heterozygous carriers of afibrinogenemia mutations and are usually asymptomatic. However, they may bleed when exposed to trauma or if they have a second associated hemostatic abnormality. Women may experience miscarriages. Liver disease occurs in rare cases (summary by de Moerloose and Neerman-Arbez, 2009).
Fetal akinesia-cerebral and retinal hemorrhage syndrome
MedGen UID:
1631944
Concept ID:
C4706410
Disease or Syndrome
Lethal congenital contracture syndrome-5 (LCCS5) is an autosomal recessive disorder characterized by decreased fetal movements, joint contractures, hypotonia, skeletal abnormalities with thin bones, and brain and retinal hemorrhages (Koutsopoulos et al., 2013). For a general phenotypic description and a discussion of genetic heterogeneity of LCCS, see LCCS1 (253310).
Spinal muscular atrophy, lower extremity-predominant, 2b, prenatal onset, autosomal dominant
MedGen UID:
1648362
Concept ID:
C4749003
Disease or Syndrome
SMALED2B is a severe neuromuscular disorder with onset in utero. Affected individuals show decreased fetal movements and are usually born with congenital contractures consistent with arthrogryposis multiplex congenita (AMC). After birth, they have severe hypotonia and muscle atrophy as well as respiratory insufficiency due to muscle weakness. Some patients may have dysmorphic facial features and/or abnormalities on brain imaging. Many patients die in early childhood (summary by Storbeck et al., 2017) For discussion of genetic heterogeneity of lower extremity-predominant spinal muscular atrophy, see SMALED1 (158600).
Congenital disorder of glycosylation, type Iw, autosomal dominant
MedGen UID:
1794278
Concept ID:
C5562068
Disease or Syndrome
Autosomal dominant congenital disorder of glycosylation type Iw (CDG1WAD) is characterized by variable skeletal anomalies, short stature, macrocephaly, and dysmorphic features; about half of patients have impaired intellectual development. Additional features include increased muscle tone and muscle cramps (Wilson et al., 2021).
Congenital myopathy 2c, severe infantile, autosomal dominant
MedGen UID:
1840969
Concept ID:
C5830333
Disease or Syndrome
Congenital myopathy-2C (CMYO2C) is an autosomal dominant disorder of the skeletal muscle characterized by severe congenital weakness usually resulting in death from respiratory failure in the first year or so of life. Patients present at birth with hypotonia, lack of antigravity movements, poor head control, and difficulties feeding or breathing, often requiring tube-feeding and mechanical ventilation. Decreased fetal movements may be observed in some cases. Of the patients with congenital myopathy caused by mutation in the ACTA1 gene, about 90% carry heterozygous mutations that are usually de novo and cause the severe infantile phenotype. Some patients with heterozygous mutations have a more typical and milder disease course with delayed motor development and proximal muscle weakness, but are able to achieve independent ambulation (CMYO2A; 161800). The severity of the disease most likely depends on the detrimental effect of the mutation, although there are probably additional modifying factors (Ryan et al., 2001; Laing et al., 2009; Sanoudou and Beggs, 2001; Agrawal et al., 2004; Nowak et al., 2013; Sewry et al., 2019; Laitila and Wallgren-Pettersson, 2021). For a discussion of genetic heterogeneity of congenital myopathy, see CMYO1A (117000).
Intellectual developmental disorder, x-linked, syndromic 37
MedGen UID:
1854940
Concept ID:
C5935567
Disease or Syndrome
X-linked syndromic intellectual developmental disorder-37 (MRXS37) is a developmental disorder showing phenotypic variability and variable severity. Male mutation carriers tend to be more severely affected than female mutation carriers, some of whom may even be asymptomatic. In general, the disorder is characterized by global developmental delay with delayed walking, speech delay, impaired intellectual development that ranges from borderline low to moderate, and behavioral abnormalities, such as autism and sleeping difficulties. Many patients are able to attend mainstream schools with assistance and work under supervision. Additional more variable features include sensorineural hearing loss, ocular anomalies, feeding difficulties, dysmorphic facial features, inguinal and umbilical hernia, genitourinary defects, congenital heart defects, musculoskeletal anomalies, and endocrine dysfunction, such as hypogonadism or hyperparathyroidism (Shepherdson et al., 2024).

Professional guidelines

PubMed

Duhaime AC, Christian CW
J Neurosurg Pediatr 2019 Nov 1;24(5):481-488. doi: 10.3171/2019.7.PEDS18394. PMID: 31675688
Macdonald RL
Neurosurg Clin N Am 2018 Oct;29(4):605-613. Epub 2018 Aug 14 doi: 10.1016/j.nec.2018.06.013. PMID: 30223973
Choudhary AK, Servaes S, Slovis TL, Palusci VJ, Hedlund GL, Narang SK, Moreno JA, Dias MS, Christian CW, Nelson MD Jr, Silvera VM, Palasis S, Raissaki M, Rossi A, Offiah AC
Pediatr Radiol 2018 Aug;48(8):1048-1065. Epub 2018 May 23 doi: 10.1007/s00247-018-4149-1. PMID: 29796797

Recent clinical studies

Etiology

Rivier CA, Kamel H, Sheth KN, Iadecola C, Gupta A, de Leon MJ, Ross E, Falcone GJ, Murthy SB
JAMA Neurol 2024 Feb 1;81(2):163-169. doi: 10.1001/jamaneurol.2023.4918. PMID: 38147345Free PMC Article
Agashe S, Brinkmann BH, Cox BC, Wong-Kisiel L, Van Gompel JJ, Marsh RW, Miller KJ, Krecke KN, Britton JW
Clin Neurophysiol 2023 Nov;155:86-93. Epub 2023 Sep 6 doi: 10.1016/j.clinph.2023.08.016. PMID: 37806180
Canty KW, Feldman KW, Bartnik-Olson B, Choudhary AK, Shiroishi MS; ENIGMA Child Abuse Working Group
Pediatr Radiol 2022 Dec;52(13):2445-2449. Epub 2022 Oct 20 doi: 10.1007/s00247-022-05534-0. PMID: 36261511
Laing J, Gabbe B, Chen Z, Perucca P, Kwan P, O'Brien TJ
JAMA Neurol 2022 Apr 1;79(4):334-341. doi: 10.1001/jamaneurol.2021.5420. PMID: 35188950Free PMC Article
Martin NA, Doberstein C, Alexander M, Khanna R, Benalcazar H, Alsina G, Zane C, McBride D, Kelly D, Hovda D
J Neurotrauma 1995 Oct;12(5):897-901. doi: 10.1089/neu.1995.12.897. PMID: 8594217

Diagnosis

Rivier CA, Kamel H, Sheth KN, Iadecola C, Gupta A, de Leon MJ, Ross E, Falcone GJ, Murthy SB
JAMA Neurol 2024 Feb 1;81(2):163-169. doi: 10.1001/jamaneurol.2023.4918. PMID: 38147345Free PMC Article
Choudhary AK, Servaes S, Slovis TL, Palusci VJ, Hedlund GL, Narang SK, Moreno JA, Dias MS, Christian CW, Nelson MD Jr, Silvera VM, Palasis S, Raissaki M, Rossi A, Offiah AC
Pediatr Radiol 2018 Aug;48(8):1048-1065. Epub 2018 May 23 doi: 10.1007/s00247-018-4149-1. PMID: 29796797
Mian M, Shah J, Dalpiaz A, Schwamb R, Miao Y, Warren K, Khan S
Fetal Pediatr Pathol 2015 Jun;34(3):169-75. Epub 2015 Jan 23 doi: 10.3109/15513815.2014.999394. PMID: 25616019
Akman CI, Cracco J
Dev Med Child Neurol 2000 Dec;42(12):843-6. doi: 10.1017/s0012162200001559. PMID: 11132259
Spaide RF, Swengel RM, Scharre DW, Mein CE
Am Fam Physician 1990 Apr;41(4):1145-52. PMID: 2181831

Therapy

Sakusic A, Rabinstein AA, Anisetti B, Mandrekar J, Wijdicks EFM, Freeman WD, Braksick SA
Neurology 2024 Aug 27;103(4):e209664. Epub 2024 Aug 5 doi: 10.1212/WNL.0000000000209664. PMID: 39102615
Rivier CA, Kamel H, Sheth KN, Iadecola C, Gupta A, de Leon MJ, Ross E, Falcone GJ, Murthy SB
JAMA Neurol 2024 Feb 1;81(2):163-169. doi: 10.1001/jamaneurol.2023.4918. PMID: 38147345Free PMC Article
Petralia CCT, Manivannan S, Shastin D, Sharouf F, Elalfy O, Zaben M
World Neurosurg 2020 Jun;138:e35-e41. Epub 2020 Feb 27 doi: 10.1016/j.wneu.2020.01.160. PMID: 32113994
Nisar MK
J Patient Saf 2018 Mar;14(1):e1-e2. doi: 10.1097/PTS.0000000000000162. PMID: 25782563
Anker-Møller T, Troldborg A, Sunde N, Hvas AM
Semin Thromb Hemost 2017 Oct;43(7):750-758. Epub 2017 Sep 6 doi: 10.1055/s-0037-1604089. PMID: 28877540

Prognosis

Agashe S, Brinkmann BH, Cox BC, Wong-Kisiel L, Van Gompel JJ, Marsh RW, Miller KJ, Krecke KN, Britton JW
Clin Neurophysiol 2023 Nov;155:86-93. Epub 2023 Sep 6 doi: 10.1016/j.clinph.2023.08.016. PMID: 37806180
Laing J, Gabbe B, Chen Z, Perucca P, Kwan P, O'Brien TJ
JAMA Neurol 2022 Apr 1;79(4):334-341. doi: 10.1001/jamaneurol.2021.5420. PMID: 35188950Free PMC Article
Shaban A, Moritani T, Al Kasab S, Sheharyar A, Limaye KS, Adams HP Jr
J Stroke Cerebrovasc Dis 2018 Jun;27(6):1435-1446. Epub 2018 Mar 16 doi: 10.1016/j.jstrokecerebrovasdis.2018.02.014. PMID: 29555403
Anker-Møller T, Troldborg A, Sunde N, Hvas AM
Semin Thromb Hemost 2017 Oct;43(7):750-758. Epub 2017 Sep 6 doi: 10.1055/s-0037-1604089. PMID: 28877540
Mian M, Shah J, Dalpiaz A, Schwamb R, Miao Y, Warren K, Khan S
Fetal Pediatr Pathol 2015 Jun;34(3):169-75. Epub 2015 Jan 23 doi: 10.3109/15513815.2014.999394. PMID: 25616019

Clinical prediction guides

Sakusic A, Rabinstein AA, Anisetti B, Mandrekar J, Wijdicks EFM, Freeman WD, Braksick SA
Neurology 2024 Aug 27;103(4):e209664. Epub 2024 Aug 5 doi: 10.1212/WNL.0000000000209664. PMID: 39102615
Peng J, Luo T, Li X, Li B, Cheng Y, Huang Q, Su J
Sci Rep 2024 Mar 12;14(1):5961. doi: 10.1038/s41598-024-56232-w. PMID: 38472247Free PMC Article
Azzam AY, Mortezaei A, Morsy MM, Essibayi MA, Ghozy S, Elamin O, Azab MA, Elswedy A, Altschul D, Kadirvel R, Brinjikji W, Kallmes DF
J Neurol Sci 2024 Apr 15;459:122948. Epub 2024 Mar 5 doi: 10.1016/j.jns.2024.122948. PMID: 38457956
Laing J, Gabbe B, Chen Z, Perucca P, Kwan P, O'Brien TJ
JAMA Neurol 2022 Apr 1;79(4):334-341. doi: 10.1001/jamaneurol.2021.5420. PMID: 35188950Free PMC Article
Duhaime AC, Durham S
Prog Brain Res 2007;161:293-302. doi: 10.1016/S0079-6123(06)61020-0. PMID: 17618985

Recent systematic reviews

Azzam AY, Mortezaei A, Morsy MM, Essibayi MA, Ghozy S, Elamin O, Azab MA, Elswedy A, Altschul D, Kadirvel R, Brinjikji W, Kallmes DF
J Neurol Sci 2024 Apr 15;459:122948. Epub 2024 Mar 5 doi: 10.1016/j.jns.2024.122948. PMID: 38457956
Zuckerman SL, Yengo-Kahn AM, Tang AR, Bailes JE, Beauchamp K, Berger MS, Bonfield CM, Camarata PJ, Cantu RC, Davis GA, Ellenbogen RG, Ellis MJ, Feuer H, Guazzo E, Harris OA, Heppner P, Honeybul S, Manley G, Maroon JC, Miele VJ, Nahed BV, Okonkwo DO, Oppenlander ME, Petty J, Sabin HI, Samadani U, Sherburn EW, Sheridan M, Tator CH, Theodore N, Timmons SD, Woodworth GF, Solomon GS, Sills AK
Neurosurgery 2021 May 13;88(6):E495-E504. doi: 10.1093/neuros/nyab041. PMID: 33693899
Srivatsan A, Mohanty A, Nascimento FA, Hafeez MU, Srinivasan VM, Thomas A, Chen SR, Johnson JN, Kan P
World Neurosurg 2019 Feb;122:613-619. Epub 2018 Nov 24 doi: 10.1016/j.wneu.2018.11.167. PMID: 30481628
Ascanio LC, Maragkos GA, Young BC, Boone MD, Kasper EM
Neurocrit Care 2019 Feb;30(1):5-15. doi: 10.1007/s12028-018-0501-4. PMID: 29476390
Anker-Møller T, Troldborg A, Sunde N, Hvas AM
Semin Thromb Hemost 2017 Oct;43(7):750-758. Epub 2017 Sep 6 doi: 10.1055/s-0037-1604089. PMID: 28877540

Supplemental Content

Table of contents

    Clinical resources

    Practice guidelines

    • PubMed
      See practice and clinical guidelines in PubMed. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.
    • Bookshelf
      See practice and clinical guidelines in NCBI Bookshelf. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.

    Consumer resources

    Recent activity

    Your browsing activity is empty.

    Activity recording is turned off.

    Turn recording back on

    See more...