The S100B protein level 72 h after injury and changes over 72 h afterward are statistically significant for the prediction of a good clinical condition 1 month after injury. The highest sensitivity (81.4%) and specificity (83.3%) for the S100B protein value after 72 h was obtained for a cut-off value of 0.114. For the change after 72 h, that is a decrease in S100B value, the optimal cut-off is 0.730, where the sum of specificity (76.3%) and sensitivity (54.2%) is the highest, or a decrease by 0.526 at the cut-off value, where sensitivity (62.5%) and specificity (62.9%) are more balanced. The S100B values were the highest at baseline; the S100B value taken 72 h after trauma negatively correlated with GCS upon discharge or transfer (r=-0.517, P<0.0001). They found no relationship between S100B protein and hypertension, diabetes mellitus, BMI, or the season when the trauma occurred. Changes in values and a higher level of S100B protein were demonstrated in polytraumas with a median of 1.070 (0.042; 8.780) μg/L compared to isolated TBI with a median of 0.421 (0.042; 11.230) μg/L.
S100B protein level with specimen collection 72 h after trauma can be used as a complementary marker of patient prognosis1).
Trnka S, Stejskal P, Jablonsky J, Krahulik D, Pohlodek D, Hrabalek L. S100Bprotein as a biomarker and predictor in traumatic brain injury. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2023 Jul 10. doi: 10.5507/bp.2023.025. Epub ahead of print. PMID: 37431619.
Chronic subdural hematoma (CSDH) is a common neurological disease with a rapidly rising incidence due to increasing age and widespread use of anticoagulants. Surgical intervention by burr holecraniotomy (BHC) is the current standard practice for symptomatic patients, but associated with complications, a chronic subdural hematoma recurrence rate of up to 30% and increased mortality. Dexamethasone (DXM) therapy is, therefore, used as a non-surgical alternative but considered to achieve a lower success rate. Furthermore, the benefit of DXM therapy appears much more deliberate than the immediate relief from BHC. Lack of evidence and clinical equipoise among caregivers prompts the need for a head-to-head randomised controlled trial. The objective of this study is to compare the effect of primary DXM therapy versus primary BHC on functional outcome and cost-effectiveness in symptomatic patients with CSDH.
From September 2016 through February 2021, we enrolled 252 patients of a planned sample size of 420; 127 were assigned to the dexamethasone group and 125 to the surgery group. The mean age of the patients was 74 years, and 77% were men. The trial was terminated early by the data and safety monitoring board owing to safety and outcome concerns in the dexamethasone group. The adjusted common odds ratio for a lower (better) score on the modified Rankin scale at 3 months with dexamethasone than with surgery was 0.55 (95% confidence interval, 0.34 to 0.90), which failed to show noninferiority of dexamethasone. The scores on the Markwalder Grading Scale and Extended Glasgow Outcome Scale were generally supportive of the results of the primary analysis. Complications occurred in 59% of the patients in the dexamethasone group and 32% of those in the surgery group, and additional surgery was performed in 55% and 6%, respectively.
In a trial that involved patients with a chronic subdural hematoma and that was stopped early, dexamethasone treatment was not found to be non-inferior to burr-hole drainage with respect to functional outcomes and was associated with more complications and a greater likelihood of later surgery. (Funded by the Netherlands Organization for Health Research and Development and others; DECSA EudraCT number, 2015-001563-39.) 1).
Consecutive patients with a CSDH with a Markwalder Grading Scale (MGS) grade 1 to 3 were randomized to treatment with DXM or BHC. The DXM treatment scheme was 16 mg DXM per day (8 mg twice daily, days 1 to 4) which is then halved every 3 days until a dosage of 0.5 mg a day on day 19 and stopped on day 20. If the treatment response is insufficient (i.e. persistent or progressive symptomatology due to insufficient hematoma resolution), additional surgery can be performed. The primary outcomes are the functional outcome by means of the modified Rankin Scale (mRS) score at 3 months and cost-effectiveness at 12 months. Secondary outcomes are quality of life at 3 and 12 months using the Short Form Health Survey (SF-36) and Quality of Life after Brain Injury Overall Scale (QOLIBRI), hematoma thickness after 2 weeks on follow-up computed tomography (CT), hematoma recurrence during the first 12 months, complications and drug-related adverse events, failure of therapy within 12 months after randomization and requiring intervention, mortality during the first 3 and 12 months, duration of hospital stay and overall healthcare and productivity costs. To test the non-inferiority of DXM therapy compared to BHC, 210 patients in each treatment arm are required (assumed adjusted common odds ratio DXM compared to BHC 1.15, the limit for inferiority < 0.9). The aim was to include a total of 420 patients in 3 years with an enrolment rate of 60%.
The present study should demonstrate whether treatment with DXM is as effective as BHC on functional outcomes, at lower costs.
TRIAL REGISTRATION:
EUCTR 2015-001563-39 . Date of registration: 29 March 2015 2)
Miah IP, Holl DC, Blaauw J, Lingsma HF, den Hertog HM, Jacobs B, Kruyt ND, van der Naalt J, Polinder S, Groen RJM, Kho KH, van Kooten F, Dirven CMF, Peul WC, Jellema K, Dammers R, van der Gaag NA; DECSA Collaborators. Dexamethasone versus Surgery for Chronic Subdural Hematoma. N Engl J Med. 2023 Jun 15;388(24):2230-2240. doi: 10.1056/NEJMoa2216767. PMID: 37314705.
Miah IP, Holl DC, Peul WC, Walchenbach R, Kruyt N, de Laat K, Koot RW, Volovici V, Dirven CMF, van Kooten F, Kho KH, den Hertog HM, van der Naalt J, Jacobs B, Groen RJM, Lingsma HF, Dammers R, Jellema K, van der Gaag NA; Dutch Subdural Hematoma Research Group (DSHR). Dexamethasone therapy versus surgery for chronic subdural haematoma (DECSA trial): study protocol for a randomised controlled trial. Trials. 2018 Oct 20;19(1):575. doi: 10.1186/s13063-018-2945-4. PubMed PMID: 30342554.
Acute activation of innate immune response in the brain, or neuroinflammation, protects this vital organ from a range of external pathogens and promotes healing after traumatic brain injury.
Level II: monitor BP and avoid hypotension (SBP <90 mm Hg).
Level III: monitor oxygenation and avoid hypoxia (PaO2 <60mm Hg or O2 saturation <90%).
Hypotension
Hypotension (shock) is rarely attributable to head injury except:
● in terminal stages (i.e. with dysfunction of medulla and cardiovascular collapse)
● in infancy, where enough blood can be lost intracranially or into the subgaleal space to cause shock
● where enough blood has been lost from scalp wounds to cause hypovolemia (exsanguination)
Hypotension (defined as a single SBP < 90 mm Hg) doubles mortality, hypoxia (apnea or cyanosis in the field, or PaO2 <60 mm Hg on ABG) also increases mortality, and the combination of both triples mortality and increases the risk bad outcome. SBP<90 mm Hg may impair CBF and exacerbate brain injury and should be avoided.
Early use of paralytics and sedation (prior to ICP monitoring)
3. severe maxillofacial trauma: patency of airway tenuous or concern for inability to maintain patency with further tissue swelling and/or bleeding
4. need for pharmacologic paralysis for evaluation or management.
There are currently no established treatments for the underlying pathophysiology in TBI and while neurorehabilitation efforts are promising, there are currently is a lack of consensus regarding rehabilitation following TBI of any severity 1).
Treating traumatic brain injuries (TBIs) during the Covid-19 pandemic requires careful considerations to ensure the safety and well-being of both patients and healthcare providers. Here are some important aspects to consider in TBI treatment during the pandemic:
Emergency care: In the event of a severe TBI, emergency medical services and hospitals continue to provide critical care. Protocols are in place to protect both patients and healthcare workers from potential exposure to the virus.
Hospital precautions: Hospitals have implemented infection control measures to minimize the risk of Covid-19 transmission. These measures include screening patients for symptoms, providing personal protective equipment (PPE) to staff, isolating Covid-19-positive patients, and maintaining enhanced cleaning and disinfection procedures.
Rehabilitation services: Rehabilitation is an essential component of TBI treatment. During the pandemic, rehabilitation facilities have implemented safety measures, such as reduced capacity, enhanced cleaning protocols, physical distancing measures, and telehealth options when appropriate.
Telehealth services: Telehealth has played a crucial role in providing ongoing care and support for TBI patients during the pandemic. Telehealth appointments allow healthcare providers to assess patients remotely, provide guidance, monitor progress, and offer therapy sessions when in-person visits are not feasible.
Mental health support: The Covid-19 pandemic has had a significant impact on mental health. It is crucial to address the emotional and psychological well-being of TBI patients, as they may face additional challenges and increased stress during these times. Teletherapy and virtual support groups can be valuable resources for providing mental health support.
Caregiver support: Caregivers play a vital role in supporting individuals with TBIs. They may face additional burdens and challenges during the pandemic. Providing caregiver support through virtual resources, educational materials, and online support groups can help them navigate these difficult circumstances.
Follow-up care: Regular follow-up appointments with healthcare providers are crucial for monitoring TBI recovery progress and addressing any ongoing concerns. Telehealth visits can be utilized for routine check-ups, medication management, and addressing non-emergency issues.
It is important to note that the specific guidelines and protocols for TBI treatment during the Covid-19 pandemic may vary depending on the location, healthcare facility, and individual circumstances.
Marklund N, Bellander BM, Godbolt A, Levin H, McCrory P, Thelin EP. Treatments and rehabilitation in the acute and chronic state of traumatic brain injury. J Intern Med. 2019 Mar 18. doi: 10.1111/joim.12900. [Epub ahead of print] PubMed PMID: 30883980.
The initial ionic flux and glutamate release result in significant energy demands and a period of metabolic crisis for the injured brain. These physiological perturbations can now be linked to clinical characteristics of concussion, including migrainous symptoms, vulnerability to repeat injury, and cognitive impairment. Furthermore, advanced neuroimaging now allows a research window to monitor postconcussion pathophysiology in humans noninvasively. There is also increasing concern about the risk for chronic or even progressive neurobehavioral impairment after concussion/mild traumatic brain injury. Critical studies are underway to better link the acute pathobiology of concussion with potential mechanisms of chronic cell death, dysfunction, and neurodegeneration 2).
Glutamate release and ionic disequilibrium
As a result of mechanical trauma, neuronal cell membranes and axons undergo disruptive stretching, leading to temporary ionic disequilibrium 3).
As a result, levels of extracellular potassium increase drastically, and indiscriminate glutamate release occurs 4).
Glutamate release activates N-methyl-D-aspartate receptors, which leads to accumulation of intracellular calcium5)6)7) , causing mitochondrial respiration dysfunction, protease activation, and often initiating apoptosis8)9). Elevated glutamate levels were also found to be significantly correlated with derangements in lactate, potassium, brain tissue pH, and brain tissue CO2 levels in human studies 10). Additionally, sodium channel upregulation, fueled by ATPase proteins depending on glucose for energy, is observed following axonal stretch injuries 11).
Energy crisis and mitochondrial dysfunction
In combination, the cellular response to the above-mentioned ionic shifts and the downstream effects of the neurotransmitter release lead to an acute energy crisis. This occurs when, to restore ionic equilibrium, adenosine-triphosphate (ATP) -dependent sodium-potassium ion transporter pump activity increases, which augments local cerebral glucose demand 12).
Further metabolic demand is incurred by ATP-dependent sodium channel upregulation. This occurs in the face of mitochondrial dysfunction, leading cells to primarily utilize glycolytic pathways instead of aerobic metabolism for energy, and causing extracellular lactate accumulation as a byproduct 13). This acidosis, caused by hyperglycolysis, has been shown to worsen membrane permeability, ionic disequilibrium, and cerebral edema 14).
Some evidence shows that the lactate produced by this process may eventually be utilized as a source of energy by the neurons once mitochondrial oxidative respiration normalizes; in fact, one study showed that in moderate to severe TBI the incidence of abnormally high levels of lactate uptake were seen in 28% of subjects 15). The same study showed that patients exhibiting a higher rate of brain lactate uptake relative to arterial lactate levels tended to have more favorable outcomes compared to others with lower relative lactate uptake.
Alterations in cerebral blood flow
Some studies have shown that cerebral blood flow decreases immediately following the insult, and the amount of time it remains lowered seems to depend on the severity of the injury 16)17).
Other studies, however, show no significant differences in CBF following mild TBI in subjects over 30 years of age 18). In pediatric studies, CBF has been seen to increase during the first day following mild TBI, followed by decreased CBF for many days after 19)20). Data comparing cerebral blood flow in pediatric TBI patients has shown impaired autoregulation in 42% of moderate and severe and 17% of mild injuries 21).
Histopathologic changes
The underlying histopathologic changes that occur are relatively unknown. In order to improve understanding of acute injury mechanisms, appropriately designed pre-clinical models must be utilized.
The clinical relevance of compression wave injury models revolves around the ability to produce consistent histopathologic deficits. Mild traumatic brain injuries activate similar neuroinflammatory cascades, cell death markers and increases in amyloid precursor protein in both humans and rodents. Humans, however, infrequently succumb to mild traumatic brain injuries and, therefore, the intensity and magnitude of impacts must be inferred. Understanding compression wave properties and mechanical loading could help link the histopathologic deficits seen in rodents to what might be happening in human brains following concussions 22).
Giza CC, Hovda DA. The new neurometabolic cascade of concussion. Neurosurgery. 2014 Oct;75 Suppl 4:S24-33. doi: 10.1227/NEU.0000000000000505. PubMed PMID: 25232881.
Farkas O, Lifshitz J, Povlishock JT. Mechanoporation induced by diffuse traumatic brain injury: an irreversible or reversible response to injury? J Neurosci. 2006 Mar 22;26(12):3130–3140.
Katayama Y, Becker DP, Tamura T, Hovda DA. Massive increases in extracellular potassium and the indiscriminate release of glutamate following concussive brain injury. J Neurosurg. 1990 Dec;73(6):889–900.
Osteen CL, Giza CC, Hovda DA. Injury-induced alterations in N-methyl-D-aspartate receptor subunit composition contribute to prolonged 45 calcium accumulation following lateral fluid percussion. Neuroscience. 2004;128(2):305–322.
Osteen CL, Moore AH, Prins ML, Hovda DA. Age-dependency of 45calcium accumulation following lateral fluid percussion: acute and delayed patterns. J Neurotrauma. 2001 Feb;18(2):141–162.
Fineman I, Hovda DA, Smith M, Yoshino A, Becker DP. Concussive brain injury is associated with a prolonged accumulation of calcium: a 45Ca autoradiographic study. Brain Research. 1993;624(1–2):94–102.
Reinert M, Hoelper B, Doppenberg E, Zauner A, Bullock R. Substrate delivery and ionic balance disturbance after severe human head injury. Acta Neurochir Suppl. 2000;76:439–444.
Yoshino A, Hovda DA, Kawamata T, Katayama Y, Becker DP. Dynamic changes in local cerebral glucose utilization following cerebral concussion in rats: evidence of a hyper- and subsequent hypometabolic state. Brain Research. 1991;561(1):106–119.
Kawamata T, Katayama Y, Hovda DA, Yoshino A, Becker DP. Lactate accumulation following concussive brain injury: the role of ionic fluxes induced by excitatory amino acids. Brain Research. 1995;674(2):196–204.
Glenn TC, Kelly DF, Boscardin WJ, et al. Energy dysfunction as a predictor of outcome after moderate or severe head injury: indices of oxygen, glucose, and lactate metabolism. J Cereb Blood Flow Metab. 2003 Oct;23(10):1239–1250.
Chan KH, Miller JD, Dearden NM. Intracranial blood flow velocity after head injury: relationship to severity of injury, time, neurological status and outcome. J Neurol Neurosurg Psychiatry. 1992 Sep;55(9):787–791.
Mandera M, Larysz D, Wojtacha M. Changes in cerebral hemodynamics assessed by transcranial Doppler ultrasonography in children after head injury. Childs Nerv Syst. 2002 Apr;18(3–4):124–128.
Lucke-Wold BP, Phillips M, Turner RC, Logsdon AF, Smith KE, Huber JD, Rosen CL, Regele JD. Elucidating the role of compression waves and impact duration for generating mild traumatic brain injury in rats. Brain Inj. 2016 Nov 23:1-8. [Epub ahead of print] PubMed PMID: 27880054.
Surgical therapies involve the irrigation and removal of the blood products, sometimes with partial resection of these vascular membranes 2).
Investigational medical therapies have employed various strategies, which include reducing the rate of microhemorrhage from the membranes, changing the osmotic environment, or altering angiogenesis 3).
Endovascular therapies are aimed at de-vascularizing these membranes 4)5)6)7).
Providing a high level of evidence to propose a standard of care for this frequent pathology is of utmost importance. However, two surveys in the UK and in France have shown a wide range of practice, without major rationale 8)9).
A variety of clinical factors must be taken into account in the treatment of chronic subdural hematoma (cSDH), and the multifaceted treatment paradigms continue to evolve 10).
There is lack of uniformity about the treatment strategies, such as the role of burr hole, twist drill, craniotomy, etc., in CSDH amongst various surgeons. There is also disagreement about the use of drain, irrigation, and steroid11)12).
Surgery is usually the treatment of choice, but conservative treatment may be a good alternative in some situations.
Soleman et al., provide a systematic review of studies analysing the conservative treatment options and the natural history of cSDH. Of 231 articles screened, 35 were included in this systematic review. Studies evaluating the natural history and conservative treatment modalities of cSDH remain sparse and are predominantly of low level of evidence. The natural history of cSDH remains unclear and is analysed only in case reports or very small case series. “Wait and watch” or “wait and scan” management is indicated in patients with no or minor symptoms (Markwalder score 0-1). However, it seems that there are no clear clinical or radiological signs indicating whether the cSDH will resolve spontaneously or not (type C recommendation). In symptomatic patients who are not worsening or in a comatose state, oral steroid treatment might be an alternative to surgery (type C recommendation). Tranexamic acid proved effective in a small patient series (type C recommendation), but its risk of increasing thromboembolic events in patients treated with antithrombotic or anticoagulant medication is unclear. Angiotensin converting-enzyme inhibitors were evaluated only as adjuvant therapy to surgery, and their effect on the rate of recurrence remains debatable. Mannitol showed promising results in small retrospective series and might be a valid treatment modality (type C recommendation). However, the long treatment duration is a major drawback. Patients presenting without paresis can be treated with a platelet activating factor receptor antagonist (type C recommendation), since they seem to promote resolution of the haematoma, especially in patients with subdural hygromas or low-density haematomas on computed tomography. Lastly, atorvastatin seems to be a safe option for the conservative treatment of asymptomatic or mildly symptomatic cSDH patients (type C recommendation). In conclusion, the knowledge of the conservative treatment modalities for cSDH is sparse and based on small case series and low grade evidence. However, some treatment modalities seem promising even in symptomatic patients with large haematomas. Randomised controlled trials are currently underway, and will hopefully provide us with good evidence for or against the conservative treatment of cSDH 14).
Surveys
The aim of a study was to survey aspects of current practice in the UK and Ireland. A 1-page postal questionnaire addressing the treatment of primary (i.e. not recurrent) CSDH was sent to consultant SBNS members in March 2006. There were 112 responses from 215 questionnaires (52%). The preferred surgical technique was burr hole drainage (92%). Most surgeons prefer not to place a drain, with 27% never using one and 58% using drain only in one-quarter of cases or less. Only 11% of surgeons always place a drain, and only 30% place one in 75% of cases or more. The closed subdural-to-external drainage was most commonly used (91%) with closed subgaleal-to-external and subdural-to-peritoneal conduit used less often (3 and 4%, respectively). Only 5% of responders claimed to know the exact recurrence rate. The average perceived recurrence rate among the surgeons that never use drains and those who always use drains, was the same (both 11%). Most operations are performed by registrars (77%). Postoperative imaging is requested routinely by 32% of respondents and 57% of surgeons prescribe bed rest. Ninety four per cent surgeons employ conservative management in less than one-quarter of cases. Forty-two per cent of surgeons never prescribe steroids, 55% prescribe them to those managed conservatively. This survey demonstrates that there are diverse practices in the management of CSDH. This may be because of sufficiently persuasive evidence either does not exist or is not always taken into account. The current literature provides Class II and III evidence and there is a need for randomized studies to address the role of external drainage, steroids and postoperative bed rest 15).
Cenic et al. developed and administered a questionnaire to Canadian Neurosurgeons with questions relating to the management of chronic and subacute subdural hematoma. Our sampling frame included all neurosurgery members of the Canadian Neurosurgical Society.
Of 158 questionnaires, 120 were returned (response rate = 76%). The respondents were neurosurgeons with primarily adult clinical practices (108/120). Surgeons preferred one and two burr-hole craniostomy to craniotomy or twist-drill craniostomy as the procedure of choice for initial treatment of subdural hematoma (35.5% vs 49.5% vs 4.7% vs 9.3%, respectively). Craniotomy and two burr-holes were preferred for recurrent subdural hematomas (43.3% and 35.1%, respectively). Surgeons preferred irrigation of the subdural cavity (79.6%), use of a subdural drain (80.6%), and no use of anti-convulsants or corticosteroids (82.1% and 86.6%, respectively). We identified a lack of consensus with keeping patients supine following surgery and post-operative antibiotic use.
The survey has identified variations in practice patterns among Canadian Neurosurgeons with respect to treatment of subacute or chronic subdural hematoma (SDH). Our findings support the need for further prospective studies and clinical trials to resolve areas of discrepancies in clinical management and hence, standardize treatment regimens 16).
Markwalder TM . The course of chronic subdural hematomas after burr-hole craniostomy with and without closed-system drainage. Neurosurg Clin N Am 2000;11:541–6.doi:10.1016/S1042-3680(18)30120-7
Sun TF , Boet R , Poon WS . Non-surgical primary treatment of chronic subdural haematoma: preliminary results of using dexamethasone. Br J Neurosurg 2005;19:327–33.doi:10.1080/02688690500305332
Link TW , Boddu S , Marcus J , et al . Middle meningeal artery embolization as treatment for chronic subdural hematoma: a case series. Oper Neurosurg 2018;14:556–62.doi:10.1093/ons/opx154
Link TW , Boddu S , Paine SM , et al . Middle meningeal artery embolization for chronic subdural hematoma: a series of 60 cases. Neurosurgery 2018;121.doi:10.1093/neuros/nyy521
Link TW , Rapoport BI , Paine SM , et al . Middle meningeal artery embolization for chronic subdural hematoma: Endovascular technique and radiographic findings. Interv Neuroradiol 2018;24:455–62.doi:10.1177/1591019918769336
Link TW , Schwarz JT , Paine SM , et al . Middle meningeal artery embolization for Chronic subdural hematoma recurrence: a case series. World Neurosurg 2018;118:e570–4.doi:10.1016/j.wneu.2018.06.241
M. Guénot, Hématome sous-dural chronique. Introduction et résultats de l’enquête de la SFNC, Neurochirurgie 4 (2001) 459–460 https://doi.org/ NCHIR-11-2001-47- 5-0028-3770-101019-ART7.
] T. Santarius, R. Lawton, P.J. Kirkpatrick, P.J. Hutchinson, The management of primary chronic subdural haematoma: a questionnaire survey of practice in the United Kingdom and the Republic of Ireland, Br. J. Neurosurg. 22 (2008) 529–534, https://doi.org/10.1080/02688690802195381.
Santarius T, Lawton R, Kirkpatrick PJ, Hutchinson PJ. The management of primary chronic subdural haematoma: a questionnaire survey of practice in the United Kingdom and the Republic of Ireland. Br J Neurosurg. 2008 Aug;22(4):529-34. doi: 10.1080/02688690802195381. PubMed PMID: 18686063.
Cenic A, Bhandari M, Reddy K. Management of chronic subdural hematoma: a national survey and literature review. Can J Neurol Sci. 2005 Nov;32(4):501-6. PubMed PMID: 16408582.
Soleman J, Noccera F, Mariani L. The conservative and pharmacological management of chronic subdural haematoma. Swiss Med Wkly. 2017 Jan 19;147:w14398. doi: smw.2017.14398. PubMed PMID: 28102879.
Cenic A, Bhandari M, Reddy K. Management of chronic subdural hematoma: a national survey and literature review. Can J Neurol Sci. 2005 Nov;32(4):501-6. PubMed PMID: 16408582.
t
A variety of clinical factors must be taken into account in the treatment of chronic subdural hematoma (cSDH), and the multifaceted treatment paradigms continue to evolve 1).
There is lack of uniformity about the treatment strategies, such as the role of burr hole, twist drill, craniotomy, etc., in CSDH amongst various surgeons. There is also disagreement about the use of drain, irrigation, and steroid2)3).
Surgery is usually the treatment of choice, but conservative treatment may be a good alternative in some situations.
Soleman et al., provide a systematic review of studies analysing the conservative treatment options and the natural history of cSDH. Of 231 articles screened, 35 were included in this systematic review. Studies evaluating the natural history and conservative treatment modalities of cSDH remain sparse and are predominantly of low level of evidence. The natural history of cSDH remains unclear and is analysed only in case reports or very small case series. “Wait and watch” or “wait and scan” management is indicated in patients with no or minor symptoms (Markwalder score 0-1). However, it seems that there are no clear clinical or radiological signs indicating whether the cSDH will resolve spontaneously or not (type C recommendation). In symptomatic patients who are not worsening or in a comatose state, oral steroid treatment might be an alternative to surgery (type C recommendation). Tranexamic acid proved effective in a small patient series (type C recommendation), but its risk of increasing thromboembolic events in patients treated with antithrombotic or anticoagulant medication is unclear. Angiotensin converting-enzyme inhibitors were evaluated only as adjuvant therapy to surgery, and their effect on the rate of recurrence remains debatable. Mannitol showed promising results in small retrospective series and might be a valid treatment modality (type C recommendation). However, the long treatment duration is a major drawback. Patients presenting without paresis can be treated with a platelet activating factor receptor antagonist (type C recommendation), since they seem to promote resolution of the haematoma, especially in patients with subdural hygromas or low-density haematomas on computed tomography. Lastly, atorvastatin seems to be a safe option for the conservative treatment of asymptomatic or mildly symptomatic cSDH patients (type C recommendation). In conclusion, the knowledge of the conservative treatment modalities for cSDH is sparse and based on small case series and low grade evidence. However, some treatment modalities seem promising even in symptomatic patients with large haematomas. Randomised controlled trials are currently underway, and will hopefully provide us with good evidence for or against the conservative treatment of cSDH 4).
Surveys
The aim of a study was to survey aspects of current practice in the UK and Ireland. A 1-page postal questionnaire addressing the treatment of primary (i.e. not recurrent) CSDH was sent to consultant SBNS members in March 2006. There were 112 responses from 215 questionnaires (52%). The preferred surgical technique was burr hole drainage (92%). Most surgeons prefer not to place a drain, with 27% never using one and 58% using drain only in one-quarter of cases or less. Only 11% of surgeons always place a drain, and only 30% place one in 75% of cases or more. The closed subdural-to-external drainage was most commonly used (91%) with closed subgaleal-to-external and subdural-to-peritoneal conduit used less often (3 and 4%, respectively). Only 5% of responders claimed to know the exact recurrence rate. The average perceived recurrence rate among the surgeons that never use drains and those who always use drains, was the same (both 11%). Most operations are performed by registrars (77%). Postoperative imaging is requested routinely by 32% of respondents and 57% of surgeons prescribe bed rest. Ninety four per cent surgeons employ conservative management in less than one-quarter of cases. Forty-two per cent of surgeons never prescribe steroids, 55% prescribe them to those managed conservatively. This survey demonstrates that there are diverse practices in the management of CSDH. This may be because of sufficiently persuasive evidence either does not exist or is not always taken into account. The current literature provides Class II and III evidence and there is a need for randomized studies to address the role of external drainage, steroids and postoperative bed rest 5).
Cenic et al. developed and administered a questionnaire to Canadian Neurosurgeons with questions relating to the management of chronic and subacute subdural hematoma. Our sampling frame included all neurosurgery members of the Canadian Neurosurgical Society.
Of 158 questionnaires, 120 were returned (response rate = 76%). The respondents were neurosurgeons with primarily adult clinical practices (108/120). Surgeons preferred one and two burr-hole craniostomy to craniotomy or twist-drill craniostomy as the procedure of choice for initial treatment of subdural hematoma (35.5% vs 49.5% vs 4.7% vs 9.3%, respectively). Craniotomy and two burr-holes were preferred for recurrent subdural hematomas (43.3% and 35.1%, respectively). Surgeons preferred irrigation of the subdural cavity (79.6%), use of a subdural drain (80.6%), and no use of anti-convulsants or corticosteroids (82.1% and 86.6%, respectively). We identified a lack of consensus with keeping patients supine following surgery and post-operative antibiotic use.
The survey has identified variations in practice patterns among Canadian Neurosurgeons with respect to treatment of subacute or chronic subdural hematoma (SDH). Our findings support the need for further prospective studies and clinical trials to resolve areas of discrepancies in clinical management and hence, standardize treatment regimens 6).
Glucocorticoids
Since glucocorticoids have been used for treatment of cSDH in 1962 their role is still discussed controversially in lack of evident data. On the basis of the ascertained inflammation cycle in cSDH dexamethasone will be an ideal substance for a short lasting, concomitant treatment protocol.
A study is designed as a double-blind randomized placebo-controlled trial 820 patients who are operated for cSDH and from the age of 25 years are included after obtaining informed consent. They are randomized for administration of dexamethasone (16-16-12-12-8-4 mg/d) or placebo (maltodextrin) during the first 48 hours after surgery. The type I error is 5% and the type II error is 20%. The primary endpoint is the reoperation within 12 weeks postoperative.
This study tests whether dexamethasone administered over 6 days is a safe and potent agent in relapse prevention for evacuated cSDH 7).
Santarius T, Lawton R, Kirkpatrick PJ, Hutchinson PJ. The management of primary chronic subdural haematoma: a questionnaire survey of practice in the United Kingdom and the Republic of Ireland. Br J Neurosurg. 2008 Aug;22(4):529-34. doi: 10.1080/02688690802195381. PubMed PMID: 18686063.
Cenic A, Bhandari M, Reddy K. Management of chronic subdural hematoma: a national survey and literature review. Can J Neurol Sci. 2005 Nov;32(4):501-6. PubMed PMID: 16408582.
Soleman J, Noccera F, Mariani L. The conservative and pharmacological management of chronic subdural haematoma. Swiss Med Wkly. 2017 Jan 19;147:w14398. doi: smw.2017.14398. PubMed PMID: 28102879.
Cenic A, Bhandari M, Reddy K. Management of chronic subdural hematoma: a national survey and literature review. Can J Neurol Sci. 2005 Nov;32(4):501-6. PubMed PMID: 16408582.
Emich S, Richling B, McCoy MR, Al-Schameri RA, Ling F, Sun L, Wang Y, Hitzl W. The efficacy of dexamethasone on reduction in the reoperation rate of chronic subdural hematoma – the DRESH study: straightforward study protocol for a randomized controlled trial. Trials. 2014 Jan 6;15(1):6. doi: 10.1186/1745-6215-15-6. PubMed PMID: 24393328; PubMed Central PMCID: PMC3891985.
A subarachnoid hemorrhage is a hemorrhage in the subarachnoid space. Subarachnoid hemorrhage (SAH) is a medical emergency that requires immediate intervention. The etiology varies between cases; however, rupture of an intracranial aneurysm accounts for 80% of medical emergencies. Early intervention and treatment are essential to prevent long-term complications. Over the years, treatment of SAH has drastically improved, which is responsible for the rapid rise in SAH survivors. Post-SAH, a significant number of patients exhibit impairments in memory and executive function and report high rates of depression and anxiety that ultimately affect daily living, return to work, and quality of life. Given the rise in SAH survivors, rehabilitation post-SAH to optimize patient outcomes becomes crucial 1)
Subarachnoid hemorrhage (SAH) has a substantial impact on quality of life and future risk for mortality in patients who survive the initial injury and hospitalization. Poor neurological status and advanced age on admission have been recognized as poor clinical prognostic factors and is one of the life-threatening diseases with high morbidity and mortality rate 11).
A neurological disease that was disgraceful fifty years ago has lost any disquieting and embarrassing significance in the present time to the light of evolution of vascular neurosurgery 12)
High SAH patient volume is robustly and strongly associated with lower inpatient mortality, fewer poor outcomes, and more discharges to home. The observed SAH patient volume association does not plateau until facilities are treating more than 100 SAH patients per year. This is a considerably higher patient volume threshold than the 20 SAH/year/facility set forth by the Joint Commission for CSC Certification.
Short-term SAH outcomes have improved. High-volume hospitals have more favorable outcomes than low-volume hospitals. This effect is substantial, even for hospitals conventionally classified as high volume. 13).
Using the Get With The Guidelines Stroke registry, Prabhakaran et al., analyzed patients with a discharge diagnosis of SAH between April 2003 and March 2012 and assessed the association of annual SAH case volume with in-hospital mortality by using multivariatelogistic regression adjusting for relevant patient, hospital, and geographic characteristics.
Among 31,973 patients with SAH from 685 hospitals, the median annual case volume per hospital was 8.5 (25th-75th percentile, 6.7-12.9) patients. Mean in-hospital mortality was 25.7%, but was lower with increasing annual SAH volume: 29.5% in quartile 1 (range, 4-6.6), 27.0% in quartile 2 (range, 6.7-8.5), 24.1% in quartile 3 (range, 8.5-12.7), and 22.1% in quartile 4 (range, 12.9-94.5). Adjusting for the patient and hospital characteristics, hospital SAH volume was independently associated with in-hospital mortality (adjusted odds ratio 0.79 for quartile 4 vs 1, 95% confidence interval, 0.67-0.92). The quartile of SAH volume also was associated with length of stay but not with discharge home or independent ambulatory status.
In a large nationwide registry, they observed that patients treated at hospitals with higher volumes of SAH patients have lower in-hospital mortality, independent of patient and hospital characteristics suggesting that experienced centers may provide more optimized care for SAH patients. 14)
Andereggen L, Neuschmelting V, von Gunten M, Widmer HR, Takala J, Jakob SM, Fandino J, Marbacher S. The Rabbit Blood-shunt Model for the Study of Acute and Late Sequelae of Subarachnoid Hemorrhage: Technical Aspects. J Vis Exp. 2014 Oct 2;(92). doi: 10.3791/52132. PubMed PMID: 25350004.
Güresir E, Schuss P, Borger V, Vatter H. Rat cisterna magna double-injection model of subarachnoid hemorrhage – background, advantages/limitations, technical considerations, modifications, and outcome measures. Acta Neurochir Suppl. 2015;120:325-9. doi: 10.1007/978-3-319-04981-6_56. PubMed PMID: 25366646.
Sehba FA. The rat endovascular perforation model of subarachnoid hemorrhage. Acta Neurochir Suppl. 2015;120:321-4. doi: 10.1007/978-3-319-04981-6_55. PubMed PMID: 25366645.
Kooijman E, Nijboer CH, van Velthoven CT, Kavelaars A, Kesecioglu J, Heijnen CJ. The rodent endovascular puncture model of subarachnoid hemorrhage: mechanisms of brain damage and therapeutic strategies. J Neuroinflammation. 2014;11:2.
Longatti P, Giombelli E, Pavesi G, Carteri A, Feletti A. Management of subarachnoid hemorrhage in two important Italian political leaders: a paradigm of ethical and technological evolution of neurosurgery during the past half-century. World Neurosurg. 2016 Jan 13. pii: S1878-8750(16)00007-3. doi: 10.1016/j.wneu.2015.12.089. [Epub ahead of print] Review. PubMed PMID: 26775232.
Prabhakaran S, Fonarow GC, Smith EE, Liang L, Xian Y, Neely M, Peterson ED, Schwamm LH. Hospital case volume is associated with mortality in patients hospitalized with subarachnoid hemorrhage. Neurosurgery. 2014 Nov;75(5):500-8. doi: 10.1227/NEU.0000000000000475. PubMed PMID: 24979097.
Burr hole trephination for chronic subdural hematoma with a closed drainage system
Double burr hole trepanation combined with a subperiostal passive closed-drainage system is a technically easy, highly effective, safe, and cost-efficient treatment strategy for symptomatic chronic subdural hematomas. The absence of a drain in direct contact with the hematoma capsule may moderate the risk of postoperative seizure and limit the secondary spread of infection to intracranial compartments 1).
The main aim of surgery should be a complete removal of the aggressive liquid. In case of many membranes that separate the hematoma into chambers like honeycomb an open procedure cannot be avoided. Nevertheless, the preferred operative therapy for most of CSDH is a burr hole craniostomy with a closed drainage system 2)3).
Preferably under general anesthesia the surgical approach should be over the thickest part of the hematoma and the patients positioned in a way that the burr hole comes to the highest point to avoid pneumocephalus.
Therefore, the head is rotated and the ipsilateral shoulder is usually padded.
The supine position is used with the patient‘s head rotated for temporal access. Extremes of head rotation can obstruct the jugular venous drainage, and a shoulder roll can combat this problem or lateral positioning (park bench position).
Skin incision
Sites of predilection are frontal about 1 cm anterior to the coronal suture or parietal posterior to the parietal eminence. The area around Kocher’s point offers a safe entry without injury of branches of the middle meningeal artery or the motor strip. Additionally, the skin incision should be brought, if possible, into alignment with an eventual future skin flap for craniotomy. A curved flap avoids a burr hole position directly under the skin cut and a possible impaired wound-healing as a consequence. Further, the base of the C-shaped incision should be opposite of the planned direction of the drain tip. Obviously, a kinking of the drain is obviated 4).
Burr Holes
A performed burr hole with a diameter of 14 mm enables a sufficient angulation of the drain tip and allows an insertion of the drainage close to the calvaria.
The dura mater is coagulated and cut in a stellate fashion.
Technical issues
Under direct vision, the external membrane is perforated by the tips of the bipolar forceps. In general, there are the open or the closed ways of evacuation of the hematoma after the drain is inserted 6)
The open variant should be chosen only if irrigation is desired: the dura and external membrane are opened widely so that the fluid of the hematoma and irrigation can drip out beside the drain during rinsing. Removal of the fluid enriched with inflammatory mediators is considered obviously as an advantage, although a remaining pneumocephalus is seen as an approved factor of recurrence 7)8).
In the closed way the aim is that no air enters the subdural space. Before the dural opening the drain is tunneled beneath the galea in the direction towards the middle of the base of the skin flap. A distance from the burr hole to the drain’s exit point of at least 5 cm prevents infection 9).
Then the dura and external membrane are incised. This opening should have the same diameter as the drain to allow for a watertight and airtight drain introduction. The hematoma can therefore be evacuated only through the drain: the more fluid that is going to be collected, the more negative pressure that will be built up, which helps the brain to unfold again.
The dura is covered with a small piece of a gelatin sponge and the burr hole is filled and with bone chips collected at the beginning.
The last steps are to connect the drain to a closed collecting system and secure the connection and the exit point from the skin with sutures.
Drain insertion after CSDH drainage is important, but position (subgaleal or subdural) and duration did not appear to influence recurrence rate or clinical outcomes. Similarly, drain location did not influence recurrence rate nor outcomes where both parietal and frontal burr holes were made. Further prospective cohort studies or randomized controlled trials could provide further clarification 10).
Weigel R, Schmiedek P, Krauss JK (2003) Outcome of contemporary surgery for chronic subdural haematoma: evidence based review. J Neurol Neurosurg Psychiatry 74:937–943
Emich S, Dollenz M, Winkler PA. Burr hole is not burr hole: technical considerations to the evacuation of chronic subdural hematomas. Acta Neurochir (Wien). 2015 Jan 13. [Epub ahead of print] PubMed PMID: 25578345.
Diren F, Ozdemir O. The effectiveness of Burr-hole sizes on midline shift and hematoma thickness in the treatment of chronic subdural hematoma. World Neurosurg. 2023 Apr 20:S1878-8750(23)00546-6. doi: 10.1016/j.wneu.2023.04.062. Epub ahead of print. PMID: 37087033.
Tosaka M, Sakamoto K, Watanabe S, Yodonawa M, Kunimine H, Aishima K, Fujii T, Yoshimoto Y (2013) Critical classification of craniostomy for chronic subdural hematoma; safer technique for hematoma aspiration. Neurol Med Chir (Tokyo) 53:273–278
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
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
Berghauser Pont LM, Dammers R, Schouten JW, Lingsma HF, Dirven CM (2012) Clinical factors associated with outcome in chronic subdural haematoma: a retrospective cohort study of patients on preoperative corticosteroid therapy. Neurosurgery 70:873–880
Glancz LJ, Poon MTC, Coulter IC, Hutchinson PJ, Kolias AG, Brennan PM. Does Drain Position and Duration Influence Outcomes in Patients Undergoing Burr-Hole Evacuation of Chronic Subdural Hematoma? Lessons from a UK Multicenter Prospective Cohort Study. Neurosurgery. 2019 Oct 1;85(4):486-493. doi: 10.1093/neuros/nyy366. PubMed PMID: 30169738.
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.
International Classification of Diseases
The ICD-10-CM (Clinical Modification) code for CSDH is S06.5×5. The code describes a traumatic subdural hematoma, which includes chronic subdural hematoma as well as acute subdural hematoma. The S06.5×5 code is used to identify and track CSDH cases in health information systems.
The ICD-11 also provides a specific code for CSDH (8A62). This code falls under the category of “intracranial and spinal haemorrhage” and provides a more detailed classification of the condition.
Yordanov et al. reported on the accuracy of diagnostic ICD codes for identifying patients with CSDH from retrospective electronic data and explore whether basic demographic data could improve the identification of CSDH.
Data were collected retrospectively from the hospital administrative system between 2014 and 2018 of all patients coded with either S065 or I620. Analysis of the ICD codes in identifying patients with CSDH diagnosis was calculated using the caretR package in RStudioR,.and stepwise logistic regression analysis was performed to evaluate the best predictive model for CSDH.
A total of 1861 patients were identified. Of these, 189 (10.2%) had a diagnosis of non-traumatic SDH (I620) and 1672 (89.8%) traumatic subdural haematomas (S065). Variables that identified CSDH as a diagnosis on univariate logistic regression included male sex (Odds Ratios (OR) – 1.606 (1.197-2.161), elderly age (OR) – 1.023 (1.015-1.032) per year for age (p < 0.001) and shorter length of hospital stay. Using stepwise regression against AIC the best model to predict CSDH included male sex, older age, and shorter LOS. The calculated sensitivity for identifying CSDH with the model is 88.4% with a specificity of 84.5% and PPV of 87.9%.
CSDH is a common neurosurgical pathology with increasing incidence and ongoing unmet clinical need. We demonstrate that case ascertainment for research purposes can be improved with the incorporation of additional demographic data but at the expense of significant case exclusion 1)
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 2)3)
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 4).
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 5).
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 6).
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 7).
The progression of CSDH is an angiogenic process, involving inflammatory mediators that affect vascular permeability, microvascular leakage, and hematoma thickness.
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 8)
A prospective, multicenter, open-label, blinded endpoint randomized controlled trial designed to include 304 participants over the age of 18-90 years presenting with a symptomatic CSDH verified on cranial computed tomography or magnetic resonance imaging. Participants will be randomly allocated to perform exhaustive drainage (treatment group) or fixed-time drainage (control group) after a one-burr hole craniostomy. The primary endpoint will be recurrence indicating a reoperation within 6 months.
This study will validate the effect and safety of exhaustive drainage after one-burr hole craniostomy in reducing recurrence rates and provide critical information to improve CSDH surgical management.
Trial registration: Clinicaltrials.gov, NCT04573387. Registered on October 5, 2020 9).
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 10).
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.
Yordanov S, Khan S, Stubbs D, Davies B, Santarius T, Hutchinson P, Joannides A. Assessing the accuracy of the International Classification of Disease (ICD) framework in the identification of patients with chronic subdural haematoma from hospital records. Surgeon. 2023 Mar 24:S1479-666X(23)00020-3. doi: 10.1016/j.surge.2023.02.001. Epub ahead of print. PMID: 36967307.
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
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
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
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.
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.
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.
Wu L, Ou Y, Zhu B, Guo X, Yu X, Xu L, Li J, Feng E, Li H, Wang X, Chen H, Sun Z, Liu Z, Yang D, Zhang H, Liu Z, Tang J, Zhao S, Zhang G, Yao J, Ma D, Sun Z, Zhou H, Liu B, Liu W; ECHO Trial Collaborators. Exhaustive drainage versus fixed-time drainage for chronic subdural hematoma after one-burr hole craniostomy (ECHO): study protocol for a multicenter randomized controlled trial. Trials. 2023 Mar 20;24(1):207. doi: 10.1186/s13063-023-07250-y. PMID: 36941714; PMCID: PMC10029260.
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).
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).
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).
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
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.
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.
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
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
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.
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).
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).
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.
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.
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.
