Complications After Surgery for Chronic Subdural Hematomas

Abstract

Chronic subdural hematoma (CSDH) is an increasing issue worldwide, due to the increasing age of the population. Despite the simple surgical technique it may be burdened by a high rate of complications (such as recurrence, acute rebleeding, infections, …). A consensus about the right management of those events.

In this chapter we clarify what are the most common complications of CSDH through a literature review and through a description of some clinical cases in order to better udestand these problems.

Keywords

CSDH, recurrence, acute rebleeding, infection, seizures

Complications After Surgery for Chronic Subdural Hematomas

Chronic subdural hematoma (CSDH) ( Fig. 45.1A–B ) is an abnormal collection of liquefied blood degradation underneath the dura matter that may result in brain tissue compression and subsequent neurologic sequelae. Due to the aging population in developed countries, chronic subdural hematoma is becoming an increasingly common neurosurgical pathology that can reach up to 58.1 per 100,000 persons in the population over 65 years of age. Toi et al., in a review of surgical databases on more than 63,000 cases, showed how the age of the patients has progressively increased in the last three decades. The high number of comorbidities at a higher age and the increasing number of surgeries for the evacuation of CSDH may lead to several complications due to a lack of evidence in the guidelines for the ideal management of this kind of hematoma.

Principal complication is a recurrence of the hematoma, which can reach a surprisingly high rate of 30% in some populations.

Pathophysiological Insights

The physiopathology of chronic subdural hematoma still remains unclear. The most probable and cited hypothesis is that it starts as an acute subdural hematoma due to intermittent rupture of bridging veins in the subdural space. The persistence of blood in subdural space, often clinically asymptomatic due to cerebral atrophy of older people, enhances an inflammatory reaction; progressive involvement of fibroblasts leads to the formation of a cortical (or inner) and a dural (or outer) membrane. Inside this new “capsule,” the clot of blood of ASDH is degraded by fibrinolytic enzymes and progressively liquefied; continuous proliferation of fibroblast may also lead to the formation of inner neomembranes. The increasing size of the newly formed hematoma is the result of the plasma effusion versus the liquid reabsorption; in most cases, this balance explains the differences in the timing of the appearance of clinical manifestations.

Surgical Management

Surgical treatment of CSDH still lacks clear indications and guidelines; however, there are a few points that should be kept in mind to avoid complications:

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Before operation, coagulation parameters should be monitored and eventually reversed; surgical treatment should be avoided until internal normalized ratio (INR) is normalized or under 1,53.
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There are no guidelines about which type of anesthesia should be performed.
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There is no correlation between the outcome and recurrence of subdural hematoma in patients operated on with twist drill (<5 mm) or burr hole (1 cm) ; however, burr hole remains the most common procedure.
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Systematic reviews have not found any difference in outcomes between one and two burr holes; however, two burr holes are recommended, especially if the operation is performed under general anesthesia. The role of a single burr hole under local anesthesia should still be evaluated.
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Placement of a postoperative drainage improves neurologic outcome and decreases the rate of recurrence ; subdural drain is recommended according to the high-quality evidence found by Santarius et al.

Complications

Recurrence

Recurrence ( Fig. 45.1E-F ) of the hematoma is the most common complication of CSDH, with an overall rate that varies between 2% and 87%. Physiopathology of this complication is not fully understood but represents a significant problem due to the fact that around 20% of the patients require at least one reoperation.

One of the most discussed explanations concerns the use and restarting of anticoagulant and/or antiplatelet therapy.

Due to the high number of comorbidities in patients with CSDH (e.g., FA, ischemic cardiopathy) there is an increasing interest in the management of anticoagulant therapy in this setting. Anticoagulant and antiplatelet therapies have been showed to be risk factors for the development and recurrence of hematoma by many groups ; however, the definition of the optimal management of these drugs is still lacking. Concerning anticoagulants, the therapy should be stopped at admission to the hospital, and the INR should be monitored to eventually normalize the level. In many patients, due to severe comorbidities or prolonged periods of immobilization, a prophylactic therapy (against deep vein thrombosis) should be started with heparin. These anticoagulant treatments, according to Kolias et al. and Tahsim-Oglou et al., increase the risk of recurrence by 18.8% and 32.1% , respectively; for these patients, a more strict surveillance should be performed. Another issue is represented by the timing of the restart of the anticoagulation. Is there an optimal range to minimize the risk? Several authors have tried to find an answer but without a clear result; at this moment the ideal timing to restart anticoagulant or antiplatelet therapy should be decided on an individual patient basis. An objective method, that has been advised by Chari et al., that can be used for patients undergoing anticoagulant therapy for atrial fibrillation is to compare the CHA2DS2-VASc thromboembolism risk score with the HAS-BLED bleeding risk score. Although this method represents a good starting point to try to solve a significant problem, it has not yet been validated by sequent RCT. This field definitely needs further study, especially due to the introduction of new anticoagulants such as Rivaroxaban.

A second variable that should be considered is the type of hematoma the patient is experiencing; it has been shown that bilateral hematomas have a higher risk of recurrence after evacuation. In 2010 Kung et al. tried to answer this question by reviewing computed tomography (CT) scans performed 14, and 30 days postoperatively. They concluded that the higher recurrence is probably related to a major shift produced by the higher volume of the lesion; this can lead to a stretch and new tearing of the bridging veins, which contributes to the reforming hematoma. This theory has not been validated by subsequent papers but still remains an interesting hypothesis.

Another possible explanation of recurrences deals with the organization of the hematoma: CSDH has a thicker outer membrane and a thinner inner membrane. These two enclose liquefied blood and often new vascularized membranes. In their randomized prospective trial, Unterhofer et al. compared two groups of 28 patients; the first group underwent enlarged burr hole surgery with opening of the inner membrane, and the second group underwent enlarged burr hole surgery without opening. This study showed no difference in the need for of a revision surgery, size of residual hematoma during the follow-up, and outcome.

The problem of inner membranes has been discussed many times over the years, and it has been proven that it is statistically significant in the recurrence of CSDH. Intraoperative opening of these septations is a common way to avoid the segregation of parts of the hematoma; however, in the case of thick or diffuse membranes, the opening could not be enough and a minicraniotomy would be required.

Another aspect to consider in the prevention of recurrency of the hematoma is the correct positioning of the patient.

Indications about the right placement of the head of the patient after surgery are not standardized. At the moment only two small randomized trials have been written about this topic with two opposite results: In 2010 Kurabe et al. found a higher risk of recidivism in the patient with the head raised to 30 to 40 degrees, and Baouzari et al. in 2007 showed no difference between the two groups of patients. Further investigations are needed to clarify this point.

The need for a validated method to predict the recurrence of CSDH has led several authors to propose scores and scales. In a work published in 2015, Jack et al. proposed a simple way to stratify the risk of recurrence; they attributed 0 or 1 point to age (<80 years = 0; >80 years = 1), CSDH volume (<160 mL = 0; >160 mL = 1) and presence of septations (absence = 0; presence = 1); the summary gives an estimation of risk of recurrence that ranges from 5% (total of 0) to >20% (total of 3). This paper represents a good starting point to stratify the risk, although more investigations are needed.

Recurrence of CSDH has not only been studied with respect to surgical factors. Schaumann et al. in 2016 published the results of the RCT “COXIBRAIN”: according to this paper the recurrence of CSDH is related to neoangiogenesis in the parietal membrane, which is VEGF-mediated. The aim of this study was to reduce the incidence of recurrence of operated CSDH by administering selective COX-2 inhibitors (Colecoxib). Unfortunately this study enrolled only 23 patients in 2 years and did not reach conclusions that can be used in clinical practice; on the other hand, it showed how 55% of patients were already treated by COX-2 inhibitors and they developed a relapse.

In the end, recurrence of CSDH is not fully understood and it still needs further investigations. Treatment of this complication is often surgical, but with a lack of high-quality evidence, it should be adapted on a case-by-case basis.

Steroid Treatment for Cdsh

The current role of steroids in the treatment of CSDH as substitute for or adjuvant to surgery has not been established. There are currently two ongoing RCTs, one promoted by the WHO (ICTRP) and the other promoted by the UK National Institute for Health Research. At the moment the only recommendation is not to treat CSDH with steroids on a systematic manner but to use steroids in a case-by-case manner.

Acute Rebleeding and Focal Brain Injury

Acute rebleeding ( Fig. 45.1C-D ) after the evacuation of CSDH, with the development of ASDH, SAH or contusions, is an uncommon situation. SAH after evacuation of CSDH has been described by only two authors. In the first case, Miyazaki et al. attributed the formation of this complication to hypertension and anticoagulation therapy taken by the patient; they also discussed, as mechanism of formation, the rapid shift of the brain after surgery with an overdrainage of subdural space and a hypoperfusion syndrome. This mechanism has also been discussed by Ogasawara et al., who attributed the formation of SAH to a loss of autoregulation of blood vessels with consequent hypertension and cortical hyperemia after reexpansion of the brain.

ICH as a complication of CSDH evacuation is a rare issue that has been described few times in the literature. This type of hematoma is usually ipsilateral to CSH; however, few cases of contralateral hematomas have been described. Pathological explication of this complication remains unclear; several authors believe that overdrainage of subdural fluid and CSF may lead to a rapid expansion of the brain and stretch of vessels with formation of acute hematomas.

This mechanism, even though not validated, could also explain another complication—namely, ASDH after evacuation of CSDH. This hematoma could also be related to a direct trauma during surgery or the ablation of subdural drain, but it remains rare and not very well explained. Spetzler et al. have found a loss of regulation and loss of CO ₂reactivity in the brains of animals with CSDH; this mechanism, though not demonstrated in humans, could be another possible explanation for the formation of ASDH and ICH in patients with CSDH.

Even though the literature remains unclear about the management of postsurgical acute bleeding, treatment should be adapted to the individual patient. Many authors also recommend a slow brain decompression to prevent rapid intracranial changes.

Infections

Infections are a rare complication of chronic subdural hematoma that lead to subdural empyema ( Figs 45.2 and 45.3 ). According to the latest review by Dabdoub et al. there are only 46 cases described in the literature, and the real overall rate of this complication is less than 1% of cases of CSDH. There are no differences in the occurrence of this complication among patients of different sexes or ages; the only factors that seem related are the immunologic state of the patient and comorbidities like diabetes, chronic infections, and chronic hepatobiliary disorders. However, in the 50% of cases described, the source of infection remains unknown. Pathogens involved usually belong to E. Coli, Salmonella, Staphylococcus aureus, and Streptococcus species.