Intracranial pressure monitoring in children

Intracranial pressure monitoring in children

Protocols for treatment of children with severe traumatic brain injury incorporate intracranial pressure monitoring as part of a comprehensive plan to minimize secondary injuries, using either ICP and/or cerebral perfusion pressure (CPP) as the therapeutic target 1).

At least 500 children enrolled in 9 studies have demonstrated at least some association between ICP and outcome 2) 3) 4) 5) 6) 7) 8) 9) 10).

As a result, most centers adopted ICP monitoring years ago, while some have argued against the need for such an approach 11).

Data suggest that there is a small, yet statistically significant, survival advantage in patients who have ICP monitors and a GCS score of 3. However, all patients with ICP monitors experienced longer hospital length of stay, longer intensive care unit stay, and more ventilator days compared with those without ICP monitors. A prospective observational study would be helpful to accurately define the population for whom ICP monitoring is advantageous 12).

EVD and IP measurements of ICP were highly correlated, although intermittent EVD ICP measurements may fail to identify ICP events when continuously draining cerebrospinal fluid. In institutions that use continuous cerebrospinal fluid diversion as a therapy, a two-monitor system may be valuable for accomplishing monitoring and therapeutic goals 13).


In the search for a reliable, cooperation-independent, noninvasive alternative to invasive intracranial pressure monitoring in children, various approaches have been proposed, but at the present time none are capable of providing fully automated, real-time, calibration-free, continuous and accurate intracranial pressure estimates. Fanelli et al. investigated the feasibility and validity of simultaneously monitored arterial blood pressure(ABP) and middle cerebral artery (MCA) cerebral blood flow velocity (CBFV) waveforms to derive noninvasive ICP (nICP) estimates.

Invasive ICP and ABP recordings were collected from 12 pediatric and young adult patients (aged 2-25 years) undergoing such monitoring as part of routine clinical care. Additionally, simultaneous transcranial Doppler (TCD) ultrasonography-based MCA CBFV waveform measurements were performed at the bedside in dedicated data collection sessions. The ABP and MCA CBFV waveforms were analyzed in the context of a mathematical model, linking them to the cerebral vasculature’s biophysical properties and ICP. The authors developed and automated a waveform preprocessing, signal-quality evaluation, and waveform-synchronization “pipeline” in order to test and objectively validate the algorithm’s performance. To generate one nICP estimate, 60 beats of ABP and MCA CBFV waveform data were analyzed. Moving the 60-beat data window forward by one beat at a time (overlapping data windows) resulted in 39,480 ICP-to-nICP comparisons across a total of 44 data-collection sessions (studies). Moving the 60-beat data window forward by 60 beats at a time (nonoverlapping data windows) resulted in 722 paired ICP-to-nICP comparisons.

Greater than 80% of all nICP estimates fell within ± 7 mm Hg of the reference measurement. Overall performance in the nonoverlapping data window approach gave a mean error (bias) of 1.0 mm Hg, standard deviation of the error (precision) of 5.1 mm Hg, and root-mean-square error of 5.2 mm Hg. The associated mean and median absolute errors were 4.2 mm Hg and 3.3 mm Hg, respectively. These results were contingent on ensuring adequate ABP and CBFV signal quality and required accurate hydrostatic pressure correction of the measured ABP waveform in relation to the elevation of the external auditory meatus. Notably, the procedure had no failed attempts at data collection, and all patients had adequate TCD data from at least one hemisphere. Last, an analysis of using study-by-study averaged nICP estimates to detect a measured ICP > 15 mm Hg resulted in an area under the receiver operating characteristic curve of 0.83, with a sensitivity of 71% and specificity of 86% for a detection threshold of nICP = 15 mm Hg.

This nICP estimation algorithm, based on ABP and bedside TCD CBFV waveform measurements, performs in a manner comparable to invasive ICP monitoring. These findings open the possibility for rational, point-of-care treatment decisions in pediatric patients with suspected raised ICP undergoing intensive care 14).


Noninvasive quantitative measures of the peripapillary retinal structure by SD-OCT were correlated with invasively measured intracranial pressure. Optical coherence tomographic parameters showed promise as surrogate, noninvasive measures of intracranial pressure, outperforming other conventional clinical measures. Spectral-domain OCT of the peripapillary region has the potential to advance current treatment paradigms for elevated intracranial pressure in children 15).

References

1)

Adelson PD, Bratton SL, Carney NA, Chesnut RM, du Coudray HE, Goldstein B, Kochanek PM, Miller HC, Partington MP, Selden NR, Warden CR, Wright DW; American Association for Surgery of Trauma; Child Neurology Society; International Society for Pediatric Neurosurgery; International Trauma Anesthesia and Critical Care Society; Society of Critical Care Medicine; World Federation of Pediatric Intensive and Critical Care Societies. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents. Chapter 19. The role of anti-seizure prophylaxis following severe pediatric traumatic brain injury. Pediatr Crit Care Med. 2003 Jul;4(3 Suppl):S72-5. PubMed PMID: 12847355.
2)

Alberico AM, Ward JD, Choi SC, Marmarou A, Young HF. Outcome after severe head injury. Relationship to mass lesions, diffuse injury, and ICP course in pediatric and adult patients. J Neurosurg. 1987;67(5):648–656.
3)

Barzilay Z, Augarten A, Sagy M, Shahar E, Yahav Y, Boichis H. Variables affecting outcome from severe brain injury in children. Intensive Care Med. 1988;14(4):417–421.
4)

Chambers IR, Treadwell L, Mendelow AD. Determination of threshold levels of cerebral perfusion pressure and intracranial pressure in severe head injury by using receiver-operating characteristic curves: an observational study in 291 patients. J Neurosurg. 2001;94(3):412–416.
5)

Downard C, Hulka F, Mullins RJ, Piatt J, Chesnut R, Quint P, Mann NC. Relationship of cerebral perfusion pressure and survival in pediatric brain-injured patients. J Trauma. 2000;49(4):654–658. discussion 658-659.
6)

Eder HG, Legat JA, Gruber W. Traumatic brain stem lesions in children. Childs Nerv Syst. 2000;16(1):21–24.
7)

Esparza J, J MP, Sarabia M, Yuste JA, Roger R, Lamas E. Outcome in children with severe head injuries. Childs Nerv Syst. 1985;1(2):109–114.
8)

Kasoff SS, Lansen TA, Holder D, Filippo JS. Aggressive physiologic monitoring of pediatric head trauma patients with elevated intracranial pressure. Pediatr Neurosci. 1988;14(5):241–249.
9)

Michaud LJ, Rivara FP, Grady MS, Reay DT. Predictors of survival and severity of disability after severe brain injury in children. Neurosurgery. 1992;31(2):254–264.
10)

Shapiro K, Marmarou A. Clinical applications of the pressure-volume index in treatment of pediatric head injuries. J Neurosurg. 1982;56(6):819–825.
11)

Salim A, Hannon M, Brown C, Hadjizacharia P, Backhus L, Teixeira PG, Chan LS, Ford H. Intracranial pressure monitoring in severe isolated pediatric blunt head trauma. Am Surg. 2008 Nov;74(11):1088-93. PubMed PMID: 19062667.
12)

Alkhoury F, Kyriakides TC. Intracranial Pressure Monitoring in Children With Severe Traumatic Brain Injury: National Trauma Data Bank-Based Review of Outcomes. JAMA Surg. 2014 Jun;149(6):544-8. doi: 10.1001/jamasurg.2013.4329. PubMed PMID: 24789426.
13)

Exo J, Kochanek PM, Adelson PD, Greene S, Clark RS, Bayir H, Wisniewski SR, Bell MJ. Intracranial pressure-monitoring systems in children with traumatic brain injury: combining therapeutic and diagnostic tools. Pediatr Crit Care Med. 2011 Sep;12(5):560-5. doi: 10.1097/PCC.0b013e3181e8b3ee. PubMed PMID: 20625341; PubMed Central PMCID: PMC3670608.
14)

Fanelli A, Vonberg FW, LaRovere KL, Walsh BK, Smith ER, Robinson S, Tasker RC, Heldt T. Fully automated, real-time, calibration-free, continuous noninvasive estimation of intracranial pressure in children. J Neurosurg Pediatr. 2019 Aug 23:1-11. doi: 10.3171/2019.5.PEDS19178. [Epub ahead of print] PubMed PMID: 31443086.
15)

Swanson JW, Aleman TS, Xu W, Ying GS, Pan W, Liu GT, Lang SS, Heuer GG, Storm PB, Bartlett SP, Katowitz WR, Taylor JA. Evaluation of Optical Coherence Tomography to Detect Elevated Intracranial Pressure in Children. JAMA Ophthalmol. 2017 Apr 1;135(4):320-328. doi: 10.1001/jamaophthalmol.2017.0025. PubMed PMID: 28241164; PubMed Central PMCID: PMC5470406.

ABC/2

ABC/2

A is the greatest diameter by CT, B is the diameter 90 degrees to A, and C is the approximate number of CT slices with hemorrhage multiplied by the slice thickness.

Intracerebral hemorrhage

The ABC/2 method for calculating intracerebral hemorrhage (ICH) volume has been well validated. However, the formula, derived from the volume of an ellipse, assumes the shape of ICH is elliptical.

Although the ABC/2 formula for calculating elliptical ICH is well validated, it must be used with caution in ICH scans where the elliptical shape of ICH is a false assumption.

Haley et al., validated the adjustment of the ABC/2.4 method in randomization, antithrombotic-associated, heterogeneous-density, and irregular-shape ICH 1).


The ICH volumes for 118 patients were evaluated in a mean of 38 seconds and correlated with planimetric measurements (R2 = 9.6). Interrater and intrarater reliability were excellent, with an intraclass correlation of .99 for both.

Kothari et al., conclude that ICH volume can be accurately estimated in less than 1 minute with the simple formula ABC/2 2).

Rapid calculation of ICH volume at the time of initial patient presentation has clinical utility. For prognosis, a model of 30-day mortality that used the Glasgow Coma Scale and hemorrhage volume in patients with ICH correctly predicted outcome with a sensitivity and specificity of 97%.

The ABC/2 technique may also be used to identify appropriate patients with ICH suitable for randomization into therapeutic trials.

For example, the technique is the measurement method used for patient eligibility assessment in the multicenter Surgical Trial of Intracerebral Hemorrhage (J. Grotta, unpublished data, 1996). In this trial, patients with ICH and anticipated good outcome are not eligible for surgery. Thus, patients with hemorrhage volumes of less than 10 cm3 and patients with lobar hemorrhage volumes of 10 to 20 cm3 with minimal or no neurological deficits are excluded.


Lisk and colleagues demonstrated the ease and power of the ABC/2 method of volume measurement in a model of outcome after ICH but did not correlate this technique with other methods of volume measurement. The ABC/2 formula can be adjusted for CT slices of varying thickness by multiplying the number of slices of the different thicknesses on which the hematoma is seen (C of ABC/2) by the slice thickness in centimeters. Other authors have estimated hematoma volume by assuming it to approximate the volume of a sphere, an ellipsoid, or a rectangulopiped.

Only estimates of volume that use the formula for an ellipsoid have been shown to correlate with planimetric techniques.

This rapid method of measuring hemorrhage volume may allow physicians to quickly select and stratify patients in future treatment trials 3).

Meningioma

Measurement of tumor growth rates over time for patients with meningiomas has important prognostic and therapeutic implications. The objective of Opalak et al. was to compare two methods of measuring meningioma volume: (1) the simplified ellipsoid (ABC/2) method; and (2) perimetric volume measurements using imaging software modules.

Patients with conservatively managed meningiomas for at least 1.5 years were retrospectively identified from the VCU Brain and Spine Tumor Registry over a 10-year period (2005-2015). Tumor volumes were independently measured using the simplified ellipsoid and computerized perimetric methods. Intra class correlations (CC) and Bland-Altman analyses were performed.

A total of 26 patients representing 29 tumors were identified. Across 146 images, there were 24 (16%) images that were non-measurable using standard application commands with the computerized perimetric method. The mean volume obtained using the ABC/2 and computerized perimetric methods were 3.2 ± 3.4 cm3 and 3.4 ± 3.5 cm3, respectively. The mean volume difference was 0.2 cm3 (SE = 0.12; p = 0.10) across measurement methods. The concordance correlation coefficient (CCC) between methods was 0.95 (95% CI 0.91, 0.98).

There is excellent correlation between the simplified ellipsoid and computerized perimetric methods of volumetric analysis for conservatively managed meningiomas. The simplified ellipsoid method remains an excellent method for meningioma volume assessment and had an advantage over the perimetric method which failed to allow measurement of roughly one in six tumors on imaging 4).

Vestibular schwannoma

Epidural hematoma

The ABC/2 method could be used for epidural hematoma volume EDHV measurement, which would contribute to treatment decision making as well as clinical outcome prediction. However, clinicians should be aware that the ABC/2 method results in a general volume overestimation. Future studies focusing on justification of the technique to improve its accuracy would be of practical value 5).

References

1)

Haley MD, Gregson BA, Mould WA, Hanley DF, Mendelow AD. Retrospective Methods Analysis of Semiautomated Intracerebral Hemorrhage Volume Quantification From a Selection of the STICH II Cohort (Early Surgery Versus Initial Conservative Treatment in Patients With Spontaneous Supratentorial Lobar Intracerebral Haematomas). Stroke. 2018 Feb;49(2):325-332. doi: 10.1161/STROKEAHA.117.016677. Epub 2018 Jan 10. PubMed PMID: 29321340.
2) , 3)

Kothari RU, Brott T, Broderick JP, Barsan WG, Sauerbeck LR, Zuccarello M, Khoury J. The ABCs of measuring intracerebral hemorrhage volumes. Stroke. 1996 Aug;27(8):1304-5. PubMed PMID: 8711791.
4)

Opalak CF, Parry M, Rock AK, Sima AP, Carr MT, Chandra V, Workman KG, Somasundaram A, Broaddus WC. Comparison of ABC/2 estimation and a volumetric computerized method for measurement of meningiomas using magnetic resonance imaging. J Neurooncol. 2019 Aug 10. doi: 10.1007/s11060-019-03205-z. [Epub ahead of print] PubMed PMID: 31401721.
5)

Hu TT, Yan L, Yan PF, Wang X, Yue GF. Assessment of the ABC/2 Method of Epidural Hematoma Volume Measurement as Compared to Computer-Assisted Planimetric Analysis. Biol Res Nurs. 2015 Mar 23. pii: 1099800415577634. [Epub ahead of print] PubMed PMID: 25802386.

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 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 3).

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 4).

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 5).


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 6).

Pneumocephalus

Remaining pneumocephalus is seen as an approved factor of recurrence 7) 8).

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 9).

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 10).

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 11).

Diabetes

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

12) 13) 14).


Balser et al. report 11% recurrence, which included individuals who recurred as late as 3 years after initial diagnosis 15).

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 16).

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 17).

Irrigation with artificial cerebrospinal fluid (ACF) decreased the rate of CSDH recurrence 18).

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 19).

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 20).

Implantation of a reservoir 21) 22) 23).

Subdural-peritoneal shunt 24).

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 25) 26) 27) 28) 29) 30).

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 31).

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 32).

Case series

Case reports

References

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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.
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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.
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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.
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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.
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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.
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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
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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
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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.
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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.
11)

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.
12)

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.
13)

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.
14)

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.
17)

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.
18)

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.
20)

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.
21)

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.
22)

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.
23)

Laumer R. Implantation of a reservoir for refractory chronic subdural hematoma. Neurosurgery. 2002 Mar;50(3):672. PubMed PMID: 11841742.
24)

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.
25)

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.
26)

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.
27)

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