Chronic subdural hematoma
Neurosurgery Department, University General Hospital of Alicante, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Alicante, Spain
Chronic subdural hematomas 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.
It was first described by Virchow, in 1857, as “an internal hemorrhagic pachymeningitis”. Later, in 1914, Trotter launched the theory of traumatic brain injury and the consecutive lesion of the “bridging veins”, as being the cause of what he called “hemorrhagic subdural cyst”.
The incidence of chronic subdural hematomas is estimated at 1,7-18/ 100.000 inhabitants of the entire population and it raises to 58/ 100.000 inhabitants in the group of patients over 65 years old. The medium age of patients with chronic subdural haematoma is of 63 years old. Due to the fact that the population continues to get old, it is expected that in 2030, its incidence will double 1) 2) 3) 4).
During the seven year period 1967-1973 a total of 64 residents of the City of Helsinki were diangosed as having chronic subdural haematomas. Forty of the patients were diagnosed during life at the Departments of Neurology and Neurosurgery, University of Helsinki, and treated surgically. Twenty four were diagnosed at autopsy at the Department of Forensic Medicine, University of Helsinki, at which the autopsies in virtually all cases of subdural haematoma in Helsinki are performed. The total of 64 cases gives an incidence of 1.72/100,000/year in the average population, the incidence increasing steeply with advancing age up to 7.35/100,000/year in the age groups 70-79 years 5).
In this a study, using data of the Miyagi Traumatic Head Injury Registry Project.
From January 2005 to December 2007, 1,445 patients with CSDH were registered in the project (M:F=1,021:424, mean age 71.2±12.8 y.o.). Using these patient’s records, the incidence of CSDH was investigated, as well as causes of head injury, severity, and outcome.
The overall incidence of CSDH was 20.6/100,000/year, with 76.5 in the age group of 70-79 y.o. and 127.1 in the over 80 y.o. group. Ground level fall was the most frequent cause of trauma in the elderly, in contrast to traffic accident, which was the most frequent cause in the younger generation. Compared to the younger generation, neurological condition was severer in the elderly at the time of admission, and the outcome was poorer at the time of discharge.
Compared to previous reports, this study demonstrates a marked increase in the incidence of CSDH. Not only population aging but also current medical trends (such as increases of the elderly patients who receive hemodialysis, anticoagulant, and/or antiplatelet therapy) may influence the increase of CSDH incidence 6).
A steady increase in the incidence of CSDH has been also observed in developing countries due to the rise in life expectancy 7).
CSDHs occurred more frequently on the left side. The anatomical asymmetry of the cranium influences the left predilection of CSDH 8).
Usually, this collection has a traumatic etiology.
Chronic subdural hematomas mainly occur amongst elderly people and usually develop after minor head injuries.
In younger patients, subdural collections may be related to hypertension, coagulopathies, vascular abnormalities, and substance abuse.
A retrospective review of 239 patients undergoing surgery for CSDH over a period of six years (2006-2011). The majority of patients (63%) in the non-trauma group were receiving anticoagulants and/or antiplatelet agent therapy prior to CSDH presentation, compared to 42% in the trauma group. 9).
Unilateral chronic subdural hematoma
Chronic subdural hematoma (CSDH) is considered to be an angiogenic disease.
Studies have suggested that local anticoagulation and inflammatory changes may be important in its pathogenesis. Most studies have used a basic bivariate statistical analysis to assess complex immunological responses in patients with this disorder, hence a more sophisticated multivariate statistical approach might be warranted.
Thirteen assigned pro-inflammatory (TNF-α, IL-1β, IL-2, IL-2R, IL-6, IL-7, IL-12, IL-15, IL-17, CCL2, CXCL8, CXCL9 and CXCL10) and five assigned anti-inflammatory (IL-1RA, IL-4, IL-5, IL-10 and IL-13) cytokines from blood and hematoma fluid samples were examined. Exploratory factor analysis indicated two major underlying immunological processes expressed by the cytokines in both blood and hematoma fluid, but with a different pattern and particularly regarding the cytokines IL-13, IL-6, IL-4 and TNF-α. Scores from confirmatory factor analysis models exhibited a higher correlation between pro- and anti-inflammatory activities in blood (r = 0.98) than in hematoma fluid samples (r = 0.92). However, correlations of inflammatory processes between blood and hematoma fluid samples were lower and non-significant.
Three major mitogen activated protein kinase (MAPK) cascade transmitters in the outer membrane of CSDH was assessed. Eleven patients whose outer membrane and CSDH fluid were successfully obtained during trepanation surgery were included in a study. Expression of extracellular signal regulated kinase (ERK), phosphorylated (p)-ERK, p38, p-p38, c-Jun N-terminal kinase (JNK), p-JNK, and actin was examined by western blotting and immunostaining. Aoyama et al. examined whether CSDH fluid could activate MAPKs in cultured endothelial cells or fibroblasts in vitro. Western blot analysis showed that p-ERK was present in all samples, while p-p38 and p-JNK were detected, but not in all cases. Immunostaining showed that all three p-MAPKs were expressed in vascular endothelium. However, only p-ERK was expressed in fibroblasts. Expression of p-extracellular signal-regulated kinase kinase (MEK) and p-ERK in endothelial cells and fibroblasts was significantly induced immediately after treatment with CSDH fluid, while p-p38 and p-JNK expression was significantly induced in endothelial cells 60 min after treatment, but not in fibroblasts. Activation of MEK was significantly inhibited by treatment with antibodies directed against interleukin-6 and vascular endothelial growth factor in endothelial cells, but not in fibroblasts. Inflammatory cytokines and growth factors in CSDH fluids might activate major MAPKs in endothelial cells, which might be associated with neovascularization in the outer membrane of CSDH. These MAPK pathways could become novel targets for treatment of CSDHs 10).
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 11).
Patients with unilateral chronic subdural hematoma had more frequent occurrence of hemiparesis than the patients with bilateral chronic subdural hematoma. It took the left-sided chronic subdural hematomas less time (about 200 hours earlier) than the right-sided ones to present its symptoms although the average hematoma diameter value was almost the same.
The site and the form of intracranial lesion-chronic subdural hematoma could have a great influence on neurological and functional condition in a patient. Although the length of time required for making diagnosis as well as clinical symptoms greatly differ and the latter are not always so clear, physicians should maintain a high level of suspicion for this disease and thus contribute to prompt diagnosis and better clinical outcome of patients12).
Its clinical symptomatology often debuting with memory and attention disorders, so that the patient is usually referred to psychiatrists or neurologists, only a paraclinical investigation (CT scan or MRI) being able to establish the diagnosis. Even the appearance of the lateral signs is subjected to many diagnosis confusions because patients deny the existence of a trauma in over 50% of the cases 13).
Density of the chronic subdural hematoma (cSDH) is variable. It often appears to be mixed density. Multiple densities of cSDH may result from multiple episodes of trauma, usually in the aged. It is hard to remember all the trivial traumas for the patients with the mixed density cSDHs. .
The cSDHs can be classified into four groups; hypodensity, homogeneous isodensity, layered type, and mixed type on the basis of CT scans 15).
CT-scan is able to provide the diagnosis of chronic subdural hematoma in more than 90% of the cases. It usually shows a peri-cerebral fluid collection along the convexity, with a convex outer border, and an irregular concave inner border. The density of the collection depends on the age of the hematoma. The main difficulties, in term of diagnosis, result from bilateral isodense chronic subdural hematoma, and differential diagnosis between hematoma, hygroma, and empyema. Some rare localisations can sometimes be seen (posterior fossa, skull base…). A double density with a sedimentation level, or heterogeneity of the hematoma, can sometimes be seen too. Chronic subdural hematoma is demonstrated by MRI in almost 100% of the cases. The intensity of the collection, in T1 and T2 sequences, depends on the age of the hematoma 16).
The MRI examination better shows the location of the chronic subdural haematoma and evidences its dimensions much clearer together with the mass effect of the adjacent structures. Moreover, it is more useful in cases of bilateral and isodense chronic subdural hematomas. The MRI examination is superior to the CT examination as far as the membranes dimensions of the chronic subdural haematoma and the presence of the septa inside the haematoma are concerned, in these conditions the surgical approach could be modified.
Based on MRI, CSDHs can be classified into five types on both T(1)- and T(2)-weighted images: low, high, and mixed intensity, isointensity, and layered. Usually, CSDHs are hyperintense on both T1- and T2-weighted MRI (the T1 values of CSDHs are significantly shorter than gray matter values and significantly longer than white matter values and the T2 values are significantly longer than both gray matter and white matter values)17) 18).
However, it can be iso- or hypointense on T1-weighted images in some cases 19) Even though MRI has advantages, CT remains the procedure of choice in the acute setting because of shorter examination time, which is important in acutely ill patients, reliability in identifying other lesions 20).
Routine post-operative CT brain for burr hole drainage of CSDH may be unnecessary in view of the good predictive value of pre-operative volume, and also because it is not predictive of the clinical outcome 23).
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 24).
Routine postoperative CT
Scheduled postoperative cranial imaging with indwelling drains was not shown to be beneficial and misses information of intracranial damage inflicted by removal of drains. Brokinkel et al recommend CT-scanning after drainage removal 25).
Chronic subdural hematoma (CSDH) is one of the most common clinical entities in daily neurosurgical practice which carries a most favorable prognosis. However, because of the advanced age and medical problems of patients, surgical therapy is frequently associated with various complications.
Failure of the brain to re-expand, pneumocephalus, incomplete evacuation, and recurrence of the fluid collection.
A wide variation in postoperative drainage volumes is observed during treatment of chronic subdural hematoma (CSDH) with twist-drill or burr-hole craniostomy and closed-system drainage.
The postoperative drainage volumes varied greatly because of differences in the outer membrane permeability of CSDH, and such variation seems to be related to the findings on the CT scans obtained preoperatively. Patients with CSDH in whom there is less postoperative drainage than expected should be carefully observed, with special attention paid to the possibility of recurrence 26).
Failure of postoperative cerebral reexpansion
Patients with high subdural pressure showed the most rapid brain expansion and clinical improvement during the first 2 days. Nevertheless, a computerized tomography (CT) scan performed on the 10th day after surgery demonstrated persisting subdural fluid in 78% of cases. After 40 days, the CT scan was normal in 27 of the 32 patients. There was no mortality and no significant morbidity. A study suggests that well developed subdural neomembranes are the crucial factors for cerebral reexpansion, a phenomenon that takes at least 10 to 20 days. However, blood vessel dysfunction and impairment of cerebral blood flow may participate in delay of brain reexpansion. It may be argued that additional surgical procedures, such as repeated tapping of the subdural fluid, craniotomy, and membranectomy or even craniectomy, should not be evaluated earlier than 20 days after the initial surgical procedure unless the patient has deteriorated markedly 27).
Remote cerebellar hemorrhage (RCH)
Is a very rare complication of supratentorial surgery, with a reported incidence of 0,08% 28).
The precise mechanism of cerebellar hemorrhage following supratentorial burr hole drainage of CSDH is uncertain, but is suspected to be multifactorial. Firstly, a history of previous hypertension and transient hypertensive peaks during the recovery period have been considered to be important factors 31) 32).
This idea is based on the fact that arterial hypertension is the most common cause of spontaneous cerebellar hemorrhage. However, only two out of nine patients (22%), reported in the literature, had a history of hypertension and in one out of them the preoperative blood pressure was consistently normal with antihypertensive drugs. Moreover all patients had perioperative normal blood pressure and only in two cases an elevation of blood pressure was reported postoperatively 33).
Another major cause of spontaneous cerebellar hemorrhages is disturbed blood coagulation, which has been considered as well to be a relevant predisposing factor for postoperative cerebellar hemorrhages 34).
Another proposed mechanism for the development of RCH is that expansion of CSF spaces after surgical removal of CSDH increases mobility of the intracranial structures. Moreover, CSF overdrainage may lead to a downward displacement of the cerebellum. These above mentioned mechanisms may cause stretching and possible tearing of the superior vermian veins leading to RCH.
Furthermore, continuous CSF drainage, intraoperatively as well as postoperatively, could even increase the transtentorial pressure gradient leading to rupture of the small supracerebellar veins and capillary bed with venous bleeding as a consequence1. A massive air reflux into the cranial cavity through the drainage tube may pose an additional risk 35).
After chronic subdural hematoma evacuation surgery, the development of epidural hematoma is a very rare entity.
Akpinar et al. report the case of a 41-year-old man with an epidural hematoma complication after chronic subdural hematoma evacuation. Under general anesthesia, the patient underwent a large craniotomy with closed system drainage performed to treat the chronic subdural hematoma. After chronic subdural hematoma evacuation, there was epidural leakage on the following day.
Although trauma is the most common risk factor in young CSDH patients, some other predisposing factors may exist. Intracranial hypotension can cause EDH. Craniotomy and drainage surgery can usually resolve the problem. Because of rapid dynamic intracranial changes, epidural leakages can occur. A large craniotomy flap and silicone drainage in the operation area are key safety points for neurosurgeons and hydration is essential36).
The National Audit of Chronic Subdural Haematoma is collecting data prospectively in order to answer “ how are patients managed in the UK and what are their outcomes? ” . A collaborative process, which was overseen by the Academic Committee of the Society of British Neurological Surgeons (SBNS), led to the development of the first set of national audit standards for chronic subdural haematoma (CSDH) on the basis of best available evidence 37).
The Audit has already collected data on over 700 patients and has therefore become the largest multicentre prospective study of CSDH worldwide, has helped to firmly establish the feasibility of collaborative research networks in the field of neurosurgery.
Establishment of collaborative networks together with the developing neurosurgical research infrastructure will ensure a bright future for clinical research in neurosurgery 38).
A high mortality index in the postoperative period was found in patients with INR (international normalized ratio) values greater than 1.25 and/or thrombocytopenia (p<0.001 and p=0.004 respectively) 39).
Surgical drainage of chronic SDHs in nonagenarians and centenarians is associated with lower incidence of inpatient death and higher 30-day and 6-month survival rates 40).
242 cases of chronic SDH. The cSDHs were classified into four groups; hypodensity, homogeneous isodensity, layered type, and mixed type on the basis of CT scans.
The density of cSDH was isodense in 115 patients, hypodense in 31 patients, mixed in 79 cases, and layered in 17 cases. The cSDH was on the left side in 115 patients, on the right side in 70 patients, and bilateral in 40 patients. The history of trauma was identifiable in 122 patients. The etiology could be identified in 67.7% of the hypodense hematomas, while it was obscure in 59.5% of the mixed hematomas.
Mixed density of cSDH results from multiple episodes of trauma, usually in the aged. It is hard to remember all the trivial traumas for the patients with the mixed density cSDHs. Although there were membranes within the mixed density hematomas, burr-holes were usually enough to drain the hematomas 41).
A case of bilateral chronic subdural hematoma (CSDH) in a 75-year-old man after exercise using a vibrating belt machine on the head. He suffered from headache and intermittent left side numbness for ten days. He denied any head injuries except eccentric exercise using a vibrating belt on his own head for 20 days. An MRI revealed bilateral CSDH. The hematoma was isodense on the CT scan. Park et al. made burr-holes on the both sides under local anesthesia and identified the neomembrane and dark red subdural fluid on both sides. In the postoperative CT scan, they found an arachnoid cyst on the left temporal pole. Although the arachnoid cyst itself is asymptomatic, trivial injury such as vibrating the head may cause a CSDH 42).
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 43).