Chronic subdural hematoma recurrence

Chronic subdural hematoma recurrence

Epidemiology

In 2 large cohorts of US patients, approximately 5% to 10% of patients who underwent surgery for nontraumatic SDH were required to undergo repeated operation within 30 to 90 days. These results may inform the design of future prospective studies and trials and help practitioners calibrate their index of suspicion to ensure that patients are referred for timely surgical care 1).

Recurrence rates after chronic subdural hematoma (CSDH) evacuation with any of actual techniques twist drillcraniostomy (TDC), burr hole craniostomy, craniotomy range from 5% to 30%. 2).

Risk factors

In the series of Han et al. independent risk factors for recurrence were as follows: age > 75 years (HR 1.72, 95% CI 1.03-2.88; p = 0.039), obesity (body mass index ≥ 25.0 kg/m2), and a bilateral operation 3).

Chon et al. shown that postoperative midline shifting (≥5 mm), diabetes mellitus, preoperative seizure, preoperative width of hematoma (≥20 mm), and anticoagulant therapy were independent predictors of the recurrence of chronic subdural hematoma.

According to internal architecture of hematoma, the rate of recurrence was significantly lower in the homogeneous and the trabecular type than the laminar and separated type 4).


The recurrence rate of chronic subdural hematoma cSDH seems to be related to the excessive neoangiogenesis in the parietal membrane, which is mediated via vascular endothelial growth factor (VEGF). This is found to be elevated in the hematoma fluid and is dependent on eicosanoid/prostaglandin and thromboxane synthesis via cyclooxygenase-2 (COX-2).

Anticoagulant therapy

Antiplatelet therapy

Antiplatelet therapy significantly influences the recurrence of CSDH 5).

Pneumocephalus

Remaining pneumocephalus is seen as an approved factor of recurrence 6) 7).

Septation

Jack et al.found a 12% reoperation rate. CSDH septation (seen on computed tomogram scan) was found to be an independent risk factor for recurrence requiring reoperation (p=0.04). Larger post-operative subdural haematoma volume was also significantly associated with requiring a second drainage procedure (p<0.001). Independent risk factors of larger post-operative haematoma volume included septations within a CSDH (p<0.01), increased pre-operative haematoma volume (p<0.01), and a greater amount of parenchymal atrophy (p=0.04). A simple scoring system for quantifying recurrence risk was created and validated based on patient age (< or ≥80 years), haematoma volume (< or ≥160cc), and presence of septations within the subdural collection (yes or no).

Septations within CSDHs are associated with larger post-operative residual haematoma collections requiring repeat drainage. When septations are clearly visible within a CSDH, craniotomy might be more suitable as a primary procedure as it allows greater access to a septated subdural collection. The proposed scoring system combining haematoma volume, age, and presence of septations might be useful in identifying patients at higher risk for recurrence 8).

Membranectomy

Opening the internal hematoma membrane does not alter the rate of patients requiring revision surgery and the number of patients showing a marked residual hematoma six weeks after evacuation of a CSDH 9).

In the study of Lee et al, an extended surgical approach with partial membranectomy has no advantages regarding the rate of reoperation and the outcome. As initial treatment, burr-hole drainage with irrigation of the hematoma cavity and closed-system drainage is recommended. Extended craniotomy with membranectomy is now reserved for instances of acute rebleeding with solid hematoma 10).

Diabetes

Surgeons should consider informing patients with diabetes mellitus that this comorbidity is associated with an increased likelihood of recurrence

11) 12) 13).


Balser et al. report 11% recurrence, which included individuals who recurred as late as 3 years after initial diagnosis 14).

Close imaging follow-up is important for CSDH patients for recurrence prediction. Using quantitative CT volumetric analysis, strong evidence was provided that changes in the residual fluid volume during the ‘self-resolution’ period can be used as significantly radiological predictors of recurrence 15).

A structural equation model showed a significant association between increased antiinflammatory activity in hematoma fluid samples and a lower risk of recurrence, but this relationship was not statistically significant in venous blood samples. Moreover, these findings indicate that anti-inflammatory activities in the hematoma may play a role in the risk of a recurrence of CSDH 16).

Irrigation with artificial cerebrospinal fluid (ACF) decreased the rate of CSDH recurrence 17).

Treatment

There is no definite operative procedure for patients with intractable chronic subdural hematoma (CSDH).

Most recurrent hematomas are managed successfully with burr hole craniostomies with postoperative closed-system drainage. Refractory hematomas may be managed with a variety of techniques, including craniotomy or subdural-peritoneal shunt placement 18).

Although many studies have reported risk factors or treatments in efforts to prevent recurrence, those have focused on single recurrence, and little cumulative data is available to analyze refractory CSDH.

Matsumoto et al. defined refractory CSDH as ≥2 recurrences, then analyzed and compared clinical factors between patients with single recurrence and those with refractory CSDH in a cohort study, to clarify whether patients with refractory CSDH experience different or more risk factors than patients with single recurrence, and whether burr-hole irrigation with closed-system drainage reduces refractory CSDH.

Seventy-five patients had at least one recurrence, with single recurrence in 62 patients and ≥2 recurrences in 13 patients. In comparing clinical characteristics, patients with refractory CSDH were significantly younger (P=0.04) and showed shorter interval to first recurrence (P<0.001). Organized CSDH was also significantly associated with refractory CSDH (P=0.02). Multivariate logistic regression analysis identified first recurrence interval <1 month (OR 6.66, P<0.001) and age <71 years (OR 4.16, P<0.001) as independent risk factors for refractory CSDH. On the other hand, burr-hole irrigation with closed-system drainage did not reduce refractory CSDH.

When patients with risk factors for refractory CSDH experience recurrence, alternative surgical procedures may be considered as the second surgery, because burr-hole irrigation with closed-system drainage did not reduce refractory CSDH 19).

Implantation of a reservoir 20) 21) 22).

Subdural-peritoneal shunt 23).

Middle meningeal artery embolization

Embolization of the MMA is effective for refractory CSDH or CSDH patients with a risk of recurrence, and is considered an effective therapeutic method to stop hematoma enlargement and promote resolution 24) 25) 26) 27) 28) 29).

A pilot study indicated that perioperative middle meningeal artery (MMA) embolization could be offered as the least invasive and most effectual means of treatment for resistant patients of CSDHs with 1 or more recurrences 30).

Chihara et al. have treated three cases of CSDH with MMA embolization to date, but there was a postoperative recurrence in one patient, which required a craniotomy for hematoma removal and capsulectomy. MMA embolization blocks the blood supply from the dura to the hematoma outer membrane in order to prevent recurrences of refractory CSDH. Histopathologic examination of the outer membrane of the hematoma excised during craniotomy showed foreign-body giant cells and neovascular proliferation associated with embolization. Because part of the hematoma was organized in this case, the CSDH did not resolve when the MMA was occluded, and the development of new collateral pathways in the hematoma outer membrane probably contributed to the recurrence. Therefore, in CSDH with some organized hematoma, MMA embolization may not be effective. Magnetic resonance imaging (MRI) should be performed in these patients before embolization 31).

Case series

Case reports

References

1)

Knopman J, Link TW, Navi BB, Murthy SB, Merkler AE, Kamel H. Rates of Repeated Operation for Isolated Subdural Hematoma Among Older Adults. JAMA Netw Open. 2018 Oct 5;1(6):e183737. doi: 10.1001/jamanetworkopen.2018.3737. PubMed PMID: 30646255.
2)

Escosa Baé M, Wessling H, Salca HC, de Las Heras Echeverría P. Use of twist-drill craniostomy with drain in evacuation of chronic subdural hematomas: independent predictors of recurrence. Acta Neurochir (Wien). 2011 May;153(5):1097-103. doi: 10.1007/s00701-010-0903-3. Epub 2010 Dec 31. PubMed PMID: 21193935.
3)

Han MH, Ryu JI, Kim CH, Kim JM, Cheong JH, Yi HJ. Predictive factors for recurrence and clinical outcomes in patients with chronic subdural hematoma. J Neurosurg. 2017 Nov;127(5):1117-1125. doi: 10.3171/2016.8.JNS16867. Epub 2016 Dec 16. PubMed PMID: 27982768.
4)

Chon KH, Lee JM, Koh EJ, Choi HY. Independent predictors for recurrence of chronic subdural hematoma. Acta Neurochir (Wien). 2012 Sep;154(9):1541-8. doi: 10.1007/s00701-012-1399-9. Epub 2012 Jun 1. PubMed PMID: 22653496.
5)

Wada M, Yamakami I, Higuchi Y, Tanaka M, Suda S, Ono J, Saeki N. Influence of antiplatelet therapy on postoperative recurrence of chronic subdural hematoma: a multicenter retrospective study in 719 patients. Clin Neurol Neurosurg. 2014 May;120:49-54. doi: 10.1016/j.clineuro.2014.02.007. Epub 2014 Feb 24. PubMed PMID: 24731576.
6)

Mori K, Maeda M (2001) Surgical treatment of chronic subdural hematoma in 500 consecutive cases: clinical characteristics, surgical outcome, complications, and recurrence rate. Neurol Med Chir (Tokyo) 41:371–381
7)

Stanišić M, Hald J, Rasmussen IA, Pripp AH, Ivanović J, Kolstad F, Sundseth J, Züchner M, Lindegaard KF (2013) Volume and densities of chronic subdural haematoma obtained from CT imaging as predictors of postoperative recurrence: a prospective study of 107 operated patients. Acta Neurochir 155:323–333
8)

Jack A, O’Kelly C, McDougall C, Max Findlay J. Predicting Recurrence after Chronic Subdural Haematoma Drainage. Can J Neurol Sci. 2015 Jan 5:1-6. [Epub ahead of print] PubMed PMID: 25557536.
9)

Unterhofer C, Freyschlag CF, Thomé C, Ortler M. Opening the Internal Hematoma Membrane does not Alter the Recurrence Rate of Chronic Subdural Hematomas – A Prospective Randomized Trial. World Neurosurg. 2016 May 2. pii: S1878-8750(16)30210-8. doi: 10.1016/j.wneu.2016.04.081. [Epub ahead of print] PubMed PMID: 27150644.
10)

Lee JY, Ebel H, Ernestus RI, Klug N. Various surgical treatments of chronic subdural hematoma and outcome in 172 patients: is membranectomy necessary? Surg Neurol. 2004 Jun;61(6):523-7; discussion 527-8. PubMed PMID: 15165784.
11)

Matsumoto K, Akagi K, Abekura M, Ryujin H, Ohkawa M, Iwasa N, Akiyama C. Recurrence factors for chronic subdural hematomas after burr-hole craniostomy and closed system drainage. Neurol Res. 1999 Apr;21(3):277-80. PubMed PMID: 10319336.
12)

Yamamoto H, Hirashima Y, Hamada H, Hayashi N, Origasa H, Endo S. Independent predictors of recurrence of chronic subdural hematoma: results of multivariate analysis performed using a logistic regression model. J Neurosurg. 2003 Jun;98(6):1217-21. PubMed PMID: 12816267.
13)

Pang CH, Lee SE, Kim CH, Kim JE, Kang HS, Park CK, Paek SH, Kim CH, Jahng TA, Kim JW, Kim YH, Kim DG, Chung CK, Jung HW, Yoo H. Acute intracranial bleeding and recurrence after bur hole craniostomy for chronic subdural hematoma. J Neurosurg. 2015 Jul;123(1):65-74. doi: 10.3171/2014.12.JNS141189. Epub 2015 Feb 13. PubMed PMID: 25679282.
14)

Balser D, Rodgers SD, Johnson B, Shi C, Tabak E, Samadani U. Evolving management of symptomatic chronic subdural hematoma: experience of a single institution and review of the literature. Neurol Res. 2013 Apr;35(3):233-42. doi: 10.1179/1743132813Y.0000000166. Review. PubMed PMID: 23485050.
15)

Xu FF, Chen JH, Leung GK, Hao SY, Xu L, Hou ZG, Mao X, Shi GZ, Li JS, Liu BY. Quantitative computer tomography analysis of post-operative subdural fluid volume predicts recurrence of chronic subdural haematoma. Brain Inj. 2014;28(8):1121-6. doi: 10.3109/02699052.2014.910702. Epub 2014 May 6. PubMed PMID: 24801643.
16)

Pripp AH, Stanišić M. The Correlation between Pro- and Anti-Inflammatory Cytokines in Chronic Subdural Hematoma Patients Assessed with Factor Analysis. PLoS One. 2014 Feb 27;9(2):e90149. doi: 10.1371/journal.pone.0090149. eCollection 2014. PubMed PMID: 24587250.
17)

Adachi A, Higuchi Y, Fujikawa A, Machida T, Sueyoshi S, Harigaya K, Ono J, Saeki N. Risk factors in chronic subdural hematoma: comparison of irrigation with artificial cerebrospinal fluid and normal saline in a cohort analysis. PLoS One. 2014 Aug 4;9(8):e103703. doi: 10.1371/journal.pone.0103703. eCollection 2014. PubMed PMID: 25089621; PubMed Central PMCID: PMC4121178.
18)

Desai VR, Scranton RA, Britz GW. Management of Recurrent Subdural Hematomas. Neurosurg Clin N Am. 2017 Apr;28(2):279-286. doi: 10.1016/j.nec.2016.11.010. Epub 2017 Jan 4. Review. PubMed PMID: 28325462.
19)

Matsumoto H, Hanayama H, Okada T, Sakurai Y, Minami H, Masuda A, Tominaga S, Miyaji K, Yamaura I, Yoshida Y, Yoshida K. Clinical investigation of refractory chronic subdural hematoma: a comparison of clinical factors between single and repeated recurrences. World Neurosurg. 2017 Aug 24. pii: S1878-8750(17)31402-X. doi: 10.1016/j.wneu.2017.08.101. [Epub ahead of print] PubMed PMID: 28844917.
20)

Sato M, Iwatsuki K, Akiyama C, Masana Y, Yoshimine T, Hayakawa T. [Use of Ommaya CSF reservoir for refractory chronic subdural hematoma]. No Shinkei Geka. 1999 Apr;27(4):323-8. Japanese. PubMed PMID: 10347846.
21)

Sato M, Iwatsuki K, Akiyama C, Kumura E, Yoshimine T. Implantation of a reservoir for refractory chronic subdural hematoma. Neurosurgery. 2001 Jun;48(6):1297-301. PubMed PMID: 11383733.
22)

Laumer R. Implantation of a reservoir for refractory chronic subdural hematoma. Neurosurgery. 2002 Mar;50(3):672. PubMed PMID: 11841742.
23)

Misra M, Salazar JL, Bloom DM. Subdural-peritoneal shunt: treatment for bilateral chronic subdural hematoma. Surg Neurol. 1996 Oct;46(4):378-83. PubMed PMID: 8876720.
24)

Mandai S, Sakurai M, Matsumoto Y. Middle meningeal artery embolization for refractory chronic subdural hematoma. Case report. J Neurosurg. 2000 Oct;93(4):686-8. PubMed PMID: 11014549.
25)

Takahashi K, Muraoka K, Sugiura T, Maeda Y, Mandai S, Gohda Y, Kawauchi M, Matsumoto Y. [Middle meningeal artery embolization for refractory chronic subdural hematoma: 3 case reports]. No Shinkei Geka. 2002 May;30(5):535-9. Japanese. PubMed PMID: 11993178.
26)

Hirai S, Ono J, Odaki M, Serizawa T, Nagano O. Embolization of the Middle Meningeal Artery for Refractory Chronic Subdural Haematoma. Usefulness for Patients under Anticoagulant Therapy. Interv Neuroradiol. 2004 Dec 24;10 Suppl 2:101-4. Epub 2008 May 15. PubMed PMID: 20587257; PubMed Central PMCID: PMC3522210.
27)

Tsukamoto Y, Oishi M, Shinbo J, Fujii Y. Transarterial embolisation for refractory bilateral chronic subdural hematomas in a case with dentatorubral-pallidoluysian atrophy. Acta Neurochir (Wien). 2011 May;153(5):1145-7. doi: 10.1007/s00701-010-0891-3. Epub 2010 Dec 2. PubMed PMID: 21125409.
28)

Mino M, Nishimura S, Hori E, Kohama M, Yonezawa S, Midorikawa H, Kaimori M, Tanaka T, Nishijima M. Efficacy of middle meningeal artery embolization in the treatment of refractory chronic subdural hematoma. Surg Neurol Int. 2010 Dec 13;1:78. doi: 10.4103/2152-7806.73801. PubMed PMID: 21206540; PubMed Central PMCID: PMC3011107.
29)

Hashimoto T, Ohashi T, Watanabe D, Koyama S, Namatame H, Izawa H, Haraoka R, Okada H, Ichimasu N, Akimoto J, Haraoka J. Usefulness of embolization of the middle meningeal artery for refractory chronic subdural hematomas. Surg Neurol Int. 2013 Aug 19;4:104. doi: 10.4103/2152-7806.116679. eCollection 2013. PubMed PMID: 24032079; PubMed Central PMCID: PMC3766342.
30)

Kim E. Embolization Therapy for Refractory Hemorrhage in Patients with Chronic Subdural Hematomas. World Neurosurg. 2017 May;101:520-527. doi: 10.1016/j.wneu.2017.02.070. Epub 2017 Feb 27. PubMed PMID: 28249828.
31)

Chihara H, Imamura H, Ogura T, Adachi H, Imai Y, Sakai N. Recurrence of a Refractory Chronic Subdural Hematoma after Middle Meningeal Artery Embolization That Required Craniotomy. NMC Case Rep J. 2014 May 9;1(1):1-5. doi: 10.2176/nmccrj.2013-0343. eCollection 2014 Oct. PubMed PMID: 28663942; PubMed Central PMCID: PMC5364934.

UpToDate: Spontaneous posterior fossa subdural hematoma

Spontaneous posterior fossa subdural hematoma

Posterior fossa subdural hematomas may be spontaneous, with no previous trauma. These cases are usually secondary to bleeding from an underlying pathology such as arteriovenous malformation (AVM), aneurysm 1),tumor or coagulation disorder2) 3).

see also Spontaneous retroclival subdural hematoma.

Posterior fossa craniectomy may be preferable in terms of diagnosis and safe treatment 4).

Outcome

Prognosis seems to be related to the clinical condition of the patient at the moment of surgery, according to the GCS. Patients with mild symptomatology usually have a good outcome, whereas, in most cases, there is no improvement if a moderate or severe neurologic deficit has already been established 5) 6).

Case reports

Finger G, Martins OG, Basso LS, Ludwig do Nascimento T, Schiavo FL, Cezimbra Dos Santos S, Stefani MA. Acute spontaneous subdural hematoma in posterior fossa: case report with great outcome. World Neurosurg. 2018 Aug 1. pii: S1878-8750(18)31700-5. doi: 10.1016/j.wneu.2018.07.220. [Epub ahead of print] PubMed PMID: 30077031.


A 69-year-old woman was admitted with nausea, headache, and mild consciousness disturbance. Computed tomography and magnetic resonance imaging showed bilateral pCSH. To prevent further neurological deterioration, we performed surgery under general anesthesia by midline suboccipital craniectomy. Unexpected bleeding from a developed circuitous occipital sinus was stopped with hemoclips. After hematoma removal, she recovered and was transferred to a rehabilitation hospital. By the 19(th) postoperative day, she had developed no neurologic deficits.

This experience demonstrates the risk of blind surgical therapy in patients with pCSH. In such patients, posterior fossa craniectomy may be preferable in terms of diagnosis and safe treatment 7).


A 83-year-old woman was admitted with recent sudden headache and dizziness. Magnetic resonance imaging showed a thin collection of blood in the subdural space adjacent to the clivus, along the wall of the posterior fossa, and at the cervical spine level. A right posterior communicating artery aneurysm was diagnosed using computed tomography angiography and digital subtraction angiography. The aneurysm had two lobes, one of which was attached to the right dorsum sellae. The aneurysm was occluded by stent-assisted coil embolization. The patient was discharged 3 weeks after admission with absence of neurological deficit.

A ruptured aneurysm of the posterior communicating artery may cause an acute SDH 8).


A rare case of concomitant cranial and spinal subdural haematoma (SDH) in a 12-year-old boy with severe thrombocytopenia due to aplastic anaemia, and review the available literature. Magnetic resonance (MR) imaging at presentation revealed a cranial SDH confined to the posterior fossa, and spinal SDH extending from the C1 to S3 segments. The child was managed conservatively due to his poor general condition and lack of any neurological deficit. Repeat MR imaging done at six weeks showed complete resolution of the spinal SDH and partial resolution of the cranial SDH. Although rare, a spontaneous spinal SDH can occur simultaneously with a cranial SDH. Urgent surgical decompression is considered the treatment of choice for spinal SDH; however, a conservative approach may succeed in patients with poor general condition, and/or mild/no neurological deficit 9).


Berhouma M, Houissa S, Jemel H, Khaldi M. Spontaneous chronic subdural hematoma of the posterior fossa. J Neuroradiol. 2007 Jul;34(3):213-5. PubMed PMID: 17572494 10).


Usul et al., present a spontaneous posterior fossa subdural hematoma in a term neonate and discuss conservative management 11).


A case of spontaneous acute subdural haematoma in the posterior fossa following anticoagulation 12).


The association of the posterior fossa chronic subdural hematoma with spontaneous parenchymal hemorrhage without anticoagulation therapy was never related in the literature. Costa et al., describe a case of a 64 year-old woman who suffered a spontaneous cerebellar hemorrhage, treated conservatively, and presented 1 month later with a chronic subdural posterior fossa hematoma 13).


Miranda et al., present a case of a posterior fossa acute subdural hematoma occurring in an anticoagulated patient who was preoperatively misdiagnosed as an intracerebellar hemorrhage 14).


A 52-year-old woman treated for acute myeloproliferative disease developed progressive stupor. CT showed obstructive hydrocephalus resulting from unexplained mass effect on the fourth ventricle. MRI revealed bilateral extra-axial collections in the posterior cranial fossa, giving high signal on T1- and T2-weighted images, suggesting subacute subdural haematomas. Subdural haematomas can be suspected on CT when there is unexplained mass effect. MRI may be essential to confirm the diagnosis and plan appropriate treatment 15).


A 70 year old female presented with progressive dizziness, vertigo and gait ataxia. She was on anticoagulation therapy for heart disease. Neuro-imaging revealed bilateral infratentorial subdural masses. The subdural masses were suspects for chronic subdural haematomas by neuroradiological criteria. Because of the progressive symptomatology, the haematomas were emptied through burrhole trepanations. Chocolate-colored fluid, not containing clotted components, gushed out under great pressure. The source of bleeding could not be identified. The patient recovered well from surgery, but died 4 months later shortly after admission to another hospital from heart failure.

The chronic subdural haematomas in this patient may have been due to rupture of bridging veins caused by a very mild trauma not noticed by the patient and possibly aggravated by the anticoagulation therapy. Infratentorial chronic subdural haematoma should at least be a part of the differential diagnosis in elderly patients with cerebellar and vestibular symptomatology even without a history of trauma 16).


A case of spontaneous acute subdural hematoma complicated with idiopathic thrombocytopenic purpura was reported. He was hospitalized complaining of sudden onset of headache and nasal bleeding without neurological deficit. CT scan revealed subdural hematoma in the posterior fossa especially below the tentorium cerebelli. Further hematological examination proved very low platelet count (1,000/mm3) and antiplatelet antibody in confirmation of a diagnosis of idiopathic thrombocytopenic purpura. As his neurological status was good, he was treated medically. His symptoms and platelet count improved gradually with corticosteroid therapy. Reviewing the literature, acute subdural hematoma with idiopathic thrombocytopenic purpura was quite rare and only three cases reported 17).


Aicher KP, Heiss E, Gawlowski J. [Spontaneous subdural hematoma in the posterior cranial fossa]. Rofo. 1988 Dec;149(6):669-70. German. PubMed PMID: 2849170 18).


Kanter et al., report a patient in whom a spontaneous subdural hematoma developed in the posterior fossa during anticoagulation therapy for mitral valve disease. This rare complication of anticoagulation has been reported in only three other patients 19).


A case of spontaneous posterior fossa subdural hematoma secondary to anticoagulation therapy with definitive diagnosis made by vertebral angiography is reported. Vertebral angiographic findings are illustrated and demonstrate primarily mass effect from posterior compartment of posterior fossa and avascular area. Carotid angiography did not show hydrocephalus. A review of the literature was made and this appears to be the first reported case in which a posterior fossa subdural hematoma has been diagnosed by vertebral angiography 20).


A report of spontaneous posterior fossa subdural haematoma associated with anticoagulation therapy. The possibility of posterior fossa lesions related to spontaneous haemorrhage is suggested by the combination of severe headache and increasing disturbance of consciousness associated with signs of brain-stem decompensation. A thorough neurological evaluation including appropriate contrast studies will help rule out a supratentorial lesion. This is a neurological emergency which can be successfully treated by early detection and prompt surgical decompression. This is the second reported case of spontaneous subdural haematoma of the posterior fossa occurring during anticoagulant therapy 21).

References

1) , 8)

Kim MS, Jung JR, Yoon SW, Lee CH. Subdural hematoma of the posterior fossa due to posterior communicating artery aneurysm rupture. Surg Neurol Int. 2012;3:39. doi: 10.4103/2152-7806.94287. Epub 2012 Mar 24. PubMed PMID: 22530173; PubMed Central PMCID: PMC3327002.
2) , 16)

Stendel R, Schulte T, Pietilä TA, Suess O, Brock M. Spontaneous bilateral chronic subdural haematoma of the posterior fossa. Case report and review of the literature. Acta Neurochir (Wien). 2002 May;144(5):497-500. Review. PubMed PMID: 12111507.
3) , 10)

Berhouma M, Houissa S, Jemel H, Khaldi M. Spontaneous chronic subdural hematoma of the posterior fossa. J Neuroradiol. 2007 Jul;34(3):213-5. PubMed PMID: 17572494.
4) , 7)

Takemoto Y, Matsumoto J, Ohta K, Hasegawa S, Miura M, Kuratsu J. Bilateral posterior fossa chronic subdural hematoma treated with craniectomy: Case report and review of the literature. Surg Neurol Int. 2016 May 6;7(Suppl 10):S255-8. doi: 10.4103/2152-7806.181979. eCollection 2016. PubMed PMID: 27213111; PubMed Central PMCID: PMC4866054.
5) , 14)

Miranda P, Alday R, Lagares A, Pérez A, Lobato RD. Posterior fossa subdural hematoma mimicking intracerebellar hemorrhage. Neurocirugia (Astur). 2003 Dec;14(6):526-8. PubMed PMID: 14710308.
6) , 15)

Pollo C, Meuli R, Porchet F. Spontaneous bilateral subdural haematomas in the posterior cranial fossa revealed by MRI. Neuroradiology. 2003 Aug;45(8):550-2. Epub 2003 May 22. PubMed PMID: 12761603.
9)

Jain V, Singh J, Sharma R. Spontaneous concomitant cranial and spinal subdural haematomas with spontaneous resolution. Singapore Med J. 2008 Feb;49(2):e53-8. Review. PubMed PMID: 18301828.
11)

Usul H, Karaarslan G, Cakir E, Kuzeyl K, Mungan L, Baykal S. Conservative management of spontaneous posterior fossa subdural hematoma in a neonate. J Clin Neurosci. 2005 Feb;12(2):196-8. PubMed PMID: 15749432.
12)

Pal D, Gnanalingham K, Peterson D. A case of spontaneous acute subdural haematoma in the posterior fossa following anticoagulation. Br J Neurosurg. 2004 Feb;18(1):68-9. PubMed PMID: 15040720.
13)

Costa LB Jr, de Andrade A, Valadão GF. Chronic subdural hematoma of the posterior fossa associated with cerebellar hemorrhage: report of rare disease with MRI findings. Arq Neuropsiquiatr. 2004 Mar;62(1):170-2. Epub 2004 Apr 28. PubMed PMID: 15122456.
17)

Saito K, Sakurai Y, Uenohara H, Seki K, Imaizumi S, Katakura R, Niizuma H. [A case of acute subdural hematoma in the posterior fossa with idiopathic thrombocytopenic purpura]. No To Shinkei. 1992 Apr;44(4):377-81. Review. Japanese. PubMed PMID: 1633035.
18)

Aicher KP, Heiss E, Gawlowski J. [Spontaneous subdural hematoma in the posterior cranial fossa]. Rofo. 1988 Dec;149(6):669-70. German. PubMed PMID: 2849170.
19)

Kanter R, Kanter M, Kirsch W, Rosenberg G. Spontaneous posterior fossa subdural hematoma as a complication of anticoagulation. Neurosurgery. 1984 Aug;15(2):241-2. PubMed PMID: 6483141.
20)

McClelland RR, Ramirez-Lassepas M. Posterior fossa subdural hematoma demonstrated by vertebral angiography. Neuroradiology. 1976;10(1):181-5. PubMed PMID: 1256644.
21)

Capistrant T, Goldberg R, Shibasaki H, Castle D. Posterior fossa subdural haematoma associated with anticoagulant therapy. J Neurol Neurosurg Psychiatry. 1971 Feb;34(1):82-5. PubMed PMID: 5313648; PubMed Central PMCID: PMC493691.

UpToDate: Subdural osteoma

Subdural osteoma

Subdural osteomas are benign neoplasms that are rarely encountered.

Case reports

Yang et al., report the case of a 64‑year‑old female patient with a left temporal subdural osteoma.

The patient presented with intermittent dizziness that first began two years earlier. Non-contrast computed tomography revealed a densely calcified left temporal extra-axial mass. Magnetic resonance imaging of the lesion revealed signal loss on T1-weighted and T2-weighted images and non-enhancement on Gadolinium enhanced T1-weighted images, and Diffusion weighted magnetic resonance imaging and ADC images demonstrated reduced values attributed to calcium-induced signal loss. Histologically, the lesion predominantly consisted of lamellar bone without bone marrow elements. The patient underwent stereotactic magnetic resonance imaging-guided neurosurgical resection and recovered without complication.

Subdural osteomas may not be enhanced on magnetic resonance imaging. Surgical tumourectomy can be considered for symptomatic patients with subdural osteomas 1).


A 29-year-old female presented with a 3-year history of headaches. Computed tomography scan revealed a homogeneous high-density lesion isolated from the inner table of the frontal bone (a lucent dural line) in the right frontal convexity. Magnetic resonance imaging revealed an extra-axial lesion with a broad base without dural tail sign and punctate enhancement pattern characteristic of abundant adipose tissue. Upon surgical excision, we found a hard bony mass clearly demarcated from the dura. The mass displayed characteristics of an osteoma upon histological examination. The symptom was relieved after operation 2).


Cheon JE, Kim JE, Yang HJ. CT and pathologic findings of a case of subdural osteoma. Korean J Radiol. 2002;3:211–213.


Kim JK, Lee KJ, Cho JK, et al. Intracranial intraparenchymal ostemoa. J Korean Neurosurg Soc. 1998;27:1450–1454.


Jung TY, Jung S, Jin SG, Jin YH, Kim IY, Kang SS. Solitary intracranial subdural osteoma: intraoperative findings and primary anastomosis of an involved cortical vein. J Clin Neurosci. 2007;14:468–470.


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Yang H, Niu L, Zhang Y, Jia J, Li Q, Dai J, Duan L, Pan Y. Solitary subdural osteoma: A case report and literature review. Clin Neurol Neurosurg. 2018 Jul 2;172:87-89. doi: 10.1016/j.clineuro.2018.07.004. [Epub ahead of print] PubMed PMID: 29986201.
2)

Kim EY, Shim YS, Hyun DK, Park H, Oh SY, Yoon SH. Clinical, Radiologic, and Pathologic Findings of Subdural Osteoma: A Case Report. Brain Tumor Res Treat. 2016 Apr;4(1):40-3. doi: 10.14791/btrt.2016.4.1.40. Epub 2016 Apr 29. PubMed PMID: 27195262; PubMed Central PMCID: PMC4868817.

Update: Computed Tomography for chronic subdural hematoma

Computed Tomography for chronic subdural hematoma

The routine use of Head computed tomography in most emergency facilities has made the diagnosis of a chronic subdural hematoma commonplace 1).
Density of the chronic subdural hematoma (cSDH) is variable. It often appears to be mixed density. Multiple densities of cSDH may result from multiple episodes of trauma, usually in the aged. It is hard to remember all the trivial traumas for the patients with the mixed density cSDHs.
CT-scan is able to provide the diagnosis of chronic subdural hematoma in more than 90% of the cases. It usually shows a peri-cerebral fluid collection along the convexity, with a convex outer border, and an irregular concave inner border. The density of the collection depends on the age of the intracranial hematoma. The main difficulties, in term of diagnosis, result from bilateral isodense chronic subdural hematoma, and differential diagnosis between hematoma, subdural hygroma, and subdural empyema. Some rare localisations can sometimes be seen (posterior fossa, skull base…). A double density with a sedimentation level, or heterogeneity of the hematoma, can sometimes be seen too 2).

Classification

The cSDHs can be classified into four groups; hypodensity, homogeneous isodensity, layered type, and mixed type on the basis of CT scans 3).

Routine Brain Computed Tomography after Evacuation

Routine post-operative CT brain for burr hole drainage of CSDH may be unnecessary in view of the good predictive value of pre-operative volume, and also because it is not predictive of the clinical outcome 4).
A study of Ng et al. compared pre-operative and early post-operative CT findings to determine the factors affecting residual hematoma and evaluate if early post-operative CT scans are useful in the management of CSDH.
Forty-three patients who underwent burr hole drainage of unilateral CSDH from August 2006 to January 2013 and had routine post-operative CT scans within 48 hours of surgery were selected. Data regarding age, sex, neurological deficit, Glasgow Coma Scale (GCS), pre-existing medical conditions, use of antiplatelets or anticoagulation, operative time, usage of drains, and number of burr holes were obtained. The pre-operative CSDH volume, CSDH density, and midline shift were measured. Residual volume was calculated from early post-operative CT scans. Clinical outcome was evaluated with Glasgow Outcome Scale (GOS) at the time of discharge. Statistical analysis was performed to look for correlation between the pre-operative factors and residual volume, and the residual volume and GOS.
Pre-operative volume was found to correlate significantly with post-operative residual volume. There was no significant correlation between all other pre-operative factors and residual volume. There was also no correlation between residual volume and GOS at discharge 5).


Routinely postoperative control brain CT scan 4 to 6 weeks after the evacuation of a CSDH has no clinical value 6).
In a retrospective study Pedersen et al. examined 202 patients who during a 2-year period from 2011 and 2012 underwent surgical treatment for chronic subdural hematoma (CSDH). Information on patient age, sex, alcohol consumption, anticoagulant/antiplatelet treatment, history of head trauma, Glasgow coma scale (GCS), neurological symptoms, laterality of CSDH, and surgical technique was retrieved from patient charts.
Overall, 27 out of 202 patients had a recurrence of CSDH and re-evacuation of the hematoma was performed. In all patients recurrence of neurological symptoms preceded the planned postoperative control brain CT 4 to 6 weeks after primary surgery.
Routinely postoperative control brain CT scan 4 to 6 weeks after the evacuation of a CSDH has no clinical value 7).
1)

Chen JC, Levy ML. Causes, epidemiology, and risk factors of chronic subdural hematoma. Neurosurg Clin N Am. 2000 Jul;11(3):399-406. Review. PubMed PMID: 10918008.
2)

Guénot M. [Chronic subdural hematoma: diagnostic imaging studies]. Neurochirurgie. 2001 Nov;47(5):473-8. French. PubMed PMID: 11915760.
3)

Park HR, Lee KS, Shim JJ, Yoon SM, Bae HG, Doh JW. Multiple Densities of the Chronic Subdural Hematoma in CT Scans. J Korean Neurosurg Soc. 2013 Jul;54(1):38-41. doi: 10.3340/jkns.2013.54.1.38. Epub 2013 Jul 31. PubMed PMID: 24044079; PubMed Central PMCID: PMC3772285.
4) , 5)

Ng HY, Ng WH, King NK. Value of routine early post-operative computed tomography in determining short-term functional outcome after drainage of chronic subdural hematoma: An evaluation of residual volume. Surg Neurol Int. 2014 Sep 19;5:136. doi: 10.4103/2152-7806.141299. eCollection 2014. PubMed PMID: 25298918; PubMed Central PMCID: PMC4174672.
6) , 7)

Pedersen CB, Sundbye F, Poulsen FR. No Value of Routine Brain Computed Tomography 6 Weeks after Evacuation of Chronic Subdural Hematoma. Surg J (N Y). 2017 Nov 27;3(4):e174-e176. doi: 10.1055/s-0037-1607215. eCollection 2017 Oct. PubMed PMID: 29184916; PubMed Central PMCID: PMC5703687.

Update: Atorvastatin for chronic subdural hematoma

Atorvastatin for chronic subdural hematoma

It is well known that inflammation influence chronic subdural hematoma (CSDH) formation to a large extent. Atorvastatin has pleiotropic effects on restraining inflammation and promoting angiogenesis besides its cholesterol-lowering function. Hence, atorvastatin may induce anti-inflammation effects and facilitate therapeutic effects for subdural hematoma (SDH).
Atorvastatin treatment may eliminate SDH and improve the neural function of the rats through its anti-inflammatory effects. Hence, it indicated that statin induced inflammatory modulation might play a significant role in rats 1).


Results of a preliminary prospective study showed that oral administration of atorvastatin is safe and effective in treating CSDH, offering a cost-effective alternative to surgery. A prospective randomized clinical trial is required to validate the effect of atorvastatin 2). 3).


Jiang et al. reported a clinical research trial protocol that was designed to evaluate the therapeutic effects of atorvastatin on CSDH 4).
Limited evidence suggests that oral atorvastatin may be beneficial in the management of CSDH. Further high-quality studies focused on dosage, duration, hematoma size are needed to further elucidate the role of atorvastatin in the management of CSDH 5).
A retrospective cohort comparison study has shown that CSDH with Atorvastatin had a lower rate of deterioration and burr-hole drainage 6).
The knowledge of the conservative treatment modalities for cSDH is sparse and based on small case series and low grade evidence. However, some treatment modalities seem promising even in symptomatic patients with large haematomas. Randomised controlled trials are currently underway, and will hopefully provide us with good evidence for or against the conservative treatment of cSDH 7).

Retracted articles

Atorvastatin administration may decrease the risks of recurrence.Patients with severe brain atrophy and bilateral CSDH are prone to the recurrence 8) is a retracted article 9).
Effect of atorvastatin on resolution of chronic subdural hematoma: a prospective observational study [RETRACTED] 10).
1)

Li T, Wang D, Tian Y, Yu H, Wang Y, Quan W, Cui W, Zhou L, Chen J, Jiang R, Zhang J. Effects of atorvastatin on the inflammation regulation and elimination of subdural hematoma in rats. J Neurol Sci. 2014 Jun 15;341(1-2):88-96. doi: 10.1016/j.jns.2014.04.009. Epub 2014 Apr 13. PubMed PMID: 24774750.
2)

Wang D, Li T, Tian Y, Wang S, Jin C, Wei H, Quan W, Wang J, Chen J, Dong J, Jiang R, Zhang J. Effects of atorvastatin on chronic subdural hematoma: a preliminary report from three medical centers. J Neurol Sci. 2014 Jan 15;336(1-2):237-42. doi: 10.1016/j.jns.2013.11.005. Epub 2013 Nov 14. PubMed PMID: 24269089.
3)

Xu M, Chen P, Zhu X, Wang C, Shi X, Yu B. Effects of Atorvastatin on Conservative and Surgical Treatments of Chronic Subdural Hematoma in Patients. World Neurosurg. 2016 Jul;91:23-8. doi: 10.1016/j.wneu.2016.03.067. Epub 2016 Mar 29. PubMed PMID: 27044372.
4)

Jiang R, Wang D, Poon WS, Lu YC, Li XG, Zhao SG, Wang RZ, You C, Yuan XR, Zhang JM, Feng H, Fei Z, Yu XG, Zhao YL, Hu J, Kang DZ, Yu RT, Gao GD, Zhu XD, Sun T, Hao JH, Liu XZ, Su N, Yue SY, Zhang JN. Effect of ATorvastatin On Chronic subdural Hematoma (ATOCH): a study protocol for a randomized controlled trial. Trials. 2015 Nov 18;16:528. doi: 10.1186/s13063-015-1045-y. PubMed PMID: 26581842; PubMed Central PMCID: PMC4652431.
5)

Qiu S, Zhuo W, Sun C, Su Z, Yan A, Shen L. Effects of atorvastatin on chronic subdural hematoma: A systematic review. Medicine (Baltimore). 2017 Jun;96(26):e7290. doi: 10.1097/MD.0000000000007290. Review. PubMed PMID: 28658127; PubMed Central PMCID: PMC5500049.
6)

Chan DY, Chan DT, Sun TF, Ng SC, Wong GK, Poon WS. The use of atorvastatin for chronic subdural haematoma: a retrospective cohort comparison study(). Br J Neurosurg. 2017 Feb;31(1):72-77. doi: 10.1080/02688697.2016.1208806. Epub 2016 Nov 23. PubMed PMID: 27881024.
7)

Soleman J, Noccera F, Mariani L. The conservative and pharmacological management of chronic subdural haematoma. Swiss Med Wkly. 2017 Jan 19;147:w14398. doi: smw.2017.14398. PubMed PMID: 28102879.
8)

Liu H, Luo Z, Liu Z, Yang J, Kan S. Atorvastatin May Attenuate Recurrence of Chronic Subdural Hematoma. Front Neurosci. 2016 Jun 28;10:303. doi: 10.3389/fnins.2016.00303. eCollection 2016. Retraction in: Front Neurosci. 2016 Oct 07;10 :465. PubMed PMID: 27445673; PubMed Central PMCID: PMC4923224.
9)

Frontiers Editorial Office. Retraction: Atorvastatin May Attenuate Recurrence of Chronic Subdural Hematoma. Front Neurosci. 2016 Oct 7;10:465. eCollection 2016. PubMed PMID: 27738420; PubMed Central PMCID: PMC5054353.
10)

Liu H, Liu Z, Liu Y, Kan S, Yang J, Liu H. Effect of atorvastatin on resolution of chronic subdural hematoma: a prospective observational study [RETRACTED]. J Neurosurg. 2016 Jul 29:1-10. doi: 10.3171/2015.12.JNS151991. [Epub ahead of print] Retraction in: J Neurosurg. 2017 Feb;126(2):651. PubMed PMID: 27471887.

Update: Chronic subdural hematoma recurrence

Chronic subdural hematoma recurrence

Epidemiology

Recurrence rates after chronic subdural hematoma (CSDH) evacuation with any of actual techniques twist drill craniostomy (TDC), burr hole craniostomy, craniotomy range from 5% to 30%. 1)

Risk factors

In the series of Han et al. independent risk factors for recurrence were as follows: age > 75 years (HR 1.72, 95% CI 1.03-2.88; p = 0.039), obesity (body mass index ≥ 25.0 kg/m2), and a bilateral operation 2).
Chon et al. shown that postoperative midline shifting (≥5 mm), diabetes mellitus, preoperative seizure, preoperative width of hematoma (≥20 mm), and anticoagulant therapy were independent predictors of the recurrence of chronic subdural hematoma.
According to internal architecture of hematoma, the rate of recurrence was significantly lower in the homogeneous and the trabecular type than the laminar and separated type 3).
see Chronic subdural hematoma and anticoagulant therapy.


The recurrence rate of chronic subdural hematoma cSDH seems to be related to the excessive neoangiogenesis in the parietal membrane, which is mediated via vascular endothelial growth factor (VEGF). This is found to be elevated in the hematoma fluid and is dependent on eicosanoid/prostaglandin and thromboxane synthesis via cyclooxygenase-2 (COX-2).


Antiplatelet therapy

Antiplatelet therapy significantly influences the recurrence of CSDH 4).

Pneumocephalus

Remaining pneumocephalus is seen as an approved factor of recurrence 5) 6).

Septation

Jack et al.found a 12% reoperation rate. CSDH septation (seen on computed tomogram scan) was found to be an independent risk factor for recurrence requiring reoperation (p=0.04). Larger post-operative subdural haematoma volume was also significantly associated with requiring a second drainage procedure (p<0.001). Independent risk factors of larger post-operative haematoma volume included septations within a CSDH (p<0.01), increased pre-operative haematoma volume (p<0.01), and a greater amount of parenchymal atrophy (p=0.04). A simple scoring system for quantifying recurrence risk was created and validated based on patient age (< or ≥80 years), haematoma volume (< or ≥160cc), and presence of septations within the subdural collection (yes or no).
Septations within CSDHs are associated with larger post-operative residual haematoma collections requiring repeat drainage. When septations are clearly visible within a CSDH, craniotomy might be more suitable as a primary procedure as it allows greater access to a septated subdural collection. The proposed scoring system combining haematoma volume, age, and presence of septations might be useful in identifying patients at higher risk for recurrence 7).

Membranectomy

Opening the internal hematoma membrane does not alter the rate of patients requiring revision surgery and the number of patients showing a marked residual hematoma six weeks after evacuation of a CSDH 8).
In the study of Lee et al, an extended surgical approach with partial membranectomy has no advantages regarding the rate of reoperation and the outcome. As initial treatment, burr-hole drainage with irrigation of the hematoma cavity and closed-system drainage is recommended. Extended craniotomy with membranectomy is now reserved for instances of acute rebleeding with solid hematoma 9).

Diabetes

Surgeons should consider informing patients with diabetes mellitus that this comorbidity is associated with an increased likelihood of recurrence
10) 11) 12).


Balser et al. report 11% recurrence, which included individuals who recurred as late as 3 years after initial diagnosis 13).
Close imaging follow-up is important for CSDH patients for recurrence prediction. Using quantitative CT volumetric analysis, strong evidence was provided that changes in the residual fluid volume during the ‘self-resolution’ period can be used as significantly radiological predictors of recurrence 14).
A structural equation model showed a significant association between increased antiinflammatory activity in hematoma fluid samples and a lower risk of recurrence, but this relationship was not statistically significant in venous blood samples. Moreover, these findings indicate that anti-inflammatory activities in the hematoma may play a role in the risk of a recurrence of CSDH 15).
Irrigation with artificial cerebrospinal fluid (ACF) decreased the rate of CSDH recurrence 16).

Treatment

There is no definite operative procedure for patients with intractable chronic subdural hematoma (CSDH).
Most recurrent hematomas are managed successfully with burr hole craniostomies with postoperative closed-system drainage. Refractory hematomas may be managed with a variety of techniques, including craniotomy or subdural-peritoneal shunt placement 17).
Although many studies have reported risk factors or treatments in efforts to prevent recurrence, those have focused on single recurrence, and little cumulative data is available to analyze refractory CSDH.
Matsumoto et al. defined refractory CSDH as ≥2 recurrences, then analyzed and compared clinical factors between patients with single recurrence and those with refractory CSDH in a cohort study, to clarify whether patients with refractory CSDH experience different or more risk factors than patients with single recurrence, and whether burr-hole irrigation with closed-system drainage reduces refractory CSDH.
Seventy-five patients had at least one recurrence, with single recurrence in 62 patients and ≥2 recurrences in 13 patients. In comparing clinical characteristics, patients with refractory CSDH were significantly younger (P=0.04) and showed shorter interval to first recurrence (P<0.001). Organized CSDH was also significantly associated with refractory CSDH (P=0.02). Multivariate logistic regression analysis identified first recurrence interval <1 month (OR 6.66, P<0.001) and age <71 years (OR 4.16, P<0.001) as independent risk factors for refractory CSDH. On the other hand, burr-hole irrigation with closed-system drainage did not reduce refractory CSDH.
When patients with risk factors for refractory CSDH experience recurrence, alternative surgical procedures may be considered as the second surgery, because burr-hole irrigation with closed-system drainage did not reduce refractory CSDH 18).
Implantation of a reservoir 19) 20) 21).
Subdural-peritoneal shunt 22).

Middle meningeal artery embolization

Embolization of the MMA is effective for refractory CSDH or CSDH patients with a risk of recurrence, and is considered an effective therapeutic method to stop hematoma enlargement and promote resolution 23) 24) 25) 26) 27) 28).
A pilot study indicated that perioperative middle meningeal artery (MMA) embolization could be offered as the least invasive and most effectual means of treatment for resistant patients of CSDHs with 1 or more recurrences 29).
Chihara et al. have treated three cases of CSDH with MMA embolization to date, but there was a postoperative recurrence in one patient, which required a craniotomy for hematoma removal and capsulectomy. MMA embolization blocks the blood supply from the dura to the hematoma outer membrane in order to prevent recurrences of refractory CSDH. Histopathologic examination of the outer membrane of the hematoma excised during craniotomy showed foreign-body giant cells and neovascular proliferation associated with embolization. Because part of the hematoma was organized in this case, the CSDH did not resolve when the MMA was occluded, and the development of new collateral pathways in the hematoma outer membrane probably contributed to the recurrence. Therefore, in CSDH with some organized hematoma, MMA embolization may not be effective. Magnetic resonance imaging (MRI) should be performed in these patients before embolization 30).

Case series

2017

A retrospective analysis of 756 consecutive patients with CSDH who underwent bur hole surgery at the Hanyang University Medical Center (Seoul and Guri) between January 1, 2004, and December 31, 2014. During the 6-month follow-up, 104 patients (13.8%) with recurrence after surgery for CSDH were identified. Independent risk factors for recurrence were as follows: age > 75 years (HR 1.72, 95% CI 1.03-2.88; p = 0.039), obesity (body mass index ≥ 25.0 kg/m2), and a bilateral operation.
This study determined the risk factors for recurrence of CSDH and their effects on outcomes. Further studies are needed to account for these observations and to determine their underlying mechanisms 31).

2016

Chronic subdural hematomas (cSDHs) have shown an increasing incidence in an ageing population over the last 20 years, while unacceptable recurrence rates of up to 30 % persist. The chronic subdural hematoma recurrence rate seems to be related to the excessive neoangiogenesis in the parietal membrane, which is mediated via vascular endothelial growth factor (VEGF). This is found to be elevated in the haematoma fluid and is dependent on eicosanoid/prostaglandin and thromboxane synthesis via cyclooxygenase-2 (COX 2). With this investigator-initiated trial (IIT) it was thought to diminish the recurrence rate of operated-on cSDHs by administering a selective COX-2 inhibitor (Celecoxib) over 4 weeks’ time postoperatively in comparison to a control group.
The thesis of risk reduction of cSDH recurrence in COX-2-inhibited patients was to be determined in a prospective, randomised, two-armed, open phase-II/III study with inclusion of 180 patients over a 2-year time period in four German university hospitals. The treated- and untreated-patient data were to be analysed by Fisher’s exact test (significance level of alpha, 0.05 [two-sided]).
After screening of 246 patients from January 2009 to April 2010, the study had to be terminated prematurely as only 23 patients (9.3 %) could be enrolled because of on-going non-steroid anti-rheumatic (NSAR) drug treatment or contraindication to Celecoxib medication. In the study population, 13 patients were treated in the control group (six women, seven men; average age 66.8 years; one adverse event (AE)/serious adverse event (SAE) needing one re-operation because of progressive cSDH (7.7 %); ten patients were treated in the treatment group (one woman, nine men; average age 64.7 years; five AEs/SAEs needing two re-operations because of one progressive cSDH and one wound infection [20 %]). Significance levels are obsolete because of insufficient patient numbers.
The theoretical advantage of COX-2 inhibition in the recurrent cSDH could not be transferred into the treatment of German cSDH patients as 66.6 % of the patients showed strict contraindications for Celecoxib. Furthermore, 55 % of the patients were already treated with some kind of COX-2 inhibition and, nevertheless, developed cSDH. Thus, although conceptually appealing, an anti-angiogenic therapy with COX-2 inhibitors for cSDH could not be realised in this patient population due to the high prevalence of comorbidities excluding the administration of COX2 inhibitors 32).

2010

Recurrence rates after chronic subdural hematoma (CSDH) evacuation with any of actual techniques twist drill craniostomy (TDC), burr hole craniostomy, craniotomy range from 5% to 30%. Use of drain has improved recurrence rates when used with burr-hole craniostomy. Now, we analyze predictors of recurrence of TDC with drain.
Three hundred twelve consecutive patients with CSDH have been studied in a retrospective study. Operative technique in all patients consisted in TDC with drain. Data recorded included any associated comorbidity. Radiologic measures of the CSDH before and after the procedure were studied. Clinical evaluation included Modified Rankin Scale, Glasgow Coma Scale (GCS), and neurological deficits. Two groups were compared: recurrence group and nonrecurrence group. Follow-up was for at least 1 year.
Twelve percent experienced recurrence. Preoperative CSDH width, preoperative midline shift, postoperative midline width, postoperative CSDH width, and residual CSDH 1 month later were significantly associated with CSDH recurrence. The logistic regression model for the multivariate analysis revealed that postoperative midline shift and postoperative neurological deficit were significantly associated with CSDH recurrence. The duration of treatment with dexamethasone was found not to be related with recurrence. Mortality before hospital discharge was 1%. Hospital stay was 2.5 days.
TDC with drain has similar results in recurrence rates, morbidity, mortality, and outcome as other techniques as burr-hole craniostomy with drain. Preoperative and postoperative hematoma width and midline shift are independent predictors of recurrence. Brain re-expansion and time of drain maintenance are important factors related with recurrence of CSDH. Future CSDH reservoirs must avoid negative pressure and sudden pressure changes inside the whole closed drain system 33).

Case reports

2016

Mewada et al. report a case with right hemiparesis and aphasia 1 month after a fall from a bicycle. Computed tomography scan of the head showed left chronic subdural hematoma, which was evacuated by burr-hole drainage. The postoperative course was complicated by reaccumulation within short period of time. On superselective digital subtraction angiography of MMA, iatrogenic dAVF was found on left side. We embolized successfully it using n-butyl cyanoacrylate after a third irrigation. No reaccumulation found in the postoperative period or at last follow-up. They proposed a treatment protocol based on the own experience and literature review.
Refractory chronic subdural hematoma with reaccumulation within a short interval should be subjected to digital subtraction angiography of the MMA. Embolization of ipsilateral MMA is safe, effective, and a useful option for the treatment of iatrogenic dAVF and resolution of hematoma 34).


An 85-year-old male presented with left CSDH, which recurred five times. The hematoma was irrigated and drained through a left frontal burr hole during the first to third surgery and through a left parietal burr hole during the fourth and fifth surgery. The hematoma had no septation and was well-evacuated during each surgery. Antiplatelet therapy for preventing ischemic heart disease was stopped after the second surgery, the hematoma cavity was irrigated with artificial cerebrospinal fluid at the third surgery, and the direction of the drainage tube was changed to reduce the postoperative subdural air collection at the fourth surgery. However, none of these interventions was effective. He was successfully treated by fibrin glue injection into the hematoma cavity after the fifth surgery.
This procedure may be effective for refractory CSDH in elderly patients 35).


A 67-year-old man with dural arteriovenous fistula (AVF) presenting as a non-traumatic chronic subdural hematoma (CSDH). This previously healthy patient was hospitalized due to progressive headache with subacute onset. He underwent burr-hole surgery twice for evacuating the left CSDH that was thickest at the posterior temporal area. The operative procedure and finding was not extraordinary, but subdural hematoma slowly progressed for days following the revision surgery. After investigation by super-selective external carotid angiography, a dural AVF found near the transverse-sigmoid sinus was diagnosed. Dural AVF was completely occluded with trans-arterial injecting polyvinyl alchol particles into the petrosquamosal branch of the middle meningeal artery. The patient showed a good neurological outcome with no additional intervention. Brain surgeons have to consider the possibility of dural AVF and perform cerebral angiogram if necessary when they manage the cases that have a spontaneously occurred and repeatedly recurring CSDH 36).

2007

Spontaneous intracranial hypotension (SIH) is reported to cause chronic subdural hematoma (SDH), however diagnosis of SIH in patients with SDH is not always easy.
Takahashi et al. report a case of chronic SDH refractory to repeated drainage, which was attributed to SIH. A forty-five-year-old man who had been suffering from orthostatic headache for one month was admitted to our hospital presenting with unconsciousness and hemiparesis. CT on admission revealed a chronic subdural hematoma, which was successfully treated once with subdural drainage. However, the patient fell into unconscious again with recurrence of the hematoma within several days. After two more sessions of drainage, SIH due to cerebrospinal fluid leakage was diagnosed with spinal magnetic resonance imaging (MRI) and radionuclide cisternography. Spinal MRI demonstrated abnormal fluid accumulation in the thoracic epidural space, and the radionuclide cisternogram showed early excretion of tracer into urine as well as absence of intracranial tracer filling. After treatment with epidural blood patching, the hematoma rapidly disappeared and he was discharged without symptoms. In the treatment of chronic SDH, especially in young to middle aged patient without preceding trauma or hematological disorders, physicians should pay attention to underlying SIH to avoid multiple surgery. MRI of the spine as well as radionuclide cisternography is useful in evaluation of this condition 37).
1) , 33)

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Pang CH, Lee SE, Kim CH, Kim JE, Kang HS, Park CK, Paek SH, Kim CH, Jahng TA, Kim JW, Kim YH, Kim DG, Chung CK, Jung HW, Yoo H. Acute intracranial bleeding and recurrence after bur hole craniostomy for chronic subdural hematoma. J Neurosurg. 2015 Jul;123(1):65-74. doi: 10.3171/2014.12.JNS141189. Epub 2015 Feb 13. PubMed PMID: 25679282.
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Balser D, Rodgers SD, Johnson B, Shi C, Tabak E, Samadani U. Evolving management of symptomatic chronic subdural hematoma: experience of a single institution and review of the literature. Neurol Res. 2013 Apr;35(3):233-42. doi: 10.1179/1743132813Y.0000000166. Review. PubMed PMID: 23485050.
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Xu FF, Chen JH, Leung GK, Hao SY, Xu L, Hou ZG, Mao X, Shi GZ, Li JS, Liu BY. Quantitative computer tomography analysis of post-operative subdural fluid volume predicts recurrence of chronic subdural haematoma. Brain Inj. 2014;28(8):1121-6. doi: 10.3109/02699052.2014.910702. Epub 2014 May 6. PubMed PMID: 24801643.
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Pripp AH, Stanišić M. The Correlation between Pro- and Anti-Inflammatory Cytokines in Chronic Subdural Hematoma Patients Assessed with Factor Analysis. PLoS One. 2014 Feb 27;9(2):e90149. doi: 10.1371/journal.pone.0090149. eCollection 2014. PubMed PMID: 24587250.
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Adachi A, Higuchi Y, Fujikawa A, Machida T, Sueyoshi S, Harigaya K, Ono J, Saeki N. Risk factors in chronic subdural hematoma: comparison of irrigation with artificial cerebrospinal fluid and normal saline in a cohort analysis. PLoS One. 2014 Aug 4;9(8):e103703. doi: 10.1371/journal.pone.0103703. eCollection 2014. PubMed PMID: 25089621; PubMed Central PMCID: PMC4121178.
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Desai VR, Scranton RA, Britz GW. Management of Recurrent Subdural Hematomas. Neurosurg Clin N Am. 2017 Apr;28(2):279-286. doi: 10.1016/j.nec.2016.11.010. Epub 2017 Jan 4. Review. PubMed PMID: 28325462.
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Matsumoto H, Hanayama H, Okada T, Sakurai Y, Minami H, Masuda A, Tominaga S, Miyaji K, Yamaura I, Yoshida Y, Yoshida K. Clinical investigation of refractory chronic subdural hematoma: a comparison of clinical factors between single and repeated recurrences. World Neurosurg. 2017 Aug 24. pii: S1878-8750(17)31402-X. doi: 10.1016/j.wneu.2017.08.101. [Epub ahead of print] PubMed PMID: 28844917.
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Sato M, Iwatsuki K, Akiyama C, Masana Y, Yoshimine T, Hayakawa T. [Use of Ommaya CSF reservoir for refractory chronic subdural hematoma]. No Shinkei Geka. 1999 Apr;27(4):323-8. Japanese. PubMed PMID: 10347846.
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Sato M, Iwatsuki K, Akiyama C, Kumura E, Yoshimine T. Implantation of a reservoir for refractory chronic subdural hematoma. Neurosurgery. 2001 Jun;48(6):1297-301. PubMed PMID: 11383733.
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Laumer R. Implantation of a reservoir for refractory chronic subdural hematoma. Neurosurgery. 2002 Mar;50(3):672. PubMed PMID: 11841742.
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Misra M, Salazar JL, Bloom DM. Subdural-peritoneal shunt: treatment for bilateral chronic subdural hematoma. Surg Neurol. 1996 Oct;46(4):378-83. PubMed PMID: 8876720.
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Mandai S, Sakurai M, Matsumoto Y. Middle meningeal artery embolization for refractory chronic subdural hematoma. Case report. J Neurosurg. 2000 Oct;93(4):686-8. PubMed PMID: 11014549.
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Takahashi K, Muraoka K, Sugiura T, Maeda Y, Mandai S, Gohda Y, Kawauchi M, Matsumoto Y. [Middle meningeal artery embolization for refractory chronic subdural hematoma: 3 case reports]. No Shinkei Geka. 2002 May;30(5):535-9. Japanese. PubMed PMID: 11993178.
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Hirai S, Ono J, Odaki M, Serizawa T, Nagano O. Embolization of the Middle Meningeal Artery for Refractory Chronic Subdural Haematoma. Usefulness for Patients under Anticoagulant Therapy. Interv Neuroradiol. 2004 Dec 24;10 Suppl 2:101-4. Epub 2008 May 15. PubMed PMID: 20587257; PubMed Central PMCID: PMC3522210.
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Tsukamoto Y, Oishi M, Shinbo J, Fujii Y. Transarterial embolisation for refractory bilateral chronic subdural hematomas in a case with dentatorubral-pallidoluysian atrophy. Acta Neurochir (Wien). 2011 May;153(5):1145-7. doi: 10.1007/s00701-010-0891-3. Epub 2010 Dec 2. PubMed PMID: 21125409.
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Mino M, Nishimura S, Hori E, Kohama M, Yonezawa S, Midorikawa H, Kaimori M, Tanaka T, Nishijima M. Efficacy of middle meningeal artery embolization in the treatment of refractory chronic subdural hematoma. Surg Neurol Int. 2010 Dec 13;1:78. doi: 10.4103/2152-7806.73801. PubMed PMID: 21206540; PubMed Central PMCID: PMC3011107.
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Hashimoto T, Ohashi T, Watanabe D, Koyama S, Namatame H, Izawa H, Haraoka R, Okada H, Ichimasu N, Akimoto J, Haraoka J. Usefulness of embolization of the middle meningeal artery for refractory chronic subdural hematomas. Surg Neurol Int. 2013 Aug 19;4:104. doi: 10.4103/2152-7806.116679. eCollection 2013. PubMed PMID: 24032079; PubMed Central PMCID: PMC3766342.
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Kim E. Embolization Therapy for Refractory Hemorrhage in Patients with Chronic Subdural Hematomas. World Neurosurg. 2017 May;101:520-527. doi: 10.1016/j.wneu.2017.02.070. Epub 2017 Feb 27. PubMed PMID: 28249828.
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Chihara H, Imamura H, Ogura T, Adachi H, Imai Y, Sakai N. Recurrence of a Refractory Chronic Subdural Hematoma after Middle Meningeal Artery Embolization That Required Craniotomy. NMC Case Rep J. 2014 May 9;1(1):1-5. doi: 10.2176/nmccrj.2013-0343. eCollection 2014 Oct. PubMed PMID: 28663942; PubMed Central PMCID: PMC5364934.
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Schaumann A, Klene W, Rosenstengel C, Ringel F, Tüttenberg J, Vajkoczy P. COXIBRAIN: results of the prospective, randomised, phase II/III study for the selective COX-2 inhibition in chronic subdural haematoma patients. Acta Neurochir (Wien). 2016 Nov;158(11):2039-2044. PubMed PMID: 27605230.
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Takahashi T, Senbokuya N, Horikoshi T, Sato E, Nukui H, Kinouchi H. [Refractory chronic subdural hematoma due to spontaneous intracranial hypotension]. No Shinkei Geka. 2007 Aug;35(8):799-806. Japanese. PubMed PMID: 17695779.

Update: Bilateral chronic subdural hematoma

Data on bilateral chronic subdural hematomas (CSHs) are scant 1) , including information on the frequency of symptoms, response to various treatments, and postoperative complications, compared with data on unilateral CSH. Bilateral CSHs constitute a fair portion of CSHs, especially in patients older than 75 years and in those with coagulopathy.

Clinical features

The presenting symptoms are those of raised intracranial pressure and mass effect.
The frequency of focal neurological deficits was found to be lesser in patients with bilateral CSDH, and it may confound the diagnosis and delay treatment 2).

Diagnosis

Computed tomography


Bilateral hematomas may lead to medial compression of both ventricles resulting in a narrow, slit-like elongated ventricle (the anterior horns sharply pointed and approaching one another so called ‘squeezed ventricle,’ ‘hare’s ears sign, or ‘rabbit’s ears’) 3) 4)5) 6).
see also Bilateral isodense chronic subdural hematoma

Magnetic resonance imaging

Magnetic resonance imaging is a more sensitive modality.

Differential diagnosis

If the lesion is placed more anteriorly and medially, hyperdense in intensity and enclosed in thick capsule, it may look biconvex in shape and can mimic extradural hematoma. This location of the lesion will also displace the frontal horns of the lateral ventricles laterally than medially, as in the present case. To avoid this confusion, if available, magnetic resonance imaging (MRI) would be better than CT in identifying these lesions 7) 8) 9) 10) 11).

Treatment

Occasionally patients with bilateral CSDH undergo unilateral surgery because the contralateral hematoma is deemed to be asymptomatic, and in some of these patients the contralateral hematoma may subsequently enlarge, requiring additional surgery.
Treatment of bilateral CSHs presents its own unique set of problems. New hemorrhage on the contralateral side and shift of midline structures are concerns and can be avoided by simultaneous bilateral decompression 12) 13). and significantly lowers the risk of retreatment compared with unilateral intervention and should be considered when choosing a surgical procedure 14).
To prevent neurological deterioration resulting from the thicker hematomas, early surgical decompression for bilateral CSDH should be implemented 15).

Outcome

Mixed high and low intensity in T2WI or low intensity in T1WI is the most predictable factor to show rapid aggravation 16).
Clinicians must be aware of the higher recurrent rate of bilateral CSDH after burr hole craniostomy 17).

Case series

2017

Two hundred ninety-one patients with bCSDH were identified, and 264 of them underwent unilateral (136 patients) or bilateral (128 patients) surgery. The overall retreatment rate was 21.6% (57 of 264 patients). Cases treated with unilateral surgery had twice the risk of retreatment compared with cases undergoing bilateral surgery (28.7% vs 14.1%, respectively, p = 0.002). In accordance with previous studies, the data also showed that a separated hematoma density and the absence of postoperative drainage were independent predictors of retreatment.
In bCSDHs bilateral surgical intervention significantly lowers the risk of retreatment compared with unilateral intervention and should be considered when choosing a surgical procedure 18).


Ninety-three patients with bilateral CSDH who underwent unilateral bur hole surgery at Aizu Chuo Hospital were included in a retrospective analysis. Findings on preoperative MRI, preoperative thickness of the drained hematoma, and the influence of antiplatelet or anticoagulant drugs were considered and evaluated in univariate and multivariate analyses.
The overall growth rate was 19% (18 of 93 hematomas), and a significantly greater percentage of the hematomas that were iso- or hypointense on preoperative T1-weighted imaging showed growth compared with other hematomas (35.4% vs 2.3%, p < 0.001). Multivariate logistic regression analysis showed that findings on preoperative T1-weighted MRI were the sole significant predictor of hematoma growth, and other factors such as antiplatelet or anticoagulant drug use, patient age, patient sex, thickness of the treated hematoma, and T2-weighted MRI findings were not significantly related to hematoma growth. The adjusted odds ratio for hematoma growth in the T1 isointense/hypointense group relative to the T1 hyperintense group was 25.12 (95% CI 3.89-51.58, p < 0.01).
The findings of preoperative MRI, namely T1-weighted sequences, may be useful in predicting the growth of hematomas that did not undergo bur hole surgery in patients with bilateral CSDH 19).

2013

Huang et al., identified 25 of 98 CSDH (25.51%). The patients with bilateral lesions had a lower incidence of hemiparesis than those having unilateral lesions (p = 0.004). Analysis of the neuro-images revealed significant differences in the presence of a midline shift (p = 0.001) and thickness of the hematoma (p < 0.001).
The mean Markwalder grading score at admission was 1.89 ± 0.66 and 1.64 ± 0.49 in the unilateral and bilateral hematoma groups, respectively (p = 0.010). After a minimum follow-up period of 6 months, the mean Glasgow Outcome Scale was not significantly different (p = 0.060). The recurrence rate of up to 28.00% observed for the bilateral disease was found to be higher than 9.59% observed for the unilateral disease (p = 0.042) 20).

Case reports

2017

A 72-year-old man with bilateral chronic subdural hematomas was admitted and treated using a YL-1 type hematoma aspiration needle. The treatment was complicated by hemorrhage of the basal ganglia and brainstem. This patient had no history of hypertension. Chen et al evaluated the relevant literature to analyze the causes of cerebral hemorrhage in similar patients.
This case report illustrates that the stability of the intracranial pressure should be closely monitored during the surgical treatment of chronic subdural hematomas, and large fluctuations in the cerebral perfusion pressure should be avoided during the operation. They also propose improvements in the technical details of the operative treatment of chronic subdural hematomas 21).


Calcified chronic subdural hematomas are an occurrence rarely seen in neurosurgical clinical practice. And when they occur bilaterally, the radiologic image they present is fascinating, as is the clinical presentation, but their management may be challenging. They have been reported to present with a multitude of neurologic deficits but never with diabetes insipidus, which is described by Siddiqui et al.
Due to the rarity of this pathology, the management protocol is not well defined, though there have been quite a few papers on this condition. This review article gathers information published over the years on this rare entity to suggest a treatment protocol 22).

2006

An 81-year-old man suffered blunt trauma to his chest resulting from a road traffic accident. On admission a chest X-ray showed multiple rib fractures but a computerized tomography scan of the head ruled out any post-traumatic lesion. He had a background diagnosis of mild Alzheimer’s dementia for which he was being treated with galantamine. He lived a reasonably independent life with his wife and was driving the car himself when the accident occurred. After a fortnight he was discharged from hospital.
Two months later he developed progressive deterioration in mobility. His wife noted an increasing level of forgetfulness and intermittent episodes of confusion. His general practitioner noted a shuffling gait and rigidity affecting lower limbs and made a working diagnosis of parkinsonism. A trial of Madopar (Levodopa and benserazide: 62.5 mg three times a day for 2 weeks) was given by the GP but this failed to improve the situation and he became virtually bed-bound. He was referred back to the hospital for further investigation.
On admission he was confused and marked rigidity affecting upper and lower limbs was detected. No resting tremor was noted but gait could not be tested, as he was unable to get out of bed. In view of the clinical presentation a computerized tomography scan of the head was repeated which showed bilateral fronto-parietal chronic subdural haematoma (Figure 1a,b). He was referred to the regional neurosurgical centre where he underwent bilateral burrhole drainage. Postoperative recovery was unremarkable and on examination there was complete resolution of previous rigidity affecting upper and lower limbs. He was able to converse normally with his wife and began walking with the aid of a stick by third postoperative day. A week later he was discharged from the hospital having regained his previous level of mobility and independence with activities of daily living 23).
1)

Schaller B, Radziwill AJ, Wasner M, Gratzl O, Steck AJ. [Intermittent paraparesis as manifestation of a bilateral chronic subdural hematoma]. Schweiz Med Wochenschr. 1999 Jul 27;129(29-30):1067-72. German. PubMed PMID: 10464909.
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Huang YH, Yang KY, Lee TC, Liao CC. Bilateral chronic subdural hematoma: what is the clinical significance? Int J Surg. 2013;11(7):544-8. doi: 10.1016/j.ijsu.2013.05.007. Epub 2013 May 24. PubMed PMID: 23707986.
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Marcu H, Becker H. Computed-tomography of bilateral isodense chronic subdural hematomas. Neuroradiology. 1977;14:81–3.
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Ellis GL. Subdural haematoma in the elderly. Emerg Med Clin North Am. 1990;8:281–94.
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Karasawa H, Tomita S, Suzuki S. Chronic subdural haematomas: Time density curve and iodine concentrations in enhanced CT. Neuroradiology. 1987;29:36–9.
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Kim KS, Hemmati M, Weinberg P. Computed tomography in isodense subdural haematoma. Radiology. 1978;128:71–4.
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Fujisawa H, Nomura S, Kajiwara K, Kato S, Fujii M, Suzuki M. Various magnetic resonance imaging patterns of chronic subdural hematomas: indicators of the pathogenesis? Neurol Med Chir (Tokyo) 2006;46:333–9.
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Kelly AB, Zimmerman RD, Snow RB, Gandy SE, Heier LA, Deck MD. Head trauma: Comparison of MR and CT experience in 100 patients. AJNR Am J Neuroradiol. 1988;9:699–708.
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Guenot M. Chronic subdural haematoma: diagnostic imaging studies. Neurochirurgie. 2001;47:473–8.
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Hosoda K, Tamaki N, Masumura M, Matsumoto S, Maeda F. Magnetic resonance images of chronic subdural hematomas. J Neurosurg. 1987;67:677–83.
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Agrawal A. Bilateral biconvex frontal chronic subdural hematoma mimicking extradural hematoma. J Surg Tech Case Rep. 2010 Jul;2(2):90-1. doi: 10.4103/2006-8808.73625. PubMed PMID: 22091345; PubMed Central PMCID: PMC3214288.
12)

Sadrolhefazi A, Bloomfield SM. Interhemispheric and bilateral chronic subdural hematoma. Neurosurg Clin N Am. 2000 Jul;11(3):455-63. Review. PubMed PMID: 10918015.
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Kurokawa Y, Ishizaki E, Inaba K. Bilateral chronic subdural hematoma cases showing rapid and progressive aggravation. Surg Neurol. 2005 Nov;64(5):444-9; discussion 449. PubMed PMID: 16253697.
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Andersen-Ranberg NC, Poulsen FR, Bergholt B, Hundsholt T, Fugleholm K. Bilateral chronic subdural hematoma: unilateral or bilateral drainage? J Neurosurg. 2017 Jun;126(6):1905-1911. doi: 10.3171/2016.4.JNS152642. Epub 2016 Jul 8. PubMed PMID: 27392267.
19)

Fujitani S, Ishikawa O, Miura K, Takeda Y, Goto H, Maeda K. Factors predicting contralateral hematoma growth after unilateral drainage of bilateral chronic subdural hematoma. J Neurosurg. 2017 Mar;126(3):755-759. doi: 10.3171/2016.1.JNS152655. PubMed PMID: 27081904.
21)

Chen L, Dong L, Wang XD, Zhang HZ, Wei M, She L. Bilateral Chronic Subdural Hematoma Treated by YL-1 Type Hematoma Aspiration Needle Complicated by Hemorrhage of the Basal Ganglia and Brainstem. World Neurosurg. 2017 Jan;97:761.e11-761.e13. doi: 10.1016/j.wneu.2016.09.074. PubMed PMID: 27702707.
22)

Siddiqui SA, Singh PK, Sawarkar D, Singh M, Sharma BS. Bilateral Ossified Chronic Subdural Hematoma Presenting as Diabetes Insipidus-Case Report and Literature Review. World Neurosurg. 2017 Feb;98:520-524. doi: 10.1016/j.wneu.2016.11.031. Review. PubMed PMID: 27867130.
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Suman S, Meenakshisundaram S, Woodhouse P. Bilateral chronic subdural haematoma: a reversible cause of parkinsonism. J R Soc Med. 2006 Feb;99(2):91-2. PubMed PMID: 16449784; PubMed Central PMCID: PMC1360497.

Chronic subdural hematoma complications

Chronic subdural hematoma complications

Failure of the brain to re-expand, pneumocephalus, incomplete evacuation, and recurrence of the fluid collection are the most frequently.

Brain herniation

Chronic subdural hematoma (CSDH) with brain herniation signs is rarely seen in the emergent department. As such, there are few cumulative data to analyze such cases.

Failure of postoperative cerebral reexpansion

A wide variation in postoperative drainage volumes is observed during treatment of chronic subdural hematoma (CSDH) with twist-drill or burr-hole craniostomy and closed-system drainage.
The postoperative drainage volumes varied greatly because of differences in the outer membrane permeability of CSDH, and such variation seems to be related to the findings on the CT scans obtained preoperatively. Patients with CSDH in whom there is less postoperative drainage than expected should be carefully observed, with special attention paid to the possibility of recurrence 1).
Patients with high subdural pressure showed the most rapid brain expansion and clinical improvement during the first 2 days. Nevertheless, a computerized tomography (CT) scan performed on the 10th day after surgery demonstrated persisting subdural fluid in 78% of cases. After 40 days, the CT scan was normal in 27 of the 32 patients. There was no mortality and no significant morbidity. A study suggests that well developed subdural neomembranes are the crucial factors for cerebral reexpansion, a phenomenon that takes at least 10 to 20 days. However, blood vessel dysfunction and impairment of cerebral blood flow may participate in delay of brain reexpansion. It may be argued that additional surgical procedures, such as repeated tapping of the subdural fluid, craniotomy, and membranectomy or even craniectomy, should not be evaluated earlier than 20 days after the initial surgical procedure unless the patient has deteriorated markedly 2).

Recurrence

Postoperative pneumocephalus

Remote cerebellar hemorrhage (RCH)

Epidural hematoma

After chronic subdural hematoma evacuation surgery, the development of epidural hematoma is a very rare entity.
Akpinar et al. report the case of a 41-year-old man with an epidural hematoma complication after chronic subdural hematoma evacuation. Under general anesthesia, the patient underwent a large craniotomy with closed system drainage performed to treat the chronic subdural hematoma. After chronic subdural hematoma evacuation, there was epidural leakage on the following day.
Although trauma is the most common risk factor in young CSDH patients, some other predisposing factors may exist. Intracranial hypotension can cause EDH. Craniotomy and drainage surgery can usually resolve the problem. Because of rapid dynamic intracranial changes, epidural leakages can occur. A large craniotomy flap and silicone drainage in the operation area are key safety points for neurosurgeons and hydration is essential 3).

Intracranial subdural empyema

A case of intracranial subdural empyema following chronic subdural hematoma drainage 4)


1)

Kwon TH, Park YK, Lim DJ, Cho TH, Chung YG, Chung HS, Suh JK. Chronic subdural hematoma: evaluation of the clinical significance of postoperative drainage volume. J Neurosurg. 2000 Nov;93(5):796-9. PubMed PMID: 11059660.
2)

Markwalder TM, Steinsiepe KF, Rohner M, Reichenbach W, Markwalder H. The course of chronic subdural hematomas after burr-hole craniostomy and closed-system drainage. J Neurosurg. 1981 Sep;55(3):390-6. PubMed PMID: 7264730.
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Akpinar A, Ucler N, Erdogan U, Yucetas CS. Epidural Hematoma Complication after Rapid Chronic Subdural Hematoma Evacuation: A Case Report. Am J Case Rep. 2015 Jul 6;16:430-433. PubMed PMID: 26147957.
4)

Ovalioglu AO, Aydin OA. A case of subdural empyema following chronic subdural hematoma drainage. Neurol India. 2013 Mar-Apr;61(2):207-9. doi: 10.4103/0028-3886.111165. PubMed PMID: 23644343.

Update: Magnetic resonance imaging for chronic subdural hematoma

The Magnetic Resonance Imaging (MRI) examination better shows the location of the chronic subdural hematoma and evidences its dimensions much clearer together with the mass effect of the adjacent structures1).

Moreover, it is more useful in cases of bilateral chronic subdural hematoma and isodense chronic subdural hematomas. The MRI examination is superior to the CT examination as far as the membranes dimensions of the chronic subdural haematoma and the presence of the septa inside the haematoma are concerned, and in determining the size and internal structures of chronic subdural hematomas 2).
In these conditions the surgical approach could be modified 3).
Even though MRI has advantages, CT remains the procedure of choice in the acute setting because of shorter examination time, which is important in acutely ill patients, reliability in identifying other lesions 4).

Classification

Based on MRI, CSDHs can be classified into five types on both T(1)- and T(2)-weighted images: low, high, and mixed intensity, isointensity, and layered.
Usually, CSDHs are hyperintense on both T1- and T2-weighted MRI (the T1 values of CSDHs are significantly shorter than gray matter values and significantly longer than white matter values and the T2 values are significantly longer than both gray matter and white matter values) 5).

Axial T1-weighted magnetic resonance imaging demonstrates bilateral subacute subdural hematomas with increased signal intensity. Areas of intermediate intensity represent more acute hemorrhage into the subacute collections.
In the series of Hosoda et al. in many ways, MRI was superior to CT for demonstrating the hematomas. In general, chronic subdural hematomas were hyperintense on both T1- and T2-weighted MRI. The T1 values of chronic subdural hematomas were significantly shorter than gray matter values and significantly longer than white matter values. The T2 values were significantly longer than both gray matter and white matter values. These findings were consistent with previous reports. However, six hematomas (30%) were iso- or hypointense on T1-weighted images. Possible mechanisms responsible for the difference in intensity of chronic subdural hematoma on MRI are discussed, and the important role of methemoglobin formation is emphasized 6)

Case series

2017

Ninety-three patients with bilateral CSDH who underwent unilateral bur hole surgery at Aizu Chuo Hospital were included in a retrospective analysis. Findings on preoperative MRI, preoperative thickness of the drained hematoma, and the influence of antiplatelet or anticoagulant drugs were considered and evaluated in univariate and multivariate analyses.
The overall growth rate was 19% (18 of 93 hematomas), and a significantly greater percentage of the hematomas that were iso- or hypointense on preoperative T1-weighted imaging showed growth compared with other hematomas (35.4% vs 2.3%, p < 0.001). Multivariate logistic regression analysis showed that findings on preoperative T1-weighted MRI were the sole significant predictor of hematoma growth, and other factors such as antiplatelet or anticoagulant drug use, patient age, patient sex, thickness of the treated hematoma, and T2-weighted MRI findings were not significantly related to hematoma growth. The adjusted odds ratio for hematoma growth in the T1 isointense/hypointense group relative to the T1 hyperintense group was 25.12 (95% CI 3.89-51.58, p < 0.01).
The findings of preoperative MRI, namely T1-weighted sequences, may be useful in predicting the growth of hematomas that did not undergo bur hole surgery in patients with bilateral CSDH 7).

2015

Preoperative MRI and postoperative computed tomography (CT) were performed and the influence of the preoperative use of antiplatelet or anticoagulant drugs was also studied. The overall recurrence rate was 9.3% (47 of 505 hematomas). The MRI T1-iso/hypointensity group showed a significantly higher recurrence rate (18.2%, 29 of 159) compared to the other groups (5.2%, 18 of 346; p < 0.001). Multivariate logistic regression analysis showed T1 classification was the solo significant prognostic predictor among various factors such as bilateral hematoma, antiplatelet or anticoagulant drug usage, residual hematoma on postoperative CT, and MRI classification (p < 0.001): adjusted odds ratio for the recurrence in T1-iso/hypointensity group relative to the T1-hyperintensity group was 5.58 [95% confidence interval (CI), 2.09-14.86] (p = 0.001). Postoperative residual hematoma and antiplatelet or anticoagulant drug usage did not increase the recurrence risk. The preoperative MRI findings, especially T1WI findings, have predictive value for postoperative recurrence of CSDH and the T1-iso/hypointensity group can be assumed to be a high recurrence risk group 8).

2010

CT and MR images of 48 chronic subdural haematomas of 34 patients were reviewed retrospectively. The thickness measurements and imaging characteristics of haematomas were compared.
Levelling was observed in 25% of haematomas, and most of them (60%) had intrahaematomal membranes. All membranes could be delineated by MR imaging, whereas only 27% were defined by CT. Mixed density (52%) and T1 hyperintensity (59%) were commonly observed in membraned haematomas, but the difference was not statistically significant. Haematomas were measured significantly thicker on MR images. All patients had been treated with burr hole craniotomy and irrigation.
MR imaging is more sensitive than CT in determining the size and internal structures of chronic subdural haematomas 9).

1987

Magnetic resonance imaging (MRI) and computerized tomography (CT) scans of 18 patients with 20 chronic subdural hematomas were compared. In many ways, MRI was superior to CT for demonstrating the hematomas. In general, chronic subdural hematomas were hyperintense on both T1- and T2-weighted MRI. The T1 values of chronic subdural hematomas were significantly shorter than gray matter values and significantly longer than white matter values. The T2 values were significantly longer than both gray matter and white matter values. These findings were consistent with previous reports. However, six hematomas (30%) were iso- or hypointense on T1-weighted images. Possible mechanisms responsible for the difference in intensity of chronic subdural hematoma on MRI are discussed, and the important role of methemoglobin formation is emphasized 10).
1)

Williams VL, Hogg JP. Magnetic resonance imaging of chronic subdural hematoma. Neurosurg Clin N Am. 2000 Jul;11(3):491-8. Review. PubMed PMID: 10918019.
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Goto H, Ishikawa O, Nomura M, Tanaka K, Nomura S, Maeda K. Magnetic resonance imaging findings predict the recurrence of chronic subdural hematoma. Neurol Med Chir (Tokyo). 2015;55(2):173-8. doi: 10.2176/nmc.oa.2013-0390. PubMed PMID: 25746312; PubMed Central PMCID: PMC4533403.

Update: Infantile acute subdural hematoma

Etiology

Acute subdural hematoma in infants is distinct from that occurring in older children or adults because of differences in mechanism, injury thresholds, and the frequency with which the question of nonaccidental injury is encountered.
When trauma occur the motor vehicle accidents are the most frequent.
In the series of Loh et al. the most common cause of injury was shaken baby syndrome 1).
The accuracy of the history obtained from the caregivers of infants may be low in severe infantile head trauma. Therefore, medical professionals should treat the mechanism of injury obtained from caregivers as secondary information and investigate for possible abusive head trauma (AHT) in cases with inconsistencies between the history that was taken and the severity of the injury observed 2).


Chronic subdural effusions in infancy may arise from trauma, from various types of meningitis, from severe dehydration, or “idiopathically” 3).

Diagnosis

Diagnosis can be made by computed tomography or magnetic resonance imaging 4).

Large subdural hematoma of the right convexity up to 3 cm thick, which causes severe cerebral compression, with cingulate herniation and transtentorial herniation.
The hematoma shows liquid-liquid levels, with a higher density lower in relation to sedimented hematoma.
Signs of diffuse brain edema.

Outcome

Early recognition and suitable treatment may improve the outcome of this injury. If treatment is delayed or the condition is undiagnosed, acute subdural hematoma may cause severe morbidity or even fatality 5).

Case series

2002

Medical records and films of 21 cases of infantile acute subdural hematoma were reviewed retrospectively. Diagnosis was made by computed tomography or magnetic resonance imaging. Medical records were reviewed for comparison of age, gender, cause of injury, clinical presentation, surgical management, and outcome.
Twenty-one infants (9 girls and 12 boys) were identified with acute subdural hematoma, with ages ranging from 6 days to 12 months. The most common cause of injury was shaken baby syndrome. The most common clinical presentations were seizure, retinal hemorrhage, and consciousness disturbance. Eight patients with large subdural hematomas underwent craniotomy and evacuation of the blood clot. None of these patients developed chronic subdural hematoma. Thirteen patients with smaller subdural hematomas were treated conservatively. Among these patients, 11 developed chronic subdural hematomas 15 to 80 days (mean = 28 days) after the acute subdural hematomas. All patients with chronic subdural hematomas underwent burr hole and external drainage of the subdural hematoma. At follow-up, 13 (62%) had good recovery, 4 (19%) had moderate disability, 3 (14%) had severe disability, and 1 (5%) died. Based on GCS on admission, one (5%) had mild (GCS 13-15), 12 (57%) had moderate (GCS 9-12), and 8 (38%) had severe (GCS 8 or under) head injury. Good recovery was found in 100% (1/1), 75% (8/12), and 50% (4/8) of the patients with mild, moderate, and severe head injury, respectively. Sixty-three percent (5/8) of those patients undergoing operation for acute subdural hematomas and 62% (8/13) of those patients treated conservatively had good outcomes.
Infantile acute subdural hematoma if treated conservatively or neglected, is an important cause of infantile chronic subdural hematoma. Early recognition and suitable treatment may improve the outcome of this injury. If treatment is delayed or the condition is undiagnosed, acute subdural hematoma may cause severe morbidity or even fatality 6).

2000

Hwang et al., reviewed a total of 16 infant head injury patients under 12 months of age who were treated in from 1989 to 1997. Birth head injury was excluded. The most common age group was 3-5 months. Early seizures were noted in 7 cases, and motor weakness in 6. Three patients with acute intracranial hematoma and another 3 with depressed skull fracture were operated on soon after admission. Chronic subdural hematomas (SDHs) developed in 3 infants. Initial CT scans showed a small amount of SDH that needed no emergency operation. Resolution of the acute SDH and development of subdural hygroma appeared on follow-up CT scans within 2 weeks of injury. Two of these infants developed early seizures. Chronic SDH was diagnosed on the 68th and 111th days after the injuries were sustained, respectively. The third patient was the subject of close follow-up with special attention to the evolution of chronic SDH in view of our experience in the previous 2 cases, and was found to have developed chronic SDH on the 90th day after injury. All chronic SDH patients were successively treated by subduro-peritoneal shunting. In conclusion, the evolution of chronic SDH from acute SDH is relatively common following infantile head injury. Infants with head injuries, especially if they are associated with acute SDH and early development of subdural hygroma, should be carefully followed up with special attention to the possible development of chronic SDH 7).

1987

A retrospective analysis of the infantile acute subdural hematoma was made by Ikeda et al., with special reference to its pathogenesis.
In 11 of 15 cases, the hematomas were bilateral or a contralateral subdural fluid collection was present. In 7 of 11 patients who underwent operation the collection was bloody fluid and/or clotted blood. In 3 patients, a subdural membrane, as seen in adult chronic subdural hematoma, was found. In only 1 patient with unilateral hematoma was clotted blood present without subdural membrane. The thickest collection of clotted blood was in the parasagittal region. It is postulated that in most cases hemorrhage occurs after minor head injury, from the bridging veins near the superior sagittal sinus, into a pre-existing subdural fluid collection such as chronic subdural hematoma or subdural effusion with cranio-cerebral disproportion, and that infants without intracranial disproportion are unlikely to have acute subdural hematoma caused by minor head injury 8).

1986

Aoki et al. report six Japanese cases of child abuse with subdural hematoma and discuss differences from those in the United States. The majority of abused children with subdural hematomas in Japan have suffered direct violence to the face and head, resulting in external signs of trauma. Failure to detect these external traces of trauma, however, might result in an incorrect diagnosis of infantile acute subdural hematoma attributed to accidental trivial head injury. Child abuse with subdural hematoma in the United States is frequently caused by whiplash shaking injury in which external signs of trauma may not be evident. In the United States, retinal hemorrhage and subdural hematoma together suggest child abuse; some cases of infantile acute subdural hematoma might be mistakenly diagnosed as child abuse. Thus, the constellation of retinal bleeding and subdural hematoma combined with the absence of visible signs of trauma is differently interpreted in the United States and Japan 9).

1984

Twenty-six cases of infantile acute subdural hematoma treated between 1972 and 1983 were reviewed. The series was limited to infants with acute subdural hematoma apparently due to minor head trauma without loss of consciousness, and not associated with cerebral contusion. Twenty-three of the patients were boys, and three were girls, showing a clear male predominance. The patients ranged in age between 3 and 13 months, with an average age of 8.1 months, the majority of patients being between 7 and 10 months old. Most of the patients were brought to the hospital because of generalized tonic convulsion which developed soon after minor head trauma, and all patients had retinal and preretinal hemorrhage. The cases were graded into mild, intermediate, and fulminant types, mainly on the basis of the level of consciousness and motor weakness. Treatment for fulminant cases was emergency craniotomy, and that for mild cases was subdural tapping alone. For intermediate cases, craniotomy or subdural tapping was selected according to the contents of the hematoma. The follow-up results included death in two cases, mild physical retardation in one case, and epilepsy in one case. The remaining 23 patients showed normal development. The relationship between computerized tomography (CT) findings and clinical grading was analyzed. Because some mild and intermediate cases could be missed on CT, the importance of noting the characteristic clinical course and of funduscopic examination is stressed 10).

Case reports

 2008
An unusual case of ruptured infantile cerebral aneurysm. An eight-month-old infant was delivered to the hospital in poor condition, after convulsions, with no history of trauma. His emergent CT study revealed acute subdural hematoma. The clinical and radiological picture evoked suspicion that the hematoma was of aneurysmal origin. The infant was operated with special preparations and precautions appropriate for aneurysmal surgery, and has shown a good recovery. It is important to consider the possibility of vascular accident in infants with subdural hematoma of nontraumatic origin. A good outcome may be achieved when appropriate preparations are made prior to surgery 11).

2005

Huang et al. the case of an infant with a traumatic acute subdural hematoma that resolved within 65 hours. A 23-month-old boy fell from a height of approximately 10 m. Brain computed tomography disclosed a left subdural hematoma with midline shift. The associated clots resolved spontaneously within 65 hours of the injury. Although they may mimic more clinically significant subdural hematomas, such collections of clots are likely to be located at least partly within the subarachnoid space. Their recognition may influence decisions regarding both surgical evacuation and the likelihood of non-accidental injury. Clinical and radiographic features distinguishing these “disappearing subdural hematomas” from more typical subdural hematomas are discussed 12)

Own case report

A 1 year old , according to anamnesis provided by the parents, they consulted in the last month for cough clinic with low expectoration, nasal congestion, Tº up to 38ºC of 24 hrs evolution. According to an emergency report: the previous week the patient presents right facial edema, of 2 days duration.
Scratch injuries in legs.
In the next days vomiting with progressive decay.
In the following hours after admission coma, respiratory arrest with bradycardia

Large subdural hematoma of the right convexity up to 3 cm thick, which causes severe cerebral compression, with cingulate herniation and transtentorial herniation.
The hematoma shows liquid-liquid levels, with a higher density lower in relation to sedimented hematoma.
Signs of diffuse brain edema.
In the surgical intervention xanthochromia appears at the beginning, later dark red liquid without clots. Later a subdural membrane is seen on the arachnoid surface, very characteristic of chronic subdural hematoma.


1) , 4) , 5) , 6)

Loh JK, Lin CL, Kwan AL, Howng SL. Acute subdural hematoma in infancy. Surg Neurol. 2002 Sep-Oct;58(3-4):218-24. PubMed PMID: 12480224.
2)

Amagasa S, Matsui H, Tsuji S, Moriya T, Kinoshita K. Accuracy of the history of injury obtained from the caregiver in infantile head trauma. Am J Emerg Med. 2016 Sep;34(9):1863-7. doi: 10.1016/j.ajem.2016.06.085. PubMed PMID: 27422215.
3)

Amacher AL, Li KT. Indirect trauma as a cause of acute infantile subdural hematomas. Can Med Assoc J. 1973 Jun 23;108(12):1530. PubMed PMID: 4714878; PubMed Central PMCID: PMC1941542.
7)

Hwang SK, Kim SL. Infantile head injury, with special reference to the development of chronic subdural hematoma. Childs Nerv Syst. 2000 Sep;16(9):590-4. PubMed PMID: 11048634.
8)

Ikeda A, Sato O, Tsugane R, Shibuya N, Yamamoto I, Shimoda M. Infantile acute subdural hematoma. Childs Nerv Syst. 1987;3(1):19-22. PubMed PMID: 3594464.
9)

Aoki N, Masuzawa H. Subdural hematomas in abused children: report of six cases from Japan. Neurosurgery. 1986 Apr;18(4):475-7. PubMed PMID: 3703222.
10)

Aoki N, Masuzawa H. Infantile acute subdural hematoma. Clinical analysis of 26 cases. J Neurosurg. 1984 Aug;61(2):273-80. PubMed PMID: 6737052.
11)

Adeleye AO, Shoshan Y, Cohen JE, Spektor S. Ruptured middle cerebral artery aneurysm in an infant presenting as acute subdural hematoma: a case report. Pediatr Neurosurg. 2008;44(5):397-401. doi: 10.1159/000149908. PubMed PMID: 18703887.
12)

Huang SH, Lee HM, Lin CK, Kwan AL, Howng SL, Loh JK. Rapid resolution of infantile acute subdural hematoma: a case report. Kaohsiung J Med Sci. 2005 Jun;21(6):291-4. PubMed PMID: 16035574.
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