Steroids for chronic subdural hematoma

Since glucocorticoids have been used for treatment of chronic subdural hematoma in 1962 their role is still discussed controversially in lack of evident data. On the basis of the ascertained inflammation cycle in cSDH dexamethasone will be an ideal substance for a short lasting, concomitant treatment protocol.

Berghauser et al. stated in 2013 that the proportion of patients primarily treated with corticosteroids are increasing year by year 1)

Patients with lower grades of CSDH can be treated successfully with steroids. Female patients seem to do better with steroids 2).


In 2020 in the The New England Journal of Medicine among adults with symptomatic chronic subdural hematoma, most of whom had undergone surgery to remove their hematomas during the index admission, treatment with dexamethasone resulted in fewer favorable outcomes and more adverse events than placebo at 6 months, but fewer repeat operations were performed in the dexamethasone group. (Funded by the National Institute for Health Research Health Technology Assessment Programme; Dex-CSDH ISRCTN number, ISRCTN80782810.) 3).

Surveys

Forty-two percent of surgeons never prescribe steroids and 55% prescribe them to those managed conservatively 4).

In another Canadian survey regarding neurosurgical practice of treatment of CSDH, <15% of neurosurgeons prefer using high-dose corticosteroid 5)

Current evidence implicates a potentially beneficial role of dexamethasone in the management of CSDH. However, it remains unclear whether the rate of crossover to surgery is reduced in patients treated with corticosteroids compared with those managed conservatively. A longer duration of study with detailed analysis of individual cases and appropriately randomized cohorts are necessary to draw more reliable conclusions 6)

Scerrati et al. performed a systematic review according to PRISMA criteria of the studies analyzing the nonsurgical strategies for CSDHs. They collected all papers in the English language published between 1990 and 2019 by searching different medical databases. The chosen keywords were “chronic subdural hematoma,” “conservative treatment/management,” “pharmacological treatment,” “non-surgical,” “tranexamic acid,” “dexamethasone,” “corticosteroid,” “glucocorticoid,” “middle meningeal artery,” “endovascular treatment,” and “embolization.”

The authors ultimately collected 15 articles regarding the pharmacological management of CSDHs matching the criteria, and 14 papers included the endovascular treatment.

The results showed that surgery still represents the mainstay in cases of symptomatic patients with large CSDHs; however, adjuvant and alternative therapies can be effective and safe in a carefully selected population. Their inclusion in new guidelines is advisable 7).


A meta-analysis of Holl et al. from 29019 suggested that the addition of corticosteroids to surgery might be effective in the treatment of CSDH. However, the results must be interpreted with caution in light of the serious risk of bias of the included studies. This study stresses the need for large randomized trials to investigate the use of corticosteroids in the management of CSDH 8)


In 2017 a study of Yao et al. had no enough evidence to support DX use as an effective alternation to surgical therapy. But adjuvant DX use may facilitate the surgical therapy by reducing chronic subdural hematoma recurrence. Further study focusing on adjuvant DX was required 9)

Among adults with symptomatic chronic subdural hematoma, most of whom had undergone surgery to remove their hematomas during the index admission, treatment with dexamethasone resulted in fewer favorable outcomes and more adverse events than placebo at 6 months, but fewer repeat operations were performed in the dexamethasone group. (Funded by the National Institute for Health Research Health Technology Assessment Programme; Dex-CSDH ISRCTN number, ISRCTN80782810.) 10).

see DECSA trial.

see SUCRE trial.

A study is designed as a double-blind randomized placebo-controlled trial 820 patients who are operated for cSDH and from the age of 25 years are included after obtaining informed consent. They are randomized for administration of dexamethasone (16-16-12-12-8-4 mg/d) or placebo (maltodextrin) during the first 48 hours after surgery. The type I error is 5% and the type II error is 20%. The primary endpoint is the reoperation within 12 weeks postoperative.

This study tests whether dexamethasone administered over 6 days is a safe and potent agent in relapse prevention for evacuated cSDH 11).

Mebberson et al. presented an interim analysis of the first registered prospective randomised placebo-controlled trial (PRPCT) of adjuvant DX on RR and outcome after CSDH surgery with post-operative drainage. Participants were randomised to either placebo or a reducing DX regime over 2 weeks, with CSDH evacuation and post-operative drainage. Post-operative mortality (POMT) and RR were determined at 30 days and 6 months; modified Rankin Score (mRS) at discharge and 6 months. Post-operative morbidity (POMB) and adverse events (AEs) were determined at 30 days. Interim analysis at approximately 50% estimated sample size was performed (n = 47). Recurrences were not observed with DX: only with placebo (0/23 [0%] v 5/24 [20.83%], P = 0.049). There was no significant between-group differences in POMT, POMB, LOS, mRS or AEs. CONCLUSIONS: In this first registered PRPCT, interim analysis suggested that adjuvant DX with post-operative drainage is both safe and may significantly decrease recurrences. A 12.5% point between-groups difference may be reasonable to power a final sample size of approximately n = 89. Future studies could consider adjuvant DX for longer than the arbitrarily-chosen 2 weeks 12).


Twenty patients with imaging-confirmed CSDH were recruited from a single center and randomized to receive dexamethasone (12 mg/day for 3 weeks followed by tapering) or placebo as a conservative treatment. Patients were followed for 6 months and the rate of success of conservative treatment with dexamethasone versus placebo was measured. Parameters such as hematoma thickness and clinical changes were also compared before and after treatment with chi-square tests. Adverse events and complications were documented.

Results: During the 6-month follow-up, one of ten patients treated with corticosteroids had to undergo surgical drainage and three of ten patients were treated surgically after placebo treatment. At the end of the study, all remaining patients had complete radiological resolution. No significant differences were observed in terms of hematoma thickness profile and impression of change; however, patients experienced more severe side effects when treated with steroids as compared with placebo. Dexamethasone contributed to many serious adverse events.

Given the small sample size, these preliminary results have not shown a clear beneficial effect of dexamethasone against placebo in our patients. However, the number of secondary effects reported was much greater for corticosteroids, and dexamethasone treatment was responsible for significant complications 13).

Sunet al. prospectively studied a group of 30 patients, who were managed non-operatively: 26 patients were treated with dexamethasone (Group 1) and four patients expectantly (Group 4). Nineteen patients (73%) from Group 1 were confused or had focal neurological deficits on admission. The mean maximum thickness of the CSDH was 12 mm. Only one of these cases (4%) required surgical drainage 6 weeks after steroid therapy. One patient died of an unrelated stroke (mortality = 4%). Two patients (8%) were left severely disabled. No significant complication from steroid therapy was documented. Out of the 85 surgically treated patients, 69 patients underwent surgical drainage in addition to steroid therapy (Group 2). Thirteen patients were treated with burr-hole drainage only (Group 3). The mean maximum thickness of the CSDH for these two groups were both 16 mm. Comparing with group 1, the redrainage rate of Group 2 [4% (3/69, p = 1)] and that of Group 3 [15% (2/13, p = 0.253)] were not significantly different. 50% of patients in Group 4 (2/4, p = 0.039) required delayed surgical drainage. The mortality rates of Groups 2, 3 and 4 were 3% (2/69, p = 1), 15% (2/13, p = 0.253) and 50% (2/4, p = 0.039), respectively. Our results suggest that steroid treatment in a selected group of patients is a good option, particularly in patients with co-morbidity 14).


1)

Berghauser Pont LM, Dippel DW, Verweij BH, Dirven CM, Dammers R. Ambivalence among neurologists and neurosurgeons on the treatment of chronic subdural hematoma: a national survey. Acta Neurol Belg. 2013 Mar;113(1):55-9. doi: 10.1007/s13760-012-0130-1. Epub 2012 Sep 14. PMID: 22975837.
2)

Thotakura AK, Marabathina NR. Nonsurgical Treatment of Chronic Subdural Hematoma with Steroids. World Neurosurg. 2015 Dec;84(6):1968-72. doi: 10.1016/j.wneu.2015.08.044. Epub 2015 Sep 2. PMID: 26342776.
3) , 10)

Hutchinson PJ, Edlmann E, Bulters D, Zolnourian A, Holton P, Suttner N, Agyemang K, Thomson S, Anderson IA, Al-Tamimi YZ, Henderson D, Whitfield PC, Gherle M, Brennan PM, Allison A, Thelin EP, Tarantino S, Pantaleo B, Caldwell K, Davis-Wilkie C, Mee H, Warburton EA, Barton G, Chari A, Marcus HJ, King AT, Belli A, Myint PK, Wilkinson I, Santarius T, Turner C, Bond S, Kolias AG; British Neurosurgical Trainee Research Collaborative; Dex-CSDH Trial Collaborators. Trial of Dexamethasone for Chronic Subdural Hematoma. N Engl J Med. 2020 Dec 31;383(27):2616-2627. doi: 10.1056/NEJMoa2020473. Epub 2020 Dec 16. PMID: 33326713.
4)

Santarius T, Lawton R, Kirkpatrick PJ, Hutchinson PJ. The management of primary chronic subdural haematoma: a questionnaire survey of practice in the United Kingdom and the Republic of Ireland. Br J Neurosurg. 2008 Aug;22(4):529-34. doi: 10.1080/02688690802195381. PMID: 18686063.
5)

Cenic A, Bhandari M, Reddy K. Management of chronic subdural hematoma: a national survey and literature review. Can J Neurol Sci. 2005 Nov;32(4):501-6. doi: 10.1017/s0317167100004510. PMID: 16408582.
6)

Petralia CCT, Manivannan S, Shastin D, Sharouf F, Elalfy O, Zaben M. Effect of Steroid Therapy on Risk of Subsequent Surgery for Neurologically Stable Chronic Subdural Hemorrhage-Retrospective Cohort Study and Literature Review. World Neurosurg. 2020 Jun;138:e35-e41. doi: 10.1016/j.wneu.2020.01.160. Epub 2020 Feb 27. PMID: 32113994.
7)

Scerrati A, Visani J, Ricciardi L, Dones F, Rustemi O, Cavallo MA, De Bonis P. To drill or not to drill, that is the question: nonsurgical treatment of chronic subdural hematoma in the elderly. A systematic review. Neurosurg Focus. 2020 Oct;49(4):E7. doi: 10.3171/2020.7.FOCUS20237. PMID: 33002869.
8)

Holl DC, Volovici V, Dirven CMF, van Kooten F, Miah IP, Jellema K, Peul WC, van der Gaag NA, Kho KH, den Hertog HM, Dammers R, Lingsma HF. Corticosteroid treatment compared with surgery in chronic subdural hematoma: a systematic review and meta-analysis. Acta Neurochir (Wien). 2019 Jun;161(6):1231-1242. doi: 10.1007/s00701-019-03881-w. Epub 2019 Apr 10. PMID: 30972566.
9)

Yao Z, Hu X, Ma L, You C. Dexamethasone for chronic subdural haematoma: a systematic review and meta-analysis. Acta Neurochir (Wien). 2017 Nov;159(11):2037-2044. doi: 10.1007/s00701-017-3309-7. Epub 2017 Sep 1. PMID: 28865006.
11)

Emich S, Richling B, McCoy MR, Al-Schameri RA, Ling F, Sun L, Wang Y, Hitzl W. The efficacy of dexamethasone on reduction in the reoperation rate of chronic subdural hematoma – the DRESH study: straightforward study protocol for a randomized controlled trial. Trials. 2014 Jan 6;15(1):6. doi: 10.1186/1745-6215-15-6. PubMed PMID: 24393328; PubMed Central PMCID: PMC3891985.
12)

Mebberson K, Colditz M, Marshman LAG, Thomas PAW, Mitchell PS, Robertson K. Prospective randomized placebo-controlled double-blind clinical study of adjuvant dexamethasone with surgery for chronic subdural haematoma with post-operative subdural drainage: Interim analysis. J Clin Neurosci. 2020 Jan;71:153-157. doi: 10.1016/j.jocn.2019.08.095. Epub 2019 Sep 3. PMID: 31492485.
13)

Prud’homme M, Mathieu F, Marcotte N, Cottin S. A Pilot Placebo Controlled Randomized Trial of Dexamethasone for Chronic Subdural Hematoma. Can J Neurol Sci. 2016 Mar;43(2):284-90. doi: 10.1017/cjn.2015.393. Epub 2016 Feb 8. PMID: 26853325.
14)

Sun TF, Boet R, Poon WS. Non-surgical primary treatment of chronic subdural haematoma: Preliminary results of using dexamethasone. Br J Neurosurg. 2005 Aug;19(4):327-33. doi: 10.1080/02688690500305332. PMID: 16455539.

Chronic subdural hematoma recurrence

Chronic subdural hematoma recurrence

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 drill craniostomy (TDC), burr hole craniostomy, craniotomy range from 5% to 30%. 2).

Oslo grading system.

Hyperdense hematoma components were the strongest prognostic factor of recurrence after surgery. Awareness of these findings allows for individual risk assessment and might prompt clinicians to tailor treatment measures 3).


In the series of Santos et al. it was possible to demonstrate an age-related protective factor, analyzed as a continuous variable, regarding the recurrence of the chronic subdural hematoma (CSDH), with a lower rate of recurrence the higher the age.

The results indicate that, among possible factors associated with recurrence, only age presented a protective factor with statistical significance. The fact that no significant difference between the patients submitted to trepanning or craniotomy was found favors the preferential use of burr-hole surgery as a procedure of choice due to its fast and less complex execution 4).


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 5).


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 6).


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).

see Chronic subdural hematoma and anticoagulant therapy.

Antiplatelet therapy significantly influences the recurrence of CSDH 7).

Timing of Low-Dose Aspirin Discontinuation for chronic subdural hematoma.

Pneumocephalus

Remaining pneumocephalus is seen as an approved factor of recurrence 8) 9).

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 10).

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 11).

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 12).

Diabetes

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

13) 14) 15).


Balser et al. report 11% recurrence, which included individuals who recurred as late as 3 years after initial diagnosis 16).

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 17).

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 18).

Irrigation with artificial cerebrospinal fluid (ACF) decreased the rate of CSDH recurrence 19).

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 20).

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 21).

Implantation of a reservoir 22) 23) 24).

Subdural-peritoneal shunt 25).

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 26) 27) 28) 29) 30) 31).

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 32).

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 33).

see Chronic subdural hematoma recurrence case series.

Chronic subdural hematoma recurrence case reports.


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)

Miah IP, Tank Y, Rosendaal FR, Peul WC, Dammers R, Lingsma HF, den Hertog HM, Jellema K, van der Gaag NA; Dutch Chronic Subdural Hematoma Research Group. Radiological prognostic factors of chronic subdural hematoma recurrence: a systematic review and meta-analysis. Neuroradiology. 2020 Oct 22. doi: 10.1007/s00234-020-02558-x. Epub ahead of print. Erratum in: Neuroradiology. 2020 Nov 5;: PMID: 33094383.
4)

Santos RGD, Xander PAW, Rodrigues LHDS, Costa GHFD, Veiga JCE, Aguiar GB. Analysis of predisposing factors for chronic subdural hematoma recurrence. Rev Assoc Med Bras (1992). 2019 Jul 22;65(6):834-838. doi: 10.1590/1806-9282.65.6.834. PubMed PMID: 31340313.
5)

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.
6)

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.
7)

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.
8)

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
9)

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
10)

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.
11)

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.
12)

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.
13)

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.
14)

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.
15)

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.
16)

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.
17)

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.
18)

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.
19)

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.
20)

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.
21)

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.
22)

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.
23)

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.
24)

Laumer R. Implantation of a reservoir for refractory chronic subdural hematoma. Neurosurgery. 2002 Mar;50(3):672. PubMed PMID: 11841742.
25)

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.
26)

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.
27)

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.
28)

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.
29)

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.
30)

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.
31)

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32)

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Spontaneous spinal subdural hematoma

Spontaneous spinal subdural hematoma

Spontaneous spinal subdural hematomas are extremely rare.

A nontraumatic acute spontaneous spinal subdural hematoma (sSDH) is a rare complication after spinal surgery. Although an sSDH is often associated with anticoagulation therapy, vascular malformations, or lumbar puncture, the pathogenesis of nontraumatic spontaneous sSDH remains unclear 1)

In the majority of cases, spontaneous hematomas are idiopathic. However, when attributed to anticoagulation therapy coumarins are more common than direct factor Xa inhibitors such as apixaban. Previous reports have linked direct factor Xa inhibitors with intracranial subdural hematomas much more frequently than spinal subdural hematomas. The manifestation of severe neurological deficits, such as sensorimotor disturbances and loss of sphincter control, is common and is considered a surgical emergency 2).


An 82-year-old patient with a history of ischemic heart disease and atrial fibrillation under acenocoumarol was admitted to emergency department with sudden onset of paraplegia and intense back pain associated with urinary incontinence and anal sphincter disorder. On examination his lower limb power was MRC grade 0 out of 5 in all ranges of movement bilaterally and a complete bilateral anesthesia reaching the T12 dermatome was noted. Biological test results showed an International Normalized Ratio at 10. Magnetic resonance imaging revealed a posteriorly located spinal hematoma at T12 level, measuring 36 mm with spinal cord compression. After correction of hemostasis disorders the patient was admitted to the operating room for a T11-L1 laminectomy with evacuation of the subdural hematoma. Muscle power showed a gradual improvement in the lower limbs estimated at 3/5 with regression of sphincter disorders but unfortunately a sequellar sensory impairment persisted.

SSH is a rare situation of acenocoumarol bleeding incident, it should be evoked in any patient treated by this molecule with signs of spinal cord compression 3).


A case of a patient with a spontaneous spinal thoracic subdural hematoma secondary to apixaban use with loss of sphincter control and paraplegia. After 6 months of follow-up, the patient recovered completely 4).

Spinal subdural hematoma (S-SDH) rarely occurs after aneurysmal subarachnoid hemorrhage (SAH). Little information is known regarding the management and prognosis of patients with both S-SDH and SAH. Here, we present an illustrative Case and provide a systematic review of S-SDH in the setting of SAH. METHODS:

A systematic literature review using PRISMA guidelines revealed 11 previous cases of concurrent intracranial SAH and spinal SDH, which are presented with our new reported Case. RESULTS:

Intracranial sources of spontaneous SAH included 8 aneurysms, 1 pseudoaneurysm, and 3 angiogram negative cases. Hunt Hess grade ranged from 1-4, mean time between SAH and S-SDH was 5.8 days, and S-SDH presented most frequently in the lumbar spine. 8 patients showed significant to complete clinical recovery, 2 had continued plegia of the lower extremities, and 2 expired. Modified Rankin score ranged from 0-6, with mRS > 2 for 4 out of 12 patients. Patients with a poor clinical outcome (mRS > 2) had an initially negative cerebral angiogram, earlier presentation with less time between SAH and S-SDH (0.8 vs 7.6 days), use of antithrombotic medication, no diversion of CSF, and cervical or thoracic S-SDH. CONCLUSION:

S-SDH is an uncommon occurrence in the setting of aneurysmal SAH with better outcomes associated with lumbar location, delayed presentation, CSF diversion, and lack of antithrombotic use. Conservative treatment may be sufficient in cases with delayed S-SDH and lack of significant neurological deficits. More reported cases will allow greater understanding of this clinical entity 5).

Surgical intervention is recommended in patients presenting with severe neurologic deficits. Conservative treatment is a reasonable option for asymptomatic patients 6).

Raymaekers et al. presented the case of an intradural hematoma after an extraforaminal surgery through the Wiltse approach for an extraforaminal disk herniation at L5/S1. This 58-year-old woman experienced hypoesthesia and progressive motor dysfunction in the left leg several hours postoperation. Urgent magnetic resonance imaging revealed an intradural hematoma at the L1/L2 to L2/L3 level in the ventral dural sac proximal to the surgical level. Surgical decompression was performed. There was no evidence of trauma, coagulopathy, or anticoagulation therapy. To our knowledge, this case is the first to report an acute sSDH proximal to the surgery level after an extraforaminal spinal surgery through the Wiltse approach for an extraforaminal disk herniation. It illustrates that attentive postoperative neurologic monitoring, even in the absence of intraoperative irregularities, remains important to diagnose and treat this complication at the early stage 7)


A 55-year-old woman without malignancy or coagulopathy history presented with progressive low back pain for the past 2 weeks. Progressive bilateral leg weakness happened 1 week ago. On the day she called for help, she presented with bilateral leg grade 2 muscle power and generalized back pain. There was no headache or meningeal sign. An absent bilateral knee reflex was found. Magnetic resonance imaging showed a space-occupying lesion at the T2-T6 and T12-L1 levels in the ventral and dorsal spinal canal, leading to cord compression. Due to rapid neurologic function deterioration, emergent T12-L1 laminectomy was performed. We found a T12-L1 tense dura sac with subdural hematoma ventral to the cord. Removal of the SDH was performed. T2-T6 levels were treated conservatively. She returned ambulant 1 week after operation. Magnetic resonance images at 3 months and 1 year later showed the SDH being absorbed and replaced by adhesive arachnoid cysts along the whole T and L spine. However, these lesions are asymptomatic for at least 2 years 8).


Sanchez et al. reported a case of Reverse Takotsubo Cardiomyopathy in an otherwise healthy 23-year-old man presenting with back pain, urinary retention, bradycardia, and hypertension. Troponin levels and brain natriuretic peptide (BNP) were elevated, and echocardiogram revealed an ejection fraction (EF) of less than 20%. In addition, MRI demonstrated a spinal subdural hematoma from T1-S1 with no cord compression. Repeated echocardiogram demonstrated an EF of 20-25% with a reverse Takotsubo pattern of cardiomyopathy. With supportive care, his clinical picture improved with normalization of cardiac enzyme and BNP values. This case represents a r-TTC presenting as heart failure in a young, apparently healthy male likely incited by a spinal subdural hematoma. To our knowledge, it is the first of its kind reported 9).


A 7-yr old girl presented to Neurology Department, Mofid Hospital, ShahidBeheshti University of Medical Sciences, Tehran, Iran with limping and pain in lower extremities and acute paraplegia without history of direct trauma. The patient had muscle weakness in lower limbs and was unable to bear weight. Deep Tendon Reflexes (DTR) in lower extremities had increased. Her MRI showed spinal subdural hematoma we reextended from T2 to T6. We performed laminectomy from T2 to T5 and about 70 cc of subdural hematoma was evacuated. One month after the surgery, the patient’s neurological deficit resolved completely. The results showed the pivotal role of attention to clinical manifestation in acute spinal subdural hematoma and early diagnosis to prevent irreversible neurologic complication 10)


Spinal subdural hematoma in pediatric nonaccidental trauma 11)


A case of spontaneous, atraumatic subdural hematoma involving the thoracic region in an 80-year-old woman on warfarin is reported. The patient presented with gross motor and sensory loss, delayed onset of incontinence, and no other symptoms. An MRI suggested an epidural hematoma concentrated around the T4-T9 levels. She was taken emergently to the OR approximately 30 hours after the initial onset of symptoms for a T3-T11 laminectomy. No epidural hematoma was noted. However, discoloration and bulging of the thecal sac were noted, and the dura was incised longitudinally from T2 to T10 revealing an expansive jelly-like blood clot which was evacuated. Postoperatively, the patient had regained 1/2 sensory function in the bilateral lower extremities. At the 2-week mark, the patient was still incontinent and showed 2/2 sensory and 2/5 motor functions in select muscle groups in her bilateral lower extremities. Completely nontraumatic, spontaneous subdural hematomas of the spine are very rare, and early surgical decompression within 24 hours from symptom onset may allow neurological recovery. Large extensive laminectomies up to 10 thoracic levels have been shown to be safe and effective in a few cases, including our case 12).


Acute lumbar spinal subdural hematoma inducing paraplegia after lumbar spinal manipulation 13).


Cases of non-traumatic spinal subdural hematoma accompanied by intracranial hemorrhage are even more rare. There are a few reports of spontaneous spinal subdural hematoma with concomitant intracranial subdural or subarachnoid hemorrhage, but not with intracerebral hemorrhage. Especially in a case of Lee et al., the evaluation and diagnosis were delayed because the spontaneous intracerebral hemorrhage accompanying the unilateral spinal subdural and subarachnoid hemorrhages caused hemiplegia. They reported a case of spinal subdural and subarachnoid hemorrhage with concomitant intracerebral hemorrhage, for the first time, with a relevant literature review 14).


A 76-year-old woman with a spinal subdural hematoma (SDH) was presented with severe back pain without headache. Magnetic resonance imaging (MRI) performed 4 days after onset showed SDH extending from Th2 to L3. She was diagnosed with spontaneous SDH without neurological manifestation, and conservative treatment was selected. Transient disturbance of orientation appeared 7 days after onset. Small subarachnoid hemorrhage (SAH) was detected on head CT, and strict antihypertensive therapy was started. Symptoms changed for the better. Back pain disappeared 4 weeks after onset. On follow-up MRI at 6 months after onset, the SDH had been resolved spontaneously. Although adhesive arachnoiditis was observed at Th4-6, the recurrence of clinical symptoms was not observed at one year and a half after onset. Spinal subdural space is almost avascular; a hematoma in a subdural space is considered to come from a subarachnoid space when it is a lot. A hemorrhage in subarachnoid space was flushed by cerebral spinal fluid; hematoma or arachnoiditis was not formed in general. In this case, hemorrhage was a lot and expansion of SDH was large enough to cause cranial SAH and arachnoiditis. But longitudinally expanded SDH did not show neurological manifestation and resolved spontaneously 15).


A 38-year-old male patient presented with sudden lower back and bilateral leg pain.

A magnetic resonance imaging (MRI) scan on the third day after the onset of symptoms revealed a subdural hematoma from L1 to S1, presenting as hyperintensities on T1 weighted sequences and hypointensities to isointensities on T2 weighted sequences.

Laminectomy and subdural evacuation were performed immediately.

An abnormal ligamentum flavum was observed intraoperatively. A histological examination revealed extravasation of blood in the degenerated ligamentum flavum. Postoperatively, the lower limb pain improved immediately. At the 6-month follow-up, the pain and numbness of the lower limb disappeared, and the muscle strength of both legs recovered completely with normal gait.

Spontaneous SSDH with ligamentum flavum hematoma was caused by a sudden increase of intravenous pressure, resulting from a marked surge in the intra-abdominal or intrathoracic pressure. Consecutive MRI scans provided valuable information, leading to a diagnosis of spontaneous SSDH 16).


Oh et al. presented a case of acute nontraumatic SSDH presenting with transient left hemiplegia for 4 hours. A magnetic resonance imaging study of cervical spine confirmed SSDH with C3-6 cervical cord compression at the left side. The patient had conservative management without recurrence. Although hemiplegia is an unusual clinical manifestation of SSDH, it should be differentiated from that of cerebrovascular origin promptly. Conservative management may be an alternative therapeutic option for selective cases with transient neurological deficits 17).


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