Neurotrauma

Chronic subdural hematoma

Chronic subdural hematoma

J.Sales-Llopis

Neurosurgery Department, University General Hospital of Alicante, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Alicante, Spain

Latest articles

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Definition

Chronic subdural hematoma (CSDH) is an encapsulated collection of old blood, mostly or totally liquefied and located between the dura mater and the arachnoid mater.

They are arbitrarily defined as those hematomas presenting 21 days or more after injury. These numbers are not absolute, and a more accurate classification of a subdural hematoma usually is based on imaging characteristics.

History

Chronic subdural hematoma history

COVID-19 in chronic subdural hematoma

COVID-19 in chronic subdural hematoma

Epidemiology

Chronic subdural hematoma epidemiology.

Etiology

see Chronic subdural hematoma etiology.

Chemokines in Chronic Subdural Hematoma

Chemokines in Chronic Subdural Hematoma

Classification

see Chronic subdural hematoma classification.

Pathophysiology

Chronic subdural hematoma pathophysiology.

Pathology

cSDHs have a tendency to persist and gradually increase in volume over time. The disease is thought to be related to a cycle of chronic inflammation and angiogenesis. An original hemorrhage forms and fibrinolysis ensues with the liquefaction of the initial clot. The subsequent blood breakdown products stimulate inflammation and thickening of the inner dural layer (ie, ‘dural border cells). This process incites angiogenesis with the ingrowth of immature capillaries, which chronically leak blood. These microhemorrhages result in the progressive enlargement of the collection with increased fibrinolytic activity, inflammation, and further angiogenesis, membrane formation, and vessel proliferation. The rate of accumulation of blood products outpaces physiological reabsorption and the collection gradually enlarges. Thus the entire basis for the pathology is the formation of leaky vascular membranes, which incite a positive feedback cycle of continued hemorrhage, inflammation, and angiogenesis 1) 2)

Chronic subdural hematoma (CSDH) is characterized by an “old” encapsulated collection of blood and blood breakdown products between the brain and its outermost covering (the dura).

It is delimited by an outer and inner membrane. In between are blood, plasma, cerebrospinal fluid, membranes, and a mixture of inflammatory angiogenic fibrinolytic and coagulation factors. These factors maintain a self-perpetuating cycle of bleeding, lysis, and growing of neo-membranes and neo-capillaries 3).

Clinical Features

see Chronic subdural hematoma clinical features.

Scales

Glasgow Coma Scale.

Markwalder grading score.

Modified Rankin Scale.

Oslo grading system.

Diagnosis

Chronic subdural hematoma diagnosis

Biomarkers

The association between the biomarkers of inflammation and angiogenesis, and the clinical and radiological characteristics of CSDH patients, need further investigation. The high number of biomarkers compared to the number of observations, the correlation between biomarkers, missing data and skewed distributions may limit the usefulness of classical statistical methods.

Pripp et al. explored lasso regression to assess the association between 30 biomarkers of inflammation and angiogenesis at the site of lesions, and selected clinical and radiological characteristics in a cohort of 93 patients. Lasso regression performs both variable selection and regularization to improve the predictive accuracy and interpretability of the statistical model. The results from the lasso regression showed analysis exhibited lack of robust statistical association between the biomarkers in hematoma fluid with age, gender, brain infarct, neurological deficiencies and volume of hematoma. However, there were associations between several of the biomarkers with postoperative recurrence requiring reoperation. The statistical analysis with lasso regression supported previous findings that the immunological characteristics of CSDH are local. The relationship between biomarkers, the radiological appearance of lesions and recurrence requiring reoperation have been inclusive using classical statistical methods on these data, but lasso regression revealed an association with inflammatory and angiogenic biomarkers in hematoma fluid. They suggest that lasso regression should be a recommended statistical method in research on biological processes in CSDH patients 4).

Differential diagnosis

Chronic subdural hematoma (CSDH) is a disease of the meninges and is to be distinguished from hygroma and subdural empyema.

Subdural effusion in the setting of dural metastases is very rare and may be difficult to be distinguished from chronic subdural hematoma. Such lesions could be missed and could be the cause of recurrence in CSDH. A contrast-enhanced brain CT scan is recommended to diagnose dural metastases.

Rosai–Dorfman disease may be mistaken for a CSDH on imaging. This disease is an uncommon, benign systemic histioproliferative disease characterized by massive lymphadenopathy, particularly in the head and neck region, and is often associated with extranodal involvement. CSDH can also develop in multifocal fibrosclerosis (MFS) which is a rare disorder of unknown etiology, characterized by chronic inflammation with dense fibrosis and lymphoplasmacytic infiltration into the connective tissue of various organs. The mechanism of the formation of CSDH is presumed to involve reactive granular membrane together with subdural collection. On the other hand, the extramedullary erythropoiesis within CSDH can be confused with metastatic malignant tumors, such as lymphoma, carcinoma, and malignant melanoma 5).

A 44-year old woman with gastric adenocarcinoma was presented with headache and a hypodense subdural collection in right fronto-parietal in brain CT. Burr-hole irrigation was performed with the impression of chronic subdural hematoma, but nonhemorrhagic xantochromic fluid was evacuated without malignant cell. Brain CT on the 11th day depicted fluid re-accumulation and noticeable midline shift, necessitating craniotomy and removing the affected dura.

Because the affected dura can be supposed as the main source of subdural effusion, resection of the involved dura is obligatory for the appropriate palliative management of such patients 6).

Treatment

see Chronic subdural hematoma treatment.

Outcome

see Chronic subdural hematoma outcome.

Complications

The progression of CSDH is an angiogenic process, involving inflammatory mediators that affect vascular permeability, microvascular leakage, and hematoma thickness.

see Chronic subdural hematoma surgery complication.

Recurrence

see Chronic subdural hematoma recurrence.

Systematic Reviews

Chronic subdural hematoma systematic reviews.

Bibliometrics

A bibliometrics retrieved 1424 CSDH-related articles published since the beginning of the twenty-first century. There was a general increase in both the number of published articles and the mean number of citations. The authors, institutions, and journals that contributed the most to the field of CSDH were Jianning Zhang, Tianjin Medical University General Hospital, and world neurosurgery, respectively. The reference co-citation network identified 13 clusters with significant modularity Q scores and silhouette scores (Q = 0.7124, S = 0.8536). The major research categories were (1) the evolution of the therapeutic method and (2) the etiology and pathology of CSDH. Keyword analysis revealed that ‘middle meningeal artery embolization‘ was the latest burst keyword.

This study identified the most influential countries, authors, institutions, and journals contributing to CSDH research and discussed the hotspots and the latest subjects of CSDH research 7)

Case series

see Chronic subdural hematoma case series.

Case reports

see Chronic subdural hematoma case reports.

Research

Experimental models

Attempts to create CSDH have been made in mice, rats, cats, dogs and monkeys. Methods include injection or surgical implantation of clotted blood or various other blood products and mixtures into the potential subdural space or the subcutaneous space. No intracranial model produced a progressively expanding CSDH. Transient hematoma expansion with liquification could be produced by subcutaneous injections in some models. Spontaneous subdural blood collections were found after creation of hydrocephalus in mice by systemic injection of the neurotoxin, 6-aminonicotinamide. The histology of the hematoma membranes in several models resembles the appearance in humans. None of the models has been replicated since its first description.

D’Abbondanza et al. did not find a report of a reproducible, well-described animal model of human CSDH 8).

Retracted articles

Zhuang Y, Jiang M, Zhou J, Liu J, Fang Z, Chen Z. Surgical Treatment of Bilateral Chronic Subdural Hematoma. Comput Intell Neurosci. 2022 Jun 27;2022:2823314. doi: 10.1155/2022/2823314. Retraction in: Comput Intell Neurosci. 2022 Dec 25;2022:9806807. PMID: 35795746; PMCID: PMC9252673.

References

1)

Ito H , Yamamoto S , Komai T , et al . Role of local hyperfibrinolysis in the etiology of chronic subdural hematoma. J Neurosurg 1976;45:26–31.doi:10.3171/jns.1976.45.1.0026
2)

Edlmann E , Giorgi-Coll S , Whitfield PC , et al . Pathophysiology of chronic subdural haematoma: inflammation, angiogenesis and implications for pharmacotherapy. J Neuroinflammation 2017;14:108.doi:10.1186/s12974-017-0881-y
3)

Frati A, Salvati M, Mainiero F, Ippoliti F, Rocchi G, Raco A, Caroli E, Cantore G, Delfini R (2004) Inflammation markers and risk factors for recurrence in 35 patients with a posttraumatic chronic subdural haematoma: a prospective study. J Neurosurg 100:24–32
4)

Pripp AH, Stanišić M. Association between biomarkers and clinical characteristics in chronic subdural hematoma patients assessed with lasso regression. PLoS One. 2017 Nov 6;12(11):e0186838. doi: 10.1371/journal.pone.0186838. eCollection 2017. PubMed PMID: 29107999.
5)

Yadav YR, Parihar V, Namdev H, Bajaj J. Chronic subdural hematoma. Asian J Neurosurg. 2016 Oct-Dec;11(4):330-342. Review. PubMed PMID: 27695533; PubMed Central PMCID: PMC4974954.
6)

Mirsadeghi SM, Habibi Z, Meybodi KT, Nejat F, Tabatabai SA. Malignant subdural effusion associated with disseminated adenocarcinoma: a case report. Cases J. 2008 Nov 18;1(1):328. doi: 10.1186/1757-1626-1-328. PubMed PMID: 19019205; PubMed Central PMCID: PMC2611978.
7)

Chen R, Wei Y, Xu X, Zhang R, Tan Y, Zhang G, Yin H, Dai D, Li Q, Zhao R, Huang Q, Xu Y, Yang P, Liu J, Zuo Q. A bibliometric analysis of chronic subdural hematoma since the twenty-first century. Eur J Med Res. 2022 Dec 27;27(1):309. doi: 10.1186/s40001-022-00959-7. PMID: 36572939.
8)

D’Abbondanza JA, Loch Macdonald R. Experimental models of chronic subdural hematoma. Neurol Res. 2014 Feb;36(2):176-88. doi: 10.1179/1743132813Y.0000000279. Epub 2013 Dec 6. Review. PubMed PMID: 24172841.

Frontal sinus cranialization

Frontal sinus cranialization

Cranialization refers to the removal of the posterior table of the frontal sinus with occlusion of the inlet into the frontonasal ducts and allowing the neural structures, mainly frontal lobes of the brain and the intact dura, to move directly posterior to the anterior table of the frontal bone 1).

Frontal sinus cranialization with closure via bifrontal pericranial flaps is the gold standard for separating the nasofrontal recess from the intracranial cavity for posterior table defects. Despite the high success rate, cerebrospinal fluid (CSF) leak may persist and is particularly challenging when vascularized reconstructive options from the bicoronal incision are exhausted.

Indications

For appropriately selected patients with extensive frontal injuries, cranialization is a procedure that provides an excellent margin of long-term safety and a satisfactory esthetic outcome. Individual surgeons will continue to differ at times as to the appropriate management of a particular frontal injury. Nevertheless, for the most severe of these, cranialization continues to be the definitive treatment 2).

In the case series of Donath and Sindwani indications included extensive frontal sinus fractures involving the posterior table (78.9%), mucocele (10.5%), arteriovenous malformation (5.3%), and frontal bone osteomyelitis (5.3%). 3).

For Calis et al. it seems that isolated anterior table fractures with a maximum amount of displacement of less than 4.5 mm can be treated conservatively without leading to contour deformities. CSF leakage in the acute setting might not always require cranialization and this may spontaneously resolve within 10 days. Cranialization should be considered whenever CSF leakage lasts longer than 10 days 4).

For Echo et al. the first step in assessing frontal sinus fractures involves the assessment of the posterior table of the frontal sinus and determining the need for cranialization. Criteria for cranialization include severe posterior table fracture, CSF leak greater than 1 to 2 weeks, or in any situation where a craniotomy is otherwise indicated. Any patient who meets these criteria would undergo a cranialization of the frontal sinus, obliteration of the nasofrontal outflow tracts, and reconstruction of the anterior table 5).

Using a pedicle vascularized pericranial flap as an extra layer and an autologous fence above the dura adds more protection to the brain. This flap may reduce the risk of CSF leak and perioperative infections and improve the overall results. Yet, more prospective and randomized trials are recommended 6).

Cranialization of the frontal sinus appears to be a good option for the prevention of secondary mucocele development after open excision of benign frontal sinus lesions 7).

Technique

Frontal sinus cranialization technique

Case series

A retrospective review of 3 patients (all male; ages 42, 43, and 69 yr) with persistent CSF leak despite frontal sinus cranialization and repair with bifrontal pericranium was performed. Etiology of injury was traumatic in 2 patients and iatrogenic in 1 patient after anaplastic meningioma treatment. To create space for the flap and repair the nasofrontal ducts, endoscopic Draf III (Case 1, 3) or Draf IIb left frontal sinusotomy (Case 2) was performed. The forearm flap was harvested, passed through a Caldwell-Luc exposure, and placed within the Draf frontal sinustomy. The flap vessels were tunneled to the left neck and anastomosed to the facial vessels by the mandibular notch.

Intraoperatively, the flaps were well-seated and provided a watertight seal. Postoperative hospital courses were uncomplicated. There were no new CSF leaks or flap necrosis at 12, 14, and 16 mo.

Endoscopic endonasal free flap reconstruction through a Draf procedure is a novel viable option for persistent CSF leak after failed frontal sinus cranialization 8).

Soto et al. presented the outcome data from 28 cases of frontal sinus trauma due to gunshot wounds. There was a statistically significant difference (P = 0.049) in the type reconstructive strategy employed with each type of flap, with pericranial flaps primarily used in cranialization, temporal grafts were more likely to be used in obliteration, and free flaps were more likely to be used in cranialization. The overall major complication rate was 52% (P = 0.248), with the most common acute major complication being cerebrospinal fluid leak (39%) and the major chronic was an abscess (23.5%).

This report explores the management of frontal sinus trauma and presents short-term outcomes of treatment for penetrating gunshot wounds at a tertiary referral center 9).

Shin et al. suggested a combination flap of galea and reverse temporalis muscle as a method for reconstruction of huge skull base defect.

From 2016 to 2019, a retrospective review was conducted, assessing 7 patients with bone defect which is not just opening of frontal sinus but extends to frontal sinus and cribriform plate. Reconstructions were done by combination of galeal flap and reverse temporalis muscle flap transposition.

Defects were caused by nasal cavity tumor with intracranial extension or brain tumor with nasal cavity extension. There was no major complication in every case. During the follow up period, no patient had signs of complication such as ascending infection, herniation and CSF rhinorrhea. Postoperative radiologic images of all patients that were taken at least 6 months after the surgery showed that flaps maintained the lining and the volume well.

Conventional reconstruction of skull base defect with galeal flap is not effective enough to cover the large sized defect. In conclusion, galeal flap in combination with reverse temporalis muscle flap can effectively block the communication of nasal cavity and intracranium 10).

19 patients underwent (bilateral) frontal sinus cranialization with the pericranial flap between 2000 and 2005. Indications included extensive frontal sinus fractures involving the posterior table (78.9%), mucocele (10.5%), arteriovenous malformation (5.3%), and frontal bone osteomyelitis (5.3%). There were no intraoperative complications. A postoperative cerebrospinal fluid leak occurred in one patient with extensive skull base injuries. This was repaired endoscopically. Follow-up ranged from 9 to 55 months.

The pericranial flap is easily harvested and versatile. Using this vascularized tissue during cranialization affords added protection by providing an extra barrier between the intracranial cavity and the frontal bone and sinonasal tract. This technique is inexpensive, safe, and effective and should be considered when cranialization of the frontal sinus is performed 11).

Case reports

A 47-year-old man with adenoid cystic carcinoma who underwent secondary reconstruction of the frontal bone with a split-iliac crest bone flap based on the deep circumflex iliac artery. The patient’s course following an initial ablative procedure was complicated by recurrent periorbital cellulitis, radiation, and eventual recurrence of the malignancy. Reconstructive requirements included restoration of the superior orbital rim, cranialization of the frontal sinus, and reconstruction of a sizeable frontal bone defect. In this setting, the iliac crest served as an excellent reconstructive option owing to its natural curvature and large surface area. The split-iliac crest deep circumflex iliac artery bone flap offers a robust and valuable reconstructive option for calvarial defects in hostile surgical fields 12).

1)

https://plasticsurgerykey.com/frontal-sinus-cranialization/
2)

Ruggiero, F. P., & Zender, C. A. (2010). Frontal sinus cranialization. Operative Techniques in Otolaryngology-Head and Neck Surgery, 21(2), 143-146. https://doi.org/10.1016/j.otot.2010.03.001
3) , 11)

Donath A, Sindwani R. Frontal sinus cranialization using the pericranial flap: an added layer of protection. Laryngoscope. 2006 Sep;116(9):1585-8. doi: 10.1097/01.mlg.0000232514.31101.39. PMID: 16954984.
4)

Calis M, Kaplan GO, Küçük KY, Altunbulak AY, Akgöz Karaosmanoğlu A, Işıkay Aİ, Mavili ME, Tunçbilek G. Algorithms for the management of frontal sinus fractures: A retrospective study. J Craniomaxillofac Surg. 2022 Oct 4:S1010-5182(22)00144-5. doi: 10.1016/j.jcms.2022.09.007. Epub ahead of print. PMID: 36220677.
5)

Echo A, Troy JS, Hollier LH Jr. Frontal sinus fractures. Semin Plast Surg. 2010 Nov;24(4):375-82. doi: 10.1055/s-0030-1269766. PubMed PMID: 22550461; PubMed Central PMCID: PMC3324222.
6)

Hammad W, Mahmoud B, Alsharif S. Frontal sinus cranialization using pericranial flap: Experience in thirty cases. Saudi J Otorhinolaryngol Head Neck Surg 2021;23:55-9
7)

Horowitz G, Amit M, Ben-Ari O, Gil Z, Abergel A, Margalit N, et al. (2013) Cranialization of the Frontal Sinus for Secondary Mucocele Prevention following Open Surgery for Benign Frontal Lesions. PLoS ONE 8(12): e83820. https://doi.org/10.1371/journal.pone.0083820
8)

Lee JJ, Wick EH, Chicoine MR, Dowling JL, Leuthardt EC, Santiago P, Pipkorn P. Endonasal Free Flap Reconstruction Combined With Draf Frontal Sinusotomy for Complex Cerebrospinal Fluid Leak: A Technical Report & Case Series. Oper Neurosurg (Hagerstown). 2021 Nov 15;21(6):478-484. doi: 10.1093/ons/opab309. PMID: 34423844; PMCID: PMC8599085.
9)

Soto E, Ovaitt AK, Clark AR, Tindal RR, Chiasson KF, Aryanpour Z, Ananthasekar S, Grant JH, Myers RP. Reconstructive Management of Gunshot Wounds to the Frontal Sinus: An Urban Trauma Center’s Perspective. Ann Plast Surg. 2021 Jun 1;86(6S Suppl 5):S550-S554. doi: 10.1097/SAP.0000000000002857. PMID: 33883442; PMCID: PMC8187270.
10)

Shin D, Yang CE, Kim YO, Hong JW, Lee WJ, Lew DH, Chang JH, Kim CH. Huge Anterior Skull Base Defect Reconstruction on Communicating Between Cranium and Nasal Cavity: Combination Flap of Galeal Flap and Reverse Temporalis Flap. J Craniofac Surg. 2020 Feb 7. doi: 10.1097/SCS.0000000000006221. [Epub ahead of print] PubMed PMID: 32049922.
12)

Baudoin ME, Palines PA, Stalder MW. Frontal Cranioplasty with Vascularized Split-iliac Crest Bone Flap. Plast Reconstr Surg Glob Open. 2021 Nov 16;9(11):e3934. doi: 10.1097/GOX.0000000000003934. PMID: 34796087; PMCID: PMC8594656.

Pediatric traumatic brain injury outcome

Pediatric traumatic brain injury outcome

see also Traumatic brain injury outcome.

Latest articles

Neuropsychological and behavioral outcomes for injured children vary with the severity of the injury, child age at injury, premorbid child characteristics, family factors, and the family’s socioeconomic status. Each of these factors needs to be taken into account when designing rehabilitation strategies and assessing factors related to outcomes 1)

The Functional Status Score (FSS) can be implemented as part of routine practice in two different healthcare systems and the relationships observed between the FSS and patient characteristics can serve as a baseline for work going forward in the coming years. As a field, establishing which outcomes tests can be readily administered while also measuring relevant outcomes for various populations of children with TBI is an essential next step in developing therapies for this disorder that is highly prevalent and morbid 2).

The multi-center, prospectively collected CENTER-TBI core and registry databases were screened and patients were included when younger than 18 years at enrollment and admitted to the regular ward (admission stratum) or intensive care unit (ICU stratum) following TBI. Patient demographics, injury causes, clinical findings, brain CT imaging details, and outcome (GOSE at 6 months follow-up) were retrieved and analyzed. Injury characteristics were compared between patients admitted to the regular ward and ICU and a multivariate analysis of factors predicting an unfavorable outcome (GOSE 1-4) was performed. Results from the core study were compared to the registry dataset which includes larger patient numbers but no follow-up data. Results: Two hundred and twenty-seven patients in the core dataset and 687 patients in the registry dataset were included in this study. In the core dataset, road-traffic incidents were the most common cause of injury overall and in the ICU stratum, while incidental falls were most common in the admission stratum. Brain injury was considered serious to severe in the majority of patients and concurrent injuries in other body parts were very common. Intracranial abnormalities were detected in 60% of initial brain CTs. Intra- and extracranial surgical interventions were performed in one-fifth of patients. The overall mortality rate was 3% and the rate of unfavorable outcomes was 10%, with those numbers being considerably higher among ICU patients. GCS and the occurrence of secondary insults could be identified as independent predictors of an unfavorable outcome 3).

There are few specific prognostic models specifically developed for the pediatric traumatic brain injury (TBI) population.

Fang et al. aimed to combine multiple machine learning approaches to building hybrid models for predicting the prognosis and length of hospital stay for adults and children with TBI.

They collected relevant clinical information from patients treated at the Neurosurgery Center of the Second Affiliated Hospital of Anhui Medical University between May 2017 and May 2022, of which 80% was used for training the model and 20% for testing via screening and data splitting. They trained and tested the machine learning models using 5 cross-validations to avoid overfitting. In the machine learning models, 11 types of independent variables were used as input variables and the Glasgow Outcome Scale score, was used to evaluate patients’ prognosis, and patient length of stay was used as the output variable. Once the models were trained, we obtained and compared the errors of each machine-learning model from 5 rounds of cross-validation to select the best predictive model. The model was then externally tested using clinical data of patients treated at the First Affiliated Hospital of Anhui Medical University from June 2021 to February 2022.

Results: The final convolutional neural network-support vector machine (CNN-SVM) model predicted the Glasgow Outcome Scale score with an accuracy of 93% and 93.69% in the test and external validation sets, respectively, and an area under the curve of 94.68% and 94.32% in the test and external validation sets, respectively. The mean absolute percentage error of the final built convolutional neural network-support vector regression (CNN-SVR) model predicting inpatient time in the test set and external validation set was 10.72% and 10.44%, respectively. The coefficient of determination (R2) was 0.93 and 0.92 in the test set and external validation set, respectively. Compared with a back-propagation neural network, CNN, and SVM models built separately, our hybrid model was identified to be optimal and had high confidence.

This study demonstrates the clinical utility of 2 hybrid models built by combining multiple machine learning approaches to accurately predict the prognosis and length of stay in hospital for adults and children with TBI. Application of these models may reduce the burden on physicians when assessing TBI and assist clinicians in the medical decision-making process 4).

Mikkonen et al., tested the predictive performance of existing prognostic tools, originally developed for the adult TBI population, in pediatric TBI patients requiring stays in the ICU.

They used the Finnish Intensive Care Consortium database to identify pediatric patients (< 18 years of age) treated in 4 academic ICUs in Finland between 2003 and 2013. They tested the predictive performance of 4 classification systems-the International Mission for Prognosis and Analysis of Clinical Trials (IMPACT) TBI model, the Helsinki CT score, the Rotterdam CT score, and the Marshall CT classification-by assessing the area under the receiver operating characteristic curve (AUC) and the explanatory variation (pseudo-R2 statistic). The primary outcome was 6-month functional outcome (favorable outcome defined as a Glasgow Outcome Scale score of 3-5).

Overall, 341 patients (median age 14 years) were included; of these, 291 patients had primary head CT scans available. The IMPACT core-based model showed an AUC of 0.85 (95% CI 0.78-0.91) and a pseudo-R2 value of 0.40. Of the CT scoring systems, the Helsinki CT score displayed the highest performance (AUC 0.84, 95% CI 0.78-0.90; pseudo-R2 0.39) followed by the Rotterdam CT score (AUC 0.80, 95% CI 0.73-0.86; pseudo-R2 0.34).

Prognostic tools originally developed for the adult TBI population seemed to perform well in pediatric TBI. Of the tested CT scoring systems, the Helsinki CT score yielded the highest predictive value 5).

1)

Keenan HT, Bratton SL. Epidemiology and outcomes of pediatric traumatic brain injury. Dev Neurosci. 2006;28(4-5):256-63. doi: 10.1159/000094152. PMID: 16943649.
2)

Bell MJ. Outcomes for Children With Traumatic Brain Injury-How Can the Functional Status Scale Contribute? Pediatr Crit Care Med. 2016 Dec;17(12):1185-1186. doi: 10.1097/PCC.0000000000000950. PMID: 27918390; PMCID: PMC5142208.
3)

Riemann L, Zweckberger K, Unterberg A, El Damaty A, Younsi A; Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) Investigators and Participants. Injury Causes and Severity in Pediatric Traumatic Brain Injury Patients Admitted to the Ward or Intensive Care Unit: A Collaborative European Neurotrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) Study. Front Neurol. 2020 Apr 30;11:345. doi: 10.3389/fneur.2020.00345. PMID: 32425879; PMCID: PMC7205018.
4)

Fang C, Pan Y, Zhao L, Niu Z, Guo Q, Zhao B. A Machine Learning-Based Approach to Predict Prognosis and Length of Hospital Stay in Adults and Children With Traumatic Brain Injury: Retrospective Cohort Study. J Med Internet Res. 2022 Dec 9;24(12):e41819. doi: 10.2196/41819. PMID: 36485032.
5)

Mikkonen ED, Skrifvars MB, Reinikainen M, Bendel S, Laitio R, Hoppu S, Ala-Kokko T, Karppinen A, Raj R. Validation of prognostic models in intensive care unit-treated pediatric traumatic brain injury patients. J Neurosurg Pediatr. 2019 Jun 7:1-8. doi: 10.3171/2019.4.PEDS1983. [Epub ahead of print] PubMed PMID: 31174193.

Deep Brain Stimulation for Post-Traumatic Stress Disorder

Deep Brain Stimulation for Post-Traumatic Stress Disorder

In 2018 the application of DBS for PTSD was still strictly investigational and animal models suggest that stimulation of the amygdala, ventral striatum, hippocampus, and prefrontal cortex may be effective in fear extinction and anxiety-like behavior 1).

Neuroimaging, preclinical, and preliminary clinical data suggested that the use of DBS for the treatment of PTSD may be practical 2).

PTSD is the only potential clinical indication for DBS that shows extensive animal research prior to human applications. Nevertheless, DBS for PTSD remains highly investigational. Despite several years of government funding of DBS research in view of treating severe PTSD in combat veterans, ethical dilemmas, recruitment difficulties, and issues related to use of DBS in such a complex and heterogenous disorder remain prevalent 3).

Hamani et al. treated four posttraumatic stress disorder (PTSD) patients with DBS delivered to the subgenual cingulum and the uncinate fasciculus. In addition to validated clinical scales, patients underwent neuroimaging studies and psychophysiological assessments of fear conditioning, extinction, and recall. They show that the procedure is safe and potentially effective (55% reduction in Clinical Administered PTSD Scale scores). Posttreatment imaging data revealed metabolic activity changes in PTSD neurocircuits. During psychophysiological assessments, patients with PTSD had higher skin conductance responses when tested for recall compared to healthy controls. After DBS, this objectively measured variable was significantly reduced. Last, they found that a ratio between recall of extinguished and nonextinguished conditioned responses had a strong correlation with clinical outcomes. As this variable was recorded at baseline, it may comprise a potential biomarker of treatment response 4).

Amygdala Deep Brain Stimulation for Post-Traumatic Stress Disorder

Functional neuroimaging studies have suggested that amygdala hyperactivity is responsible for the symptoms of PTSD. Deep brain stimulation (DBS) can functionally reduce the activity of a cerebral target by delivering an electrical signal through an electrode. We tested whether DBS of the amygdala could be used to treat PTSD symptoms. Rats traumatized by inescapable shocks, in the presence of an unfamiliar object, develop the tendency to bury the object when re-exposed to it several days later. This behavior mimics the symptoms of PTSD. 10 Sprague-Dawley rats underwent the placement of an electrode in the right basolateral nucleus of the amygdala (BLn). The rats were then subjected to a session of inescapable shocks while being exposed to a conspicuous object (a ball). Five rats received DBS treatment while the other 5 rats did not. After 7 days of treatment, the rats were re-exposed to the ball and the time spent burying it under the bedding was recorded. Rats treated with BLn DBS spent on average 13 times less time burying the ball than the sham control rats. The treated rats also spent 18 times more time exploring the ball than the sham control rats. In conclusion, the behavior of treated rats in this PTSD model was nearly normalized. We argue that these results have direct implications for patients suffering from treatment-resistant PTSD by offering a new therapeutic strategy 5)

1)

Lavano A, Guzzi G, Della Torre A, Lavano SM, Tiriolo R, Volpentesta G. DBS in Treatment of Post-Traumatic Stress Disorder. Brain Sci. 2018 Jan 20;8(1):18. doi: 10.3390/brainsci8010018. PMID: 29361705; PMCID: PMC5789349.
2)

Reznikov R, Hamani C. Posttraumatic Stress Disorder: Perspectives for the Use of Deep Brain Stimulation. Neuromodulation. 2016 Dec 19. doi: 10.1111/ner.12551. [Epub ahead of print] Review. PubMed PMID: 27992092.
3)

Meeres J, Hariz M. Deep Brain Stimulation for Post-Traumatic Stress Disorder: A Review of the Experimental and Clinical Literature. Stereotact Funct Neurosurg. 2022 Jan 3:1-13. doi: 10.1159/000521130. Epub ahead of print. PMID: 34979516.
4)

Hamani C, Davidson B, Corchs F, Abrahao A, Nestor SM, Rabin JS, Nyman AJ, Phung L, Goubran M, Levitt A, Talakoub O, Giacobbe P, Lipsman N. Deep brain stimulation of the subgenual cingulum and uncinate fasciculus for the treatment of posttraumatic stress disorder. Sci Adv. 2022 Dec 2;8(48):eadc9970. doi: 10.1126/sciadv.adc9970. Epub 2022 Dec 2. PMID: 36459550.
5)

Langevin JP, De Salles AA, Kosoyan HP, Krahl SE. Deep brain stimulation of the amygdala alleviates post-traumatic stress disorder symptoms in a rat model. J Psychiatr Res. 2010 Dec;44(16):1241-5. doi: 10.1016/j.jpsychires.2010.04.022. Epub 2010 May 26. PMID: 20537659.

Serum Biomarkers for Traumatic Brain Injury

Serum Biomarkers for Traumatic Brain Injury

Traumatic brain injury (TBI) is frequently associated with abnormal blood-brain barrier function, resulting in the release of factors that can be used as molecular biomarkers of TBI, among them GFAP, UCH-L1, S100B, and NSE. Although many experimental studies have been conducted, clinical consolidation of these biomarkers is still needed to increase the predictive power and reduce the poor outcome of TBI. Interestingly, several of these TBI biomarkers are oxidatively modified to carbonyl groups, indicating that markers of oxidative stress could be of predictive value for the selection of therapeutic strategies 1).

Unlike other organ-based diseases where rapid diagnosis employing biomarkers from blood tests are clinically essential to guide diagnosis and treatment, there are no rapid, definitive diagnostic blood tests for TBI. Over the last decade there has been a myriad of studies exploring many promising biomarkers. Despite the large number of published studies there is still a lack of any FDA-approved biomarkers for clinical use in adults and children. There is now an important need to validate and introduce them into the clinical setting 2).

Richter et al. aimed to assess if day of injury serum protein biomarkers could identify critically ill TBI patients in whom the risks of transfer are compensated by the likelihood of detecting management-altering neuroimaging findings.

Data were obtained from the Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) study. Eligibility criteria included: TBI patients aged ≥ 16 years, Glasgow Coma Score (GCS) < 13 or patient intubated with unrecorded pre-intubation GCS, CT with Marshall score < 3, serum biomarkers (GFAP, NFL, NSE, S100B, Tau, UCH-L1) sampled ≤ 24 h of injury, MRI < 30 days of injury. The degree of axonal injury on MRI was graded using the Adams-Gentry classification. The association between serum concentrations of biomarkers and Adams-Gentry stage was assessed and the optimum threshold concentration identified, assuming different minimum sensitivities for the detection of brainstem injury (Adams-Gentry stage 3). A cost-benefit analysis for the USA and UK health care settings was also performed.

Among 65 included patients (30 moderate-severe, 35 unrecorded) axonal injury was detected in 54 (83%) and brainstem involvement in 33 (51%). In patients with moderate-severe TBI, brainstem injury was associated with higher concentrations of NSE, Tau, UCH-L1 and GFAP. If the clinician did not want to miss any brainstem injury, NSE could have avoided MRI transfers in up to 20% of patients. If a 94% sensitivity was accepted considering potential transfer-related complications, GFAP could have avoided 30% of transfers. There was no added net cost, with savings up to £99 (UK) or $612 (US). No associations between proteins and axonal injury were found in intubated patients without a recorded pre-intubation GCS.

Serum protein biomarkers show potential to safely reduce the number of transfers to MRI in critically ill patients with moderate-severe TBI at no added cost 3).

Systematic reviews

Mozaffari et al. created a comprehensive appraisal of the most prominent serum biomarkers used in the assessment and care of TBI.The PubMed, Scopus, Cochrane, and Web of Science databases were queried with the terms “biomarker” and “traumatic brain injury” as search terms with only full-text, English articles within the past 10 years selected. Non-human studies were excluded, and only adult patients fell within the purview of this analysis. A total of 528 articles were analyzed in the initial search with 289 selected for screening. A further 152 were excluded for primary screening. Of the remaining 137, 54 were included in the final analysis. Serum biomarkers were listed into the following broad categories for ease of discussion: immune markers and markers of inflammation, hormones as biomarkers, coagulation and vasculature, genetic polymorphisms, antioxidants and oxidative stress, apoptosis and degradation pathways, and protein markers. Glial fibrillary acidic protein(GFAP), S100, and neurons specific enolase (NSE) were the most prominent and frequently cited markers. Amongst these three, no single serum biomarker demonstrated neither superior sensitivity nor specificity compared to the other two, therefore noninvasive panels should incorporate these three serum biomarkers to retain sensitivity and maximize specificity for TBI 4).

S100B in mild traumatic brain injury

S100B in mild traumatic brain injury

Latest articles

1)

Mendes Arent A, de Souza LF, Walz R, Dafre AL. Perspectives on Molecular Biomarkers of Oxidative Stress and Antioxidant Strategies in Traumatic Brain Injury. Biomed Res Int. 2014;2014:723060. Epub 2014 Feb 13. Review. PubMed PMID: 24689052.
2)

Papa L, Edwards D, Ramia M. Exploring Serum Biomarkers for Mild Traumatic Brain Injury. In: Kobeissy FH, editor. Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects. Boca Raton (FL): CRC Press/Taylor & Francis; 2015. Chapter 22. PubMed PMID: 26269900.
3)

Richter S, Winzeck S, Czeiter E, Amrein K, Kornaropoulos EN, Verheyden J, Sugar G, Yang Z, Wang K, Maas AIR, Steyerberg E, Büki A, Newcombe VFJ, Menon DK; Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury Magnetic Resonance Imaging (CENTER-TBI MRI) Sub-study Participants and Investigators. Serum biomarkers identify critically ill traumatic brain injury patients for MRI. Crit Care. 2022 Nov 29;26(1):369. doi: 10.1186/s13054-022-04250-3. PMID: 36447266.
4)

Mozaffari K, Dejam D, Duong C, Ding K, French A, Ng E, Preet K, Franks A, Kwan I, Phillips HW, Kim DY, Yang I. Systematic Review of Serum Biomarkers in Traumatic Brain Injury. Cureus. 2021 Aug 10;13(8):e17056. doi: 10.7759/cureus.17056. PMID: 34522534; PMCID: PMC8428323.

Charlson comorbidity index (CCI)

Charlson comorbidity index (CCI)

http://touchcalc.com/calculators/cci_js

https://www.mdcalc.com/charlson-comorbidity-index-cci

The purpose of the study was to assess whether the Charlson Comorbidity Index (CCI) was associated with in-hospital death and short-term functional outcome in elderly patients (age ≥ 70) with intracerebral hemorrhage (ICH).

This was a retrospective cohort of aged ICH patients (≥70 years old) admitted within 24 hours of ICH onset. The CCI was derived using hospital discharge ICD-9 CM codes and patient history obtained from standardized case report forms. Multivariable logistic regression was used to determine the independent effect of the CCI score on clinical outcomes.

In this cohort of 248 aged ICH patients, comorbid conditions were common, with CCI scores ranging from 2 to 12. Logistic regression showed that the CCI score was independently predictive of 1-month functional outcome (OR = 1.642, P < 0.001) and in-hospital death (OR = 1.480, P = 0.003). Neither ICH volume nor the presence of IVH was an independent predictive factor for the 1-month functional outcome or in-hospital mortality (P < 0.05).

Comorbid medical conditions as assessed by the CCI independently influence short-term outcomes in aged ICH patients. The characteristics of the hematoma itself, such as intracerebral hemorrhage volume and the presence of IVH, seem to have a reduced effect on it 1).

Complications in spine trauma patients with Ankylosing spinal disorders may be driven by comorbidity burden rather than operative or injury-related factors. The Charlson Comorbidity Index (CCI) may be a valuable tool for the evaluation of this unique population 2)

Charlson Comorbidity Index (CCI) provides a simple way of predicting recurrence in patients with chronic subdural hematoma and should be incorporated into decision-making processes, when counseling patients 3).

Data show that elderly with a good performance status and few co-morbidity may be treated as younger patients; moreover, age confirms a negative impact on survival while (CCI) ≤ 2 did not correlate with overall survival (OS) 4).

Charlson comorbidity index (CCI), functional status computed by the Karnofsky performance scale (KPS)), tumor characteristics (size, location, isocitrate dehydrogenase mutation, and O-6-methylguanine-DNA methyltransferase promoter methylation status), and treatment parameters (volumetrically quantified extent of resection and adjuvant therapy), evidence that aside established prognostic parameters (age and KPS) for glioblastoma patient outcome, the CCI additionally significantly impacts outcome and may be employed for preoperative patient stratification 5).

Maximal resection and radiochemotherapy treatment completion are associated with longer OS, and age alone should not preclude elderly patients from receiving surgery and adjuvant treatment. However, only a few patients were able to finish the proposed treatments. Poor performance and high comorbidity index status might compromise the benefit of treatment aggressiveness and must be considered in therapeutic decision 6).

Latest articles

References

1)

Zhang T, Chen R, Wen D, Wang X, Ma L. The prognostic value of the Charlson comorbidity index in aged patients with intracerebral hemorrhage. BMC Neurol. 2022 Nov 28;22(1):443. doi: 10.1186/s12883-022-02980-z. PMID: 36443745.
2)

Lakomkin N, Mikula AL, Pinter ZW, Wellings E, Alvi MA, Scheitler KM, Pennington Z, Lee NJ, Freedman BA, Sebastian AS, Fogelson JL, Bydon M, Clarke MJ, Elder BD. Perioperative risk stratification of spine trauma patients with ankylosing spinal disorders: a comparison of 3 quantitative indices. J Neurosurg Spine. 2022 May 27:1-7. doi: 10.3171/2022.4.SPINE211449. Epub ahead of print. PMID: 35623371.
3)

Martinez-Perez R, Tsimpas A, Rayo N, Cepeda S, Lagares A. Role of the patient comorbidity in the recurrence of chronic subdural hematomas. Neurosurg Rev. 2020 Mar 7. doi: 10.1007/s10143-020-01274-7. [Epub ahead of print] PubMed PMID: 32146611.
4)

Balducci M, Fiorentino A, De Bonis P, Chiesa S, Manfrida S, D’Agostino GR, Mantini G, Frascino V, Mattiucci GC, De Bari B, Mangiola A, Miccichè F, Gambacorta MA, Colicchio G, Morganti AG, Anile C, Valentini V. Impact of age and co-morbidities in patients with newly diagnosed glioblastoma: a pooled data analysis of three prospective mono-institutional phase II studies. Med Oncol. 2012 Dec;29(5):3478-83. doi: 10.1007/s12032-012-0263-3. Epub 2012 Jun 7. PubMed PMID: 22674154.
5)

Ening G, Osterheld F, Capper D, Schmieder K, Brenke C. Charlson comorbidity index: an additional prognostic parameter for preoperative glioblastoma patient stratification. J Cancer Res Clin Oncol. 2015 Jan 11. [Epub ahead of print] PubMed PMID: 25577223.
6)

Pereira AF, Carvalho BF, Vaz RM, Linhares PJ. Glioblastoma in the elderly: Therapeutic dilemmas. Surg Neurol Int. 2015 Nov 16;6(Suppl 23):S573-S582. eCollection 2015. PubMed PMID: 26664927.

Subgaleal hematoma

Subgaleal hematoma

Subgaleal hematoma is a type of cephalhematoma in the potential space between the periosteum and the galea aponeurosis.

They dont calcify.

Its occurrence beyond the neonatal period is rare and is often associated with head trauma involving tangential or radial forces applied to the scalp causing emissary veins traversing the subgaleal space to be ruptured 1).

Epidemiology

In patients with traumatic intracranial hemorrhage or skull fractures, the incidence is increased.

In the newborn infant is rare, occurs early, and often bears serious consequences.

Etiology

Subgaleal hematoma etiology.

Diagnosis

The diagnosis is generally a clinical one, with a fluctuant boggy mass developing over the scalp

Laboratory studies consist of a hematocrit evaluation.

Right frontotemporoparietal intracranial acute epidural hematoma, up to 1 cm. thick, underlying a broad line of right temporoparietal Right parietal subgaleal hematoma, up to 1cm. of thickness.

Hemorrhage under the scalp

Not to confuse with subperiosteal hematoma.

Small gyriform laminar hyperdensity is observed in the left superior frontal sulcus in relation to a small subarachnoid hemorrhage. Left parietal subgaleal hematoma up to 7 mm thick.

Differential diagnosis

Subgaleal hematoma differential diagnosis.

Epidural hematoma association

Although rare, rapid spontaneous resolution of epidural hematomas in the pediatric population has even been reported 2).

Numerous theories have been proposed to explain the pathophysiology behind these cases, including egress of epidural collections through cranial discontinuities (fractures/open sutures), blood that originates in the subgaleal space, and bleeding from the cranial diploic cavity after a skull fracture that preferentially expands into the subgaleal space 3)

Treatment

Children born by use of vacuum extractor or forceps require careful monitoring by the nursing staff throughout their stay in the maternity unit 4).

In most cases, conservative treatment is the preferred option because adhesion between the galea aponeurotica and the periosteum restricts the extent of the hematoma. In special cases, however, the hematoma enlarges extraordinarily past these adhesions, and the patients thus affected suffer from progressive anemia followed by the lethargy and headache resulting from the excessive distension of the skin and the subcutaneous tissue. In such cases, hematoma removal is performed in order to relieve the symptoms 5).

The therapeutic strategy for massive subgaleal hematoma is individualized. However, treatment for massive subgaleal hematoma with skull fracture should not be considered the same as for hematoma without skull fracture. Emergent surgery is recommended before neurological deterioration is recognized in the patient if damage to the dural sinus is suspected 6).

Endoscopic techniques have been advanced along with the recent trend toward invasive neurosurgery. These minimally invasive techniques can allow sufficient removal of subgaleal hematoma with minimal morbidity, especially in patients such as ours. In addition, the utility of endoscopic techniques for the removal of subgaleal hematoma should be confirmed after long-term follow-up 7).

Complications

Usually starts as a small localized hematoma, and may become huge (with significant loss of circulating blood volume in age < 1 year, transfusion may be necessary).

A 3 kg baby was delivered by cesarean section after prolonged labor. He had massive subgaleal hematoma. He developed anemia requiring packed cell transfusions and hyperbilirubinemia requiring a total of seven exchange transfusions and highly intensive phototherapy. There were no adverse complications of the hyperbilirubinemia or the exchange transfusion 8).

Case reports

A 39-year-old healthy worker came to our emergency department (ED) due to scalp lacerations from an accident that caused severe twisting of his hair. He denied head contusion and was conscious upon arrival. Physical examination showed three lacerations over his right temporal area. The wounds depth extended to the skull, with a 10-cm subperiosteal pocket beneath the lacerations. Primary sutures were performed immediately under local anesthesia, not only for wound closure but also for hemostasis. However, he returned to our ED 3 h after the first visit for a newly developed soft lump over the left side of his forehead. Computed tomography scan of brain illustrated a huge and diffuse SGH in the left temporal region with extension to periorbital region. Although the option of incision and drainage was discussed with a neurosurgeon and a search for some case reports was done, most of the hematoma could be self-limited. Conservative management with non-elastic bandage packing direct compression was applied. The patient was then admitted for close observation and conservative treatment for 1 week. There was no recurrence of SGH in the following 3 months. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: SGH is an uncommon phenomenon that is caused by tearing of the emissary veins in the loose areolar tissue located beneath the galeal aponeurosis. Conservative treatment with bandage compression is recommended for SGH. Surgery is reserved for cases where non-invasive management fails or severe complications 9).

References

1)

Vu TT, Guerrera MF, Hamburger EK, Klein BL. Subgaleal hematoma from hair braiding.Case report and literature review. Pediatr Emerg Cure. 2004;20:821–3
2)

Chida K, Yukawa H, Mase T, Endo H, Ogasawara K. Spontaneous slow drainage of epidural hematoma into the subgaleal space through a skull fracture in an infant–case report. Neurol Med Chir (Tokyo). 2011;51(12):854-6. PubMed PMID: 22198110.
3)

Tataryn Z, Botsford B, Riesenburger R, Kryzanski J, Hwang S. Spontaneous resolution of an acute epidural hematoma with normal intracranial pressure: case report and literature review. Childs Nerv Syst. 2013 Nov;29(11):2127-30. doi: 10.1007/s00381-013-2167-8. Epub 2013 May 26. Review. PubMed PMID: 23708934.
4)

Boumahni B, Ghazouani J, Bey KJ, Carbonnier M, Staquet P. [Subgaleal hematoma in 2 neonates]. Arch Pediatr. 2010 Oct;17(10):1451-4. doi: 10.1016/j.arcped.2010.07.011. Epub 2010 Sep 18. French. PubMed PMID: 20851581.
5)

Amar AP, Aryan HE, Meltzer HS, Levy ML. Neonatal subgaleal hematoma causing brain compression: Report of two cases and review of the literature. Neurosurgery. 2003;52:1470–4.
6)

Yamada SM, Tomita Y, Murakami H, Nakane M. Delayed post-traumatic large subgaleal hematoma caused by diastasis of rhomboid skull suture on the transverse sinus. Childs Nerv Syst. 2015 Apr;31(4):621-4. doi: 10.1007/s00381-014-2531-3. Epub 2014 Aug 21. PubMed PMID: 25142690.
7)

Hayashi Y, Kita D, Furuta T, Oishi M, Hamada J. Endoscopic removal of subgaleal hematoma in a 7-year-old patient treated with anticoagulant and antiplatelet agents. Surg Neurol Int. 2014 Jun 20;5:98. doi: 10.4103/2152-7806.134911. eCollection 2014. PubMed PMID: 25024898; PubMed Central PMCID: PMC4093743.
8)

Dutta S, Singh A, Narang A. Subgaleal hematoma and seven exchange transfusions. Indian Pediatr. 2004 Mar;41(3):267-70. PubMed PMID: 15064515.
9)

Chen CE, Liao ZZ, Lee YH, Liu CC, Tang CK, Chen YR. Subgaleal Hematoma at the Contralateral Side of Scalp Trauma in an Adult. J Emerg Med. 2017 Nov;53(5):e85-e88. doi: 10.1016/j.jemermed.2017.06.007. Epub 2017 Sep 20. PMID: 28941556.

Chronic subdural hematoma recurrence prevention

Chronic subdural hematoma recurrence prevention

Systematic reviews and meta-analyses

In total, 402 studies were included in this analysis and 32 potential risk factors were evaluated. Among these, 21 were significantly associated with the postoperative recurrence of CSDH. Three risk factors (male, bilateral hematoma, and no drainage) had convincing evidence 1).

Subdural drain

The single most important factor appears to be the residual subdural space after drainage of the chronic subdural hematoma and an effort should be made by the surgeon to facilitate the expansion of the underlying brain. The presence of a functioning drain for 48–72 h draining the subdural fluid and promoting brain expansion will reduce the subdural space, thus reducing the recurrence of the CSDH. Some of the relevant surgical nuances include placement of at least two burr holes with the burr holes located to drain multiple cavities, copious irrigation of the subdural space, placement of the drain in the dependent burr hole site, near-total filling of the subdural space with irrigation to prevent a pneumocephalus and placing a subdural drain. Closure of the site with a large piece of Gelfoam prevents the subgaleal blood to migrate into the subdural space.

Postoperative subdural drain of maximal 48 h is effective in reducing recurrent hematomas. However, the shortest possible drainage time without increasing the recurrence rate is unknown

see Subdural drain for chronic subdural hematoma

Middle meningeal artery embolization

see Middle meningeal artery embolization for chronic subdural hematoma

Effect of Irrigation Fluid

The effect of a physical property of irrigation solution (at body vs room temperature) on the chronic subdural hematoma recurrence rate needs further study.

Objective: To explore whether irrigation fluid temperature has an influence on cSDH recurrence.

Design, setting, and participants: This was a multicenter randomized clinical trial performed between March 16, 2016, and May 30, 2020. The follow-up period was 6 months. The study was conducted at 3 neurosurgical departments in Sweden. All patients older than 18 years undergoing cSDH evacuation during the study period were screened for eligibility in the study.

Interventions: The study participants were randomly assigned by 1:1 block randomization to the cSDH evacuation procedure with irrigation fluid at room temperature (RT group) or at body temperature (BT group).

Main outcomes and measures: The primary end point was recurrence requiring reoperation within 6 months. Secondary end points were mortality, health-related quality of life, and complication frequency.

Results: At 6 months after surgery, 541 patients (mean [SD] age, 75.8 [9.8] years; 395 men [73%]) had a complete follow-up according to protocol. There were 39 of 277 recurrences (14%) requiring reoperation in the RT group, compared with 16 of 264 recurrences (6%) in the BT group (odds ratio, 2.56; 95% CI, 1.38-4.66; P < .001). There were no significant differences in mortality, health-related quality of life, or complication frequency.

Conclusions and Relevance: In this study, irrigation at body temperature was superior to irrigation at room temperature in terms of fewer recurrences. This is a simple, safe, and readily available technique to optimize outcome in patients with cSDH. When irrigation is used in cSDH surgery, irrigation fluid at body temperature should be considered standard of care.

Trial registration: ClincalTrials.gov Identifier: NCT02757235 2).

Half-saline solution

A study aimed to evaluate the efficacy and safety of half-saline solution for irrigation in burr hole trephination for chronic subdural hematoma.

This randomized clinical trial was conducted in university hospital referral centers from 2020 to 2021. Sixty-three patients with chronic subdural hematoma eligible for burr hole trephination were primarily enrolled. Two patients were excluded because of concurrent stroke. Sixty-one patients were randomly allocated into case (HS=30) and control (normal-saline [NS]=31) groups. HS was used to irrigate the hematoma in the case group and NS was used in the control group. The patients were followed-up. Clinical variables including demographic and medical findings, postoperative computed tomography findings, postoperative complications, hospitalization period, recurrence rate, and functional status measured by the Barthel type B index were recorded.

Forty-six of 61 patients were male (75.4%), and the patients’ mean age was 65.4±16.9 years, with equal distribution between the 2 groups. Postoperative effusion and postoperative hospital stay duration were significantly lower in the HS group than in the NS group (p=0.002 and 0.033, respectively). The postoperative recurrence within 3 months in both groups was approximately equal (6.6%). In terms of functional outcomes and postoperative complications, HS showed similar results to those of NS.

Conclusion: HS as an irrigation fluid in BHC effectively reduced postoperative effusion and hospital stay duration without considerable complications.

Trial registration: Iranian Registry of Clinical Trials Identifier: IRCT20200608047688N1 3).

Goreisan

Goreisan for chronic subdural hematoma recurrence prevention.

1)

Zhu F, Wang H, Li W, Han S, Yuan J, Zhang C, Li Z, Fan G, Liu X, Nie M, Bie L. Factors correlated with the postoperative recurrence of chronic subdural hematoma: An umbrella study of systematic reviews and meta-analyses. EClinicalMedicine. 2021 Dec 20;43:101234. doi: 10.1016/j.eclinm.2021.101234. PMID: 34988412; PMCID: PMC8703229.
2)

Bartley A, Bartek J Jr, Jakola AS, Sundblom J, Fält M, Förander P, Marklund N, Tisell M. Effect of Irrigation Fluid Temperature on Recurrence in the Evacuation of Chronic Subdural Hematoma: A Randomized Clinical Trial. JAMA Neurol. 2022 Nov 21. doi: 10.1001/jamaneurol.2022.4133. Epub ahead of print. PMID: 36409480.
3)

Mahmoodkhani M, Sharafi M, Sourani A, Tehrani DS. Half-Saline Versus Normal-Saline as Irrigation Solutions in Burr Hole Craniostomy to Treat Chronic Subdural Hematomata: A Randomized Clinical Trial. Korean J Neurotrauma. 2022 Sep 29;18(2):221-229. doi: 10.13004/kjnt.2022.18.e47. PMID: 36381457; PMCID: PMC9634318.

Pediatric Emergency Care Applied Research Network (PECARN)

Pediatric Emergency Care Applied Research Network (PECARN)

see PECARN traumatic brain injury algorithm.

The overuse of CT leads to inefficient care. Therefore, to maximize precision and minimize the overuse of CT, the Pediatric Emergency Care Applied Research Network (PECARN) previously derived clinical prediction rules for identifying children at high risk and very low risk for intra-abdominal trauma undergoing acute intervention and clinically important traumatic brain injury after blunt trauma in large cohorts of children who are injured.

A study aimed to validate the IAI and age-based TBI clinical prediction rules for identifying children at high risk and very low risk for IAIs undergoing acute intervention and clinically important TBIs after blunt trauma.

This was a prospective 6-center observational study of children aged <18 years with the blunt torso or head trauma. Consistent with the original derivation studies, enrolled children underwent a routine history and physical examinations, and the treating clinicians completed case report forms prior to knowledge of CT results (if performed). Medical records were reviewed to determine clinical courses and outcomes for all patients, and for those who were discharged from the emergency department, a follow-up survey via a telephone call or SMS text message was performed to identify any patients with missed IAIs or TBIs. The primary outcomes were IAI undergoing acute intervention (therapeutic laparotomy, angiographic embolization, blood transfusion, or intravenous fluid for ≥2 days for pancreatic or gastrointestinal injuries) and clinically important TBI (death from TBI, neurosurgical procedure, intubation for >24 hours for TBI, or hospital admission of ≥2 nights due to a TBI on CT). Prediction rule accuracy was assessed by measuring rule classification performance, using a standard point and 95% CI estimates of the operational characteristics of each prediction rule (sensitivity, specificity, positive and negative predictive values, and diagnostic likelihood ratios).

The project was funded in 2016, and enrollment was completed on September 1, 2021. Data analyses are expected to be completed by December 2022, and the primary study results are expected to be submitted for publication in 2023.

This study will attempt to validate previously derived clinical prediction rules to accurately identify children at high and very low risk for clinically important intra-abdominal trauma and traumatic brain injury. Assuming successful validation, widespread implementation is then indicated, which will optimize the care of children who are injured by better aligning CT use with need.

International registered report identifier (irrid): RR1-10.2196/43027 1).

Background

Blunt head trauma is common in children and a common reason for presentation to an emergency department. Head CT involves radiation exposure and the risk of fatal radiation-related malignancy increases with younger age at CT 2). The PECARN flow diagram flags assessment features that increase the risk of ci-TBI and weigh them against the risk of radiation exposure. Therefore, it is useful in avoiding unnecessary radiation exposure in younger patients, where it is safe to do so, and identifying those at risk that require further investigation.

In PECARN, altered mental status was defined as GCS 14 or agitation, somnolence, repetitive questioning, or slow response to verbal communication.

Severe mechanisms of injuries including:

motor vehicle crash with patient ejection

death of another passenger, or rollover

pedestrian or bicyclist without helmet struck by a motorized vehicle falls

more than 1.5 m (5 feet) for patients aged 2 years and older

more than 0.9 m (3 feet) for those younger than 2 years

head struck by a high-impact object

The algorithm was created from patients presenting to an emergency department within 24 hours of the trauma and with blunt trauma only.

Excluded criteria included:

penetrating trauma

known brain tumors

pre-existing neurological disorders complicating assessment

neuroimaging at a hospital outside before transfer

and therefore may not apply to patients with these features.

TBI on CT was defined as any of:

intracranial hemorrhage or contusion

cerebral edema

traumatic infarction

diffuse axonal injury

shearing injury

sigmoid sinus thrombosis

midline shift of intracranial contents or signs of brain herniation

diastasis of the skull

pneumocephalus

skull fracture depressed by at least the width of the table of the skull

Kuppermann et al. analyzed 42 412 children (derivation and validation populations: 8502 and 2216 younger than 2 years, and 25 283 and 6411 aged 2 years and older). We obtained CT scans on 14 969 (35.3%); ciTBIs occurred in 376 (0.9%), and 60 (0.1%) underwent neurosurgery. In the validation population, the prediction rule for children younger than 2 years (normal mental status, no scalp hematoma except frontal, no loss of consciousness or loss of consciousness for less than 5 s, non-severe injury mechanism, no palpable skull fracture, and acting normally according to the parents) had a negative predictive value for ciTBI of 1176/1176 (100.0%, 95% CI 99.7-100 0) and sensitivity of 25/25 (100%, 86.3-100.0). 167 (24.1%) of 694 CT-imaged patients younger than 2 years were in this low-risk group. The prediction rule for children aged 2 years and older (normal mental status, no loss of consciousness, no vomiting, non-severe injury mechanism, no signs of basilar skull fracture, and no severe headache) had a negative predictive value of 3798/3800 (99.95%, 99.81-99.99) and sensitivity of 61/63 (96.8%, 89.0-99.6). 446 (20.1%) of 2223 CT-imaged patients aged 2 years and older were in this low-risk group. Neither rule missed neurosurgery in validation populations.

These validated prediction rules identified children at very low risk of ciTBIs for whom CT can routinely be obviated 3).

A study applied two different machine learning (ML) models to diagnose mTBI in a paediatric population collected as part of the paediatric emergency care applied research network (PECARN) study between 2004 and 2006. The models were conducted using 15,271 patients under the age of 18 years with mTBI and had a head CT report. In the conventional model, random forest (RF) ranked the features to reduce data dimensionality and the top ranked features were used to train a shallow artificial neural network (ANN) model. In the second model, a deep ANN applied to classify positive and negative mTBI patients using the entirety of the features available. The dataset was divided into two subsets: 80% for training and 20% for testing using five-fold cross-validation. Accuracy, sensitivity, precision, and specificity were calculated by comparing the model’s prediction outcome to the actual diagnosis for each patient. RF ranked ten clinical demographic features and twelve CT-findings; the hybrid RF-ANN model achieved an average specificity of 99.96%, sensitivity of 95.98%, precision of 99.25%, and accuracy of 99.74% in identifying positive mTBI from negative mTBI subjects. The deep ANN proved its ability to carry out the task efficiently with an average specificity of 99.9%, sensitivity of 99.2%, precision of 99.9%, and accuracy of 99.9%. The performance of the two proposed models demonstrated the feasibility of using ANN to diagnose mTBI in a paediatric population. This is the first study to investigate deep ANN in a paediatric cohort with mTBI using clinical and non-imaging data and diagnose mTBI with balanced sensitivity and specificity using shallow and deep ML models. This method, if validated, would have the potential to reduce the burden of TBI evaluation in EDs and aide clinicians in the decision-making process 4).

1)

Ugalde IT, Chaudhari PP, Badawy M, Ishimine P, McCarten-Gibbs KA, Yen K, Atigapramoj NS, Sage A, Nielsen D, Adelson PD, Upperman J, Tancredi D, Kuppermann N, Holmes JF. Validation of Prediction Rules for Computed Tomography Use in Children With Blunt Abdominal or Blunt Head Trauma: Protocol for a Prospective Multicenter Observational Cohort Study. JMIR Res Protoc. 2022 Nov 24;11(11):e43027. doi: 10.2196/43027. PMID: 36422920.
2)

Brenner D, Elliston C, Hall E, Berdon W. Estimated risks of radiation-induced fatal cancer from pediatric CT. AJR Am J Roentgenol. 2001 Feb;176(2):289-96.
3)

Kuppermann N, Holmes JF, Dayan PS, Hoyle JD Jr, Atabaki SM, Holubkov R, Nadel FM, Monroe D, Stanley RM, Borgialli DA, Badawy MK, Schunk JE, Quayle KS, Mahajan P, Lichenstein R, Lillis KA, Tunik MG, Jacobs ES, Callahan JM, Gorelick MH, Glass TF, Lee LK, Bachman MC, Cooper A, Powell EC, Gerardi MJ, Melville KA, Muizelaar JP, Wisner DH, Zuspan SJ, Dean JM, Wootton-Gorges SL; Pediatric Emergency Care Applied Research Network (PECARN). Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet. 2009 Oct 3;374(9696):1160-70. doi: 10.1016/S0140-6736(09)61558-0. Epub 2009 Sep 14. Erratum in: Lancet. 2014 Jan 25;383(9914):308. PMID: 19758692.
4)

Ellethy H, Chandra SS, Nasrallah FA. The detection of mild traumatic brain injury in paediatrics using artificial neural networks. Comput Biol Med. 2021 Aug;135:104614. doi: 10.1016/j.compbiomed.2021.104614. Epub 2021 Jun 30. PMID: 34229143.

Chronic Subdural Hematoma Surgical Technique

Chronic Subdural Hematoma Surgical Technique

(1) Twist drill craniostomy for chronic subdural hematoma is a relatively safe technique that can be employed under local anesthesia and thus can be considered as first-line treatment in high-risk surgical candidates. (2) Single and double burr hole craniotomies have shown comparable results. (3) Intraoperative irrigation during burr-hole craniostomy doesn’t affect the outcome. (4) Drain insertion after hematoma evacuation lowers the recurrence risk. (5) Position of the drain is not significant but early drain removal is associated with higher recurrence rates. (6) Craniotomy is associated with high morbidity and mortality, hence should be reserved for recurrent and large septate hematoma cases. (7) Head elevation in the postoperative period reduces recurrence. (8) Embolization of the middle meningeal artery (EMMA): A novel treatment modality, is promising but requires further approval in terms of large sample-sized multicenter randomized control trials. In conclusion, further research is required on the subject to formulate guidelines regarding the management of this common neurosurgical emergency 1)

Due to the lack of consensus treatment, tissue plasminogen activator (tPA) has begun to be investigated to promote drainage and has shown promise in some early studies in reducing recurrence rates.

The most usual procedures for chronic subdural hematoma treatment include single or multiple burr hole drainage craniectomy. There is still controversy, however, about the risks and benefits of the different surgical approaches and types of drainage.

Till 1970s, craniotomy was the most commonly used method. Burr hole trephination for chronic subdural hematoma became the most preferred method from 1980s. In 1977, Twist drill craniostomy for chronic subdural hematoma was introduced. Closed system drainage after a Burr hole (BH) or a Twist drill (TD) became the most frequently used surgical method 2).

Pre-operative evaluation of radiological features of CSDHs is crucial in determining the right indication for minimally invasive drainage. Minimally invasive treatments of CSH may reduce the use of anaesthetic drugs and worsening of pre-existing neurodegenerative disorders 3).

The duration of procedure was significantly more in Burr-Hole Craniostomy BHC than in Twist-Drill Craniostomy TDC. In postoperative outcome, there was no significant difference in the GCS score, motor power improvement, motor power deterioration, overall clinical improvement, and improvement in CT scans of both the groups. Postoperative residue requiring reoperation was significantly more in TDC group. There was no significant difference in the development acute SDH, reoperation rate, complications, death, and hospital stay in both the groups. Avoiding the complications of general anesthesia and giving the equal postoperative improvement and complications of BHC, the TDC is considered as an effective alternative to the BHC in the surgical management of CSDH 4)

Although nonsurgical treatment is often successful, trephination has more advantages, such as rapid resolution of the symptoms and short period of hospitalization. Nonsurgical treatment is possible in asymptomatic patients with a small CSDH. For the symptomatic patients with CSDH, trephination is the treatment of choice, either by BH or TD. In gray zone between surgery and medical treatment, shared decision making can be an ideal approach. For chronic subdural hematoma recurrences, repeated trephination is still effective for patients with a low risk of recurrence. If the risk of recurrence is high, additional management would be helpful. For the refractory CSDHs, it is necessary to obliterate the subdural space 5).

Chronic subdural hematoma treatment in the elderly include observation, operative burr holes or craniotomy, and bedside twist drill drainage. The decision on which technique to use should be determined by weighing the comorbidities and symptoms of the patient with the potential risks and benefits.

Chronic subdural hematoma are ideally treated with surgical drainage. Despite this common practice, there is still controversy surrounding the best surgical procedure. With lack of clear evidence of a superior technique, surgeons are free to base the decision on other factors that are not related to patient care.

Originally, CSDHs were treated by open craniotomy 6) 7) 8) 9). Later burr hole trephination (BHT) was adopted because it was less invasive with lower morbidity and recurrence rates when compared with standard craniotomy 10) 11) 12) 13) 14) 15).

The traditional methods include evacuation via a burr hole with closed system drainage with or without irrigation, two burr-hole craniostomy with closed system drainage with irrigation or craniotomy, with subdural drain or without drain placement.

Minicraniotomy (MC) emerged as an attractive alternative to BHT as it allows better visualisation of the subdural cavity, enabling better haemostasis and resection of membranes.

Although bedside twist drill evacuation may avoid operating room costs and anesthetic complications in an elderly patient population and allow earlier anticoagulation resumption treatment if necessary, there is also a risk of morbidity if uncontrolled bleeding is encountered or the patient is unable to tolerate the bedside procedure. However, bedside twist drill craniostomy is a reasonable and effective option for the treatment of subacute/chronic SDH in patients who may not be optimal surgical candidates 16).

Subperiosteal vs Subdural Drain After Burr-Hole Drainage of Chronic Subdural Hematoma: A Randomized Clinical Trial (cSDH-Drain-Trial) 17).

Burr hole trephination for chronic subdural hematoma

see Burr hole trephination for chronic subdural hematoma.

Twist drill craniotomy for chronic subdural hematoma

see Twist drill craniostomy for chronic subdural hematoma.

Subdural drain for chronic subdural hematoma

see Subdural drain for chronic subdural hematoma.

Subdural evacuating port system for chronic subdural hematoma

see Subdural evacuating port system for chronic subdural hematoma.

Subperiosteal drain for chronic subdural hematoma

see Subperiosteal drain for chronic subdural hematoma

Craniotomy for chronic subdural hematoma

see Craniotomy for chronic subdural hematoma.

Neuroendoscopy

see Chronic subdural hematoma neuroendoscopy.

References

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Siddique AN, Khan SA, Khan AA, Aurangzeb A. Surgical Treatment Options For Chronic Subdural Haematoma. J Ayub Med Coll Abbottabad. 2022 Jul-Sep;34(3):550-556. doi: 10.55519/JAMC-03-10225. PMID: 36377174.
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Lee KS. How to Treat Chronic Subdural Hematoma? Past and Now. J Korean Neurosurg Soc. 2019 Mar;62(2):144-152. doi: 10.3340/jkns.2018.0156. Epub 2018 Nov 30. PubMed PMID: 30486622; PubMed Central PMCID: PMC6411568.
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Certo F, Maione M, Altieri R, Garozzo M, Toccaceli G, Peschillo S, Barbagallo GMV. Pros and cons of a minimally invasive percutaneous subdural drainage system for evacuation of chronic subdural hematoma under local anesthesia. Clin Neurol Neurosurg. 2019 Oct 10;187:105559. doi: 10.1016/j.clineuro.2019.105559. [Epub ahead of print] PubMed PMID: 31639631.
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Thavara BD, Kidangan GS, Rajagopalawarrier B. Comparative Study of Single Burr-Hole Craniostomy versus Twist-Drill Craniostomy in Patients with Chronic Subdural Hematoma. Asian J Neurosurg. 2019 Apr-Jun;14(2):513-521. doi: 10.4103/ajns.AJNS_37_19. PubMed PMID: 31143272; PubMed Central PMCID: PMC6516027.
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Ernestus R, Beldzinski P, Lanfermann H, Klug N. Chronic subdural hematoma: surgical treatment and outcome in 104 patients. Surg Neurol 1997;48:220–5.
7)

McKissock W, Richardson A, Bloom WH. Subdural hematoma: a review of 389 cases. Lancet 1960;1:1365–9.
8)

Tyson G et al. The role of craniectomy in the treatment of chronic subdural hematomas. J Neurosurg 1980;52:776–81.
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Putnam IJ, Cushing H. Chronic subdural hematoma. Its pathology, its relation to pachymeningitis hemorrhagica, and its surgical treatment. Arch Surg 1925;11:329–93.
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Chronic Almenawer S et al. Subdural hematoma management: a systematic review and meta-analysis of 34829 patients. Ann Surg 2014;259(3):449–57.
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Lee J, Ebel H, Ernestus R, Klug N. Various surgical treatments of chronic subdural hematoma and outcome in 172 patients: is membranectomy necessary? Surg Neurol 2004;61:523–5528.
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Ducruet A et al. The surgical management of chronic subdural hematoma. Neurosurg Rev 2012;35:155–69.
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Leroy H et al. Predictors of functional outcomes and recurrence of chronic subdural. J Clin Neurosci 2015;22:1895–900.
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Regan J, Worley E, Shelburne C, Pullarkat R, Burr Watson J. Hole Washout versus craniotomy for chronic subdural hematoma: patient outcome and cost analysis. PLoS One 2015;10(1):1–8.
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Mondorf Y, Abu-Owaimer M, Gaab M, Oertel J. Chronic subdural hematoma – Craniotomy versus burr hole trephination. Br J Neurosurg 2009;23(6):612–6.
16)

Garber S, McCaffrey J, Quigley EP, MacDonald JD. Bedside Treatment of Chronic Subdural Hematoma: Using Radiographic Characteristics to Revisit the Twist Drill. J Neurol Surg A Cent Eur Neurosurg. 2016 Jan 25. [Epub ahead of print] PubMed PMID: 26807616.
17)

Agrawal A, Pacheco-Hernandez A, Moscote-Salazar LR. Letter: Subperiosteal vs Subdural Drain After Burr-Hole Drainage of Chronic Subdural Hematoma: A Randomized Clinical Trial (cSDH-Drain-Trial). Neurosurgery. 2019 Aug 6. pii: nyz289. doi: 10.1093/neuros/nyz289. [Epub ahead of print] PubMed PMID: 31387117.