Medical and Surgical Management of Chronic Subdural Hematomas

This chapter includes an accompanying lecture presentation that has been prepared by the authors: .

Key Concepts

Chronic subdural hematoma (CSDH) is a common neurosurgical condition; with progressive aging of the world population, its incidence will continue to grow.
Surgery is a primary mode of treatment, unless the patient is asymptomatic or moribund.
Many surgical options exist, but bur-hole craniostomy (BHC) and mini-craniotomy are most popular; twist-drill craniotomy is also used in a number of centers around the world. Since the 2009 randomized controlled trial of drains versus no drain, bur hole with an external subdural drain has become the most commonly used technique. However, each detail of the technique needs to be carefully considered and meticulously executed, as serious complications such as brain injury with permanent neurological deficit can occur. We recommend using a frontal rather than parietal bur hole for insertion of drains, and stress the importance of using an appropriate drain and drain insertion technique. Although drainage of subdural hematoma is relatively straightforward and often left to the most junior trainees, judicious supervision may still be required if one wants to eradicate such complications. Subgaleal insertion of the drain seems to be a reasonable alternative if an appropriate drain is not available or there are difficulties with eradiation of drain-associated complications.
A large, placebo-controlled, randomized trial, published in 2020, found worse 6-month outcomes in patients treated with dexamethasone.
Early postoperative scanning is not required, as was shown in a trial reported in 2019.

Introduction and Epidemiology

Chronic subdural hematoma (CSDH) can be defined as a predominantly hypodense or isodense crescentic collection along the cerebral convexity on cranial CT, which must be differentiated from subdural empyema and hygroma. This chapter deals with the diagnosis and management of CSDH in adults only, as pediatric CSDH is a separate disease entity with distinctive etiology and management.

CSDH is considered a disease of elderly people; mean age at presentation in a large, prospective, observational study from the United Kingdom (the UK CSDH study; 1205 patients enrolled from 26 neurosurgical units) was 77 years (range, 20–99 years), with a 2:1 male-to-female ratio. However, in low- and middle-income countries the mean age at presentation is around 60 years. The incidence of CSDH is quoted at about 10 per 100,000 per year and is rising owing to the combination of an aging population and the increasing use of anticoagulant and antiplatelet medications. A population-based study from the Pirkanmaa region in Finland demonstrated that from 1990 to 2015 the overall incidence of CSDH doubled from 8.2 to 17.6 per 100,000 per year. The incidence remained stable in those younger than 70 years, whereas it increased from 32.3 to 52.1 per 100,000 per year in patients aged 70 to 79 years, from 50.7 to 130.3 per 100,000 per year in patients aged 80 to 89 years, and from 11.6 to 125 per 100,000 per year in patients age 90 years and older. The median age for a CSDH diagnosis also increased from 73 years (1990–95) to 79 years (2011–15) during the 26-year study period.

Pathogenesis

CSDH arises at the dural border cell layer, a thin layer of cells between the dura mater and arachnoid mater with less extracellular collagen and intercellular connections prone to separation ( Fig. 47.1 ). Development of CSDH requires a predisposing factor of a shrinking volume within the cranial vault (e.g., the elderly atrophic brain, the alcoholic brain, or the overdraining cerebrospinal fluid [CSF] shunt), and a precipitant trauma that can often be so minor that it is not identified in the history.

Figure 47.1, Schematic diagram of the meninges illustrating the dural border cell layer, a thin layer of cells between the dura mater and arachnoid mater with less extracellular collagen and intercellular connections prone to separation where chronic subdural hematoma (CSDH) forms.

Two possible etiologies have been hypothesized, ^, although there remains debate about what proportion of CSDH arises from each. ^,

The first etiology is associated with an acute subdural hematoma (ASDH). These usually occur in the context of trauma due to tearing of the bridging veins that traverse the dural border cell layer or, less commonly, tearing of cortical arteries or veins. An ASDH that is not surgically evacuated in the acute setting will usually be resorbed, but in certain cases this process is incomplete and the hematoma becomes chronic as the acute clot lyses ( Fig. 47.2 ). Chronic hematomas expand as a result of a local inflammatory reaction, ^, resulting in fibrinolysis of the clot and the production of angiogenic factors that promote neovascularization and bleeding from fragile capillaries. ^, ^, Studies have demonstrated that roughly 20% of conservatively managed ASDH will become chronic, although the factors that predispose to this have not been identified. ^,

Figure 47.2, Example of evolution of acute subdural hematoma (ASDH) into chronic subdural hematoma (CSDH) in a 90-year-old man on warfarin presenting with reduced consciousness after a fall.

The second etiology involves a subdural hygroma, a collection of CSF in the subdural space caused by the splitting of the dural border cell layer at points of tension between the dura mater and arachnoid mater. This can occur spontaneously, especially in asymmetrical skulls in which the tension may not be spread evenly. In the subdural space, neomembranes form through proliferation of the dural border cells, and neovascularization occurs. Hemorrhage and the resulting inflammatory response from these new vessels leads to the formation and expansion of a CSDH.

Regardless of the primary insult, inflammation, angiogenesis, and fibrinolysis play a key role in the pathogenesis of CSDH. Formation of neomembranes is one of the main features of CSDH; in particular, the outer neomembranes are a well-recognized source of inflammatory and angiogenic mediators, such as tissue plasminogen activator (tPA), thrombomodulin, angiopoietin-2 (Ang-2), vascular endothelial growth factor (VEGF), and matrix metalloproteinases (MMPs). Some of these mediators may also have a role to play as biomarkers; for example, high levels of interleukin (IL)-6 and IL-8 in the subdural fluid correlate with increased risk of CSDH recurrence.

A range of risk factors have been identified including advancing age, a history of falls or minor head injury, use of anticoagulants or antiplatelet drugs, bleeding diatheses, alcohol use (contributing to global brain atrophy, higher risk of falls, and hepatogenic coagulopathy), epilepsy, low intracranial pressure states, and hemodialysis. ^, Around 60% of patients have a history of head injury. Perhaps one of the most important risk factors that has contributed to the increasing incidence of CSDH is the use of anticoagulant and antiplatelet medications. The population-based study from Finland found that the percentage of patients receiving anticoagulant or antiplatelet medication has almost doubled since the 1990s (27% in 1990–95 versus 49% in 2011–15). The widespread use of these agents has made quantification of risk difficult, but they have been shown to increase the incidence of both de novo and recurrent CSDH. However, other studies have found that antithrombotic drugs do not increase recurrence.

Clinical Presentation

CSDH can present heterogeneously, and symptom onset and progression can vary from days to weeks. Common presenting symptoms and signs include headache, limb and gait disturbance, hemiparesis or hemiplegia, cognitive decline, and confusion ( Table 47.1 ). It is important to remember, however, that a significant proportion (20%–30%) of CSDHs may be completely asymptomatic and discovered incidentally. Consciousness level at presentation is usually normal or only slightly altered, although a minority of patients (20%) may present with a Glasgow Coma Scale (GCS) score <13.

TABLE 47.1

Presenting Symptoms and Admission Glasgow Coma Scale (GCS) Score of Patients With Chronic Subdural Hematoma (CSDH) ^a

Modified from Santarius T, Kirkpatrick PJ, Ganesan D, et al. Use of drains versus no drains after burr-hole evacuation of chronic subdural haematoma: a randomised controlled trial. Lancet. 2009;374(9695):1067–1073.

Presenting Symptoms (n = 205)
	Gait disturbance and falls	116	(55.5%)
	Mental deterioration	71	(34.0%)
	Limb weakness	71	(34.0%)
	Acute confusion	67	(32.1%)
	Headache	36	(17.2%)
	Drowsiness or coma	20	(9.6%)
	Speech impairment	12	(5.7%)
	Nonspecific deterioration	7	(3.3%)
	Collapse	2	(1.0%)
	Seizure	2	(1.0%)
	Incontinence	1	(0.5%)
	Visual disturbance	1	(0.5%)
	Vomiting	1	(0.5%)
GCS Score at Presentation (n = 202)
	13–15	163	(80.7%)
	9–12	25	(12.4%)
	3–8	14	(6.9%)

a Presenting symptoms and admission GCS score of patients with CSDH from a prospective randomized controlled trial at our institution examining the role of subdural drains in addition to bur-hole craniostomy for treatment of CSDH.

There is evidence to suggest that prognosis can be predicted based on the GCS and modified Rankin Scale (mRS) scores at admission. ^, ^, ^, An alternative to the GCS used in many CSDH studies is the Markwalder grading system ; although historically popular, it is rather imprecise in its descriptions, and therefore we prefer to use a combination of GCS, focal neurological signs, and a measure of function (e.g., mRS) to provide a comprehensive approach to assessing patients both at admission and at follow-up, especially in the academic context.

Diagnosis

The mainstay for diagnosis is CT. CSDH is seen as a hypodense (<30 HU) crescentic collection along the convexity but may have isodense (subacute, 30–60 HU) or hyperdense (acute, >60 HU) components. ^, Subacute CSDH may be overlooked, especially if it is bilateral or does not cause midline shift. Features that can be helpful include medial displacement of the gray matter–white matter interface and failure of the convexity sulci to reach the inner table of the skull. Differential diagnoses for a hypodense crescentic collection include subdural hygroma (discussed earlier) and subdural empyema. The clinical picture and MRI findings will help in making the correct diagnosis.

Nakaguchi et al. categorized CSDH into four subtypes (homogeneous, laminar, separated, and trabeculated), hypothesizing that they were four stages in the natural history of the disease process. They found higher recurrence rates in the separated subtype (36%) and lower recurrence rates in the trabecular subtype (0%) as compared with the homogeneous (15%) and laminar (19%) subtypes, findings that have since been corroborated. However, this has not led to a stratified approach to the treatment of CSDH in routine clinical practice. MRI does not currently have a role in routine clinical practice and is usually performed when other diagnoses were originally suspected.

Management

Preoperative Optimization

The typical patient undergoing surgical intervention for CSDH is often an elderly patient with multiple comorbidities. Those who are taking anticoagulant and antiplatelet medications often have significant cardiovascular disease and therefore must undergo a thorough preoperative assessment. The assessment should include cardiorespiratory examination, routine blood tests (full blood count, urea and electrolytes, clotting studies) and electrocardiography; further tests such as chest radiography and echocardiography may be required in selected patients. This assessment can aid with decisions about whether or not surgical intervention is appropriate and if so, the type of surgical intervention (see “Conservative Management” section later in this chapter). Medical optimization, such as treatment of concomitant lower respiratory tract infections or optimization of cardiovascular medications, may be required prior to surgical intervention if the clinical situation allows.

Correction of Coagulopathy and Thrombopathy

Correction of coagulopathy or thrombopathy is crucial to reduce the risks of bleeding during operative intervention and recurrence. Correction of coagulopathy and temporary cessation of antiplatelet medications are usually recommended in nonoperatively managed patients to prevent further expansion.

There is evidence that platelet function fully recovers in 4 to 6 days and 7 to 10 days after discontinuation of aspirin and clopidogrel, respectively. Hence the option of discontinuing these drugs and planning surgery after a few days could be made available to patients who are neurologically stable and have mild symptoms. If urgent surgery is indicated, a platelet transfusion should be considered. The UK CSDH study found that nearly one-third of patients on a single antiplatelet agent received a perioperative platelet transfusion. The median intervals between discontinuation of the antiplatelet drug and the operation in patients with and without platelet transfusion were 1 and 5 days, respectively.

Details about the management of specific anticoagulant and antiplatelet drugs in the perioperative setting can be found in Chapter 18 . The involvement of hematologists and cardiologists should be considered, especially in patients with recent myocardial infarctions, recent venous thromboembolism, insertion of coronary stents, and cardiac valve replacements.

Adjuvant Treatments

There are two main adjuvant medical therapies used for the treatment of CSDH, namely steroids and antiepileptic medications.

A systematic review published in 2019, which included a total of 1119 patients, concluded that the need for reintervention was lower in patients who had corticosteroids as an adjunct to surgery (CS group) compared with patients who had corticosteroids as a monotherapy (C group) (relative risk [RR], 3.34 [95% confidence interval {CI}, 1.53–7.29]; P <.01). Moreover, the CS group had a lower risk of intervention when compared with patients treated with surgery alone (RR, 0.44 [95% CI, 0.27–0.72]; P <.01).

The findings of the first, multicenter, placebo-controlled, randomized trial of a tapering 2-week course of dexamethasone, which enrolled 748 patients with a symptomatic CSDH admitted to a neurosurgical unit, were published in 2020. It confirmed that the risk of repeat surgery for a recurrence was lower in patients who received dexamethasone (1.7% versus 7.1% for patients in the placebo group). However, analysis of the primary end point, which was functional outcome at 6 months (assessed with the use of the mRS), showed that patients in the dexamethasone group fared worse compared with patients in the placebo group. ^, Specifically, a favorable outcome was reported in 286 of 341 patients (83.9%) in the dexamethasone group and in 306 of 339 patients (90.3%) in the placebo group, for a difference of −6.4 percentage points (95% CI, −11.4 to −1.4) favoring the placebo group. As the majority of the enrolled patients had surgery for their CSDH (94%), it is not clear if these results apply to patients managed with a primary nonoperative intent. However, the subgroup of patients who did not have an operation (38 patients) had a similar direction of effect as the primary endpoint (18/22 patients [82%] in the dexamethasone group had a favorable outcome versus 16/16 patients [100%] in the placebo group). Therefore, owing to the clear signal of harm associated with dexamethasone, we recommend that the use of dexamethasone for CSDH should be avoided, unless it is happening as part of a research study. This recommendation may need to be revisited after the ongoing DECSA (Dexamethasone Therapy in Symptomatic Patients With Chronic Subdural Hematoma) trial has been reported, as it is specifically examining the role of dexamethasone as a stand-alone therapy (i.e., alternative to surgery).

The use of prophylactic antiepileptic medication was examined in a Cochrane review, which found a highly variable but generally low incidence of preoperative and postoperative seizures (2.3%–17% and 1.0%–23%, respectively). In the three retrospective studies that were analyzed, preoperative antiepileptic prophylaxis was shown to reduce postoperative seizure rate but not discharge outcome. Hence there is currently no evidence to advocate the use of prophylactic antiepileptic medication in this patient population.

Many other agents have been suggested as adjunctive or stand-alone therapies, including statins, tranexamic acid, and angiotensin-converting enzyme (ACE) inhibitors. We do not use any of these agents routinely, but we note that a number of randomized trials are currently in progress, which may change practice in the future. A phase 2 placebo-controlled trial of atorvastatin (20 mg daily for 8 weeks) conducted in China found an adjusted odds ratio of 1.957 for clinical improvement (95% CI, 1.07–3.58; P =.03) favoring the drug. Eleven patients (11.2%) who were on atorvastatin and 23 (23.5%) on placebo underwent surgery during the trial for an enlarging hematoma and/or a deteriorating clinical condition (hazard ratio, 0.47 [95% CI, 0.24–0.92]; P =.03). These results cannot be considered definitive, and we do not recommend any practice changes on this basis.

Conservative Management

In general, nonoperative treatment is offered to patients in whom operative risks are believed to outweigh the benefits of surgery. This includes asymptomatic patients with small collections at one end of the spectrum and moribund patients with poor baseline function at the other end.

For the asymptomatic patients with small collections, there are no specific management guidelines. During the initial admission, efforts must be made to reverse coagulopathy and thrombopathy (see section “Correction of Coagulopathy and Thrombopathy” for further details). Following discharge, repeat CT scanning may be performed after a few weeks to confirm that the hematoma is not expanding, or after development of new symptoms.

At the other end of the spectrum, patients managed conservatively because of either poor baseline condition or high surgical risk should be managed in conjunction with other specialties, especially elderly care physicians. A course of steroids may be trialed, notwithstanding the aforementioned limitations. Important to note, the patient (whenever possible) and the next of kin should be consulted about the appropriateness of escalation of care should the patient’s condition deteriorate.

Surgical Intervention

In general, there is consensus that patients with symptoms that can be attributed to a radiologically confirmed CSDH should be treated surgically. Surgical treatment of symptomatic CSDH results in a rapid improvement of patient symptoms and results in a favorable outcome in about 80% of patients. ^, ^, Coupled with relatively low surgical risk, surgical evacuation is currently the mainstay of management for symptomatic patients.

There are three primary surgical techniques used: twist-drill craniostomy (TDC), involving small openings (<10 mm) made using a twist drill; bur-hole craniostomy (BHC), involving openings of 10 to 30 mm; and craniotomy, involving larger openings. The following sections describe each of these surgical techniques.

Within each of these three broad categories a number of specific techniques have been described and are used by individual surgeons. ^, ^, Usually one or two techniques are used by a surgeon or institution to treat most of presenting CSDHs. Although it is likely that certain techniques are more suitable for certain subtypes of CSDHs, this has not been shown in the published literature.

The three main techniques vary in their invasiveness, and this needs to be taken into account, balancing the physiologic frailty and multiple comorbidities inherent to the elderly population against the risk of recurrence, as judge based on published evidence and experience; this will be discussed in more detail later in the “Outcomes” section. Here we describe the techniques as used and viewed based on the experience from our institution.

Bur-Hole Craniostomy

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