CSDH is one of the most commonly treated neurosurgical disorders and BHD is a universal surgical treatment.[11, 18, 27] The rate of CSDH recurrence following BHD is 4–38% and the complications rate is 0–38%.[6-12, 24, 26] In this study, we found the CSDH recurrence rate after BDH was 13.4% and the complication rate was 27.2%. Of the 122 patients with complications, 23 had postoperative AIH (5.1% incidence). Pang et al. similarly reported an incidence of postoperative AIH of 4.57%. According to the literature, the mortality rate due to CSDH is 1.8–32%, however, in this study, only one patient died of respiratory failure, giving a lower mortality rate of 0.2%.[6, 23] Comparing our results with previous studies, our definition of CSDH, postoperative recurrence of CSDH and postoperative AIH are in accordance with medical norms and logic.
CSDHs are usually unilateral, but do present as bilateral in ~9.2–34.9% of cases.[5, 28-30] However, not all patients with bilateral CSDH warrant evacuation of both sides at initial presentation. The major determinants of unilateral or bilateral evacuation are preoperative maximal thickness, the degree of midline shift, and lateralized clinical symptoms, followed by surgical treatment of only the largest or the symptomatic hematoma, leaving the other hematoma non-operated. In our study, 154 patients (34.4%) had bilateral CSDH. Fifty-four (12.1%) had unilateral evacuation and 100 (22.3%) were evacuated bilaterally. Previous studies have shown that simultaneous bilateral decompression in bilateral CSDH reduces complications and the rate of CSDH recurrence, however, others have not corroborated this result.[31-33] In our study, there was no significant difference between the rate of CSDH recurrence and incidence of AIH following unilateral or bilateral evacuation in bilateral CSDH.
The recurrence rate in unilateral CSDH is lower than that of bilateral CSDH, making bilateral hematoma a risk factor for CSDH recurrence.[16, 19] This could be due to poor brain re-expansion in bilateral CSDH compared to unilateral CSDH, which may result in a brain parenchymal shift, tearing of the blood vessels, postoperative pneumocephalus and cerebrospinal ﬂuid accumulation in the hematoma cavity, leading to a higher recurrence rate.[19, 34, 35] Another theory is that patients with bilateral CSDH tend to have a history of brain atrophy, which leads to poor re-expansion, resulting in a higher recurrence rate.[19, 35] In our study, bilateral hematoma was found to be a risk factor for postoperative recurrence of CSDH, but was not a risk factor for postoperative AIH. Whether the brain re-expansion theory or the brain atrophy theory were correct will require time to accumulate results. In our study, the mean time interval (4.7±2.9 days) between initial surgery and postoperative AIH was significantly lower than the mean time interval (40.8±28.3 days) between initial surgery and postoperative recurrence.
Some studies have reported that male sex is an independent risk factor of CSDH recurrence, and that males likely have more trauma and more frequent complications than females. However, other studies have suggested that gender is not associated with CSDH recurrence.[13, 36] In our study, 295 patients had a history of trauma, including 233 males and 62 females. According to multivariate logistic regression analysis, there was no significant correlation between gender and CSDH recurrence. To date, no literature has reported the relationship between gender and postoperative AIH. We found that gender was not significantly associated with postoperative AIH.
The clinical presentation of CSDH varies from asymptomatic to headache, limb weakness, incontinence, etc. According to our study, preoperative headache is an independent risk factor for postoperative AIH. When CSDH presents as a clinical manifestation of headache, it indicates a higher intracranial pressure and a secondary cerebral blood flow reduction in the deep cerebral regions, causing blood vessels to spasm and increasing the risk of vascular accidents. Thus, when blood flow in the brain changes or intracranial pressure changes significantly in a short period of time, blood vessels rupture, resulting in bleeding.
Many studies suggest that preoperative hematoma density is associated with CSDH recurrence, and hyperdense hematoma is an independent risk factor for CSDH recurrence.[13, 38] In present study, although nearly 1/3 of the patients had hyperdense imaging findings, according to our clinical experience and our definition of CSDH, neurosurgeons evaluated patients with subdural hematoma no matter what the density of subdural hematoma on imaging, once they were able to be treated with BHD, these patients could be managed as patients with CSDH. In our study, hyperdense hematoma were more prone to CSDH recurrence than mixed density (OR, 0.433; 95%CI, 0.229–0.818; P = 0.010, hyperdense as reference). The relationship between hematoma density and postoperative AIH has not been reported in the literature. In our study, hematoma density was not significantly associated with postoperative AIH. We suspect that when hyperdense hematoma are compared with the other three types of hematoma density, repeated microhemorrhages from the immature capillary network in the outer membrane take place and accumulate over time, causing CSDH recurrence.
Preoperative hematoma thickness has been reported as an independent risk factor for CSDH recurrence. It is thought that hematoma thickness has an increased tendency to recur because the subdural space is larger than a small lesion postoperatively.[7, 36] As hematoma thickness is related to many factors, such as age, midline shift and brain atrophy, it may not be a useful predictor of CSDH recurrence and postoperative AIH. However, other studies have shown no significant relationship between hematoma thickness and CSDH recurrence,[13, 39] and the relationship between hematoma thickness and postoperative AIH has not been reported. In our study, the hematoma thickness of 20mm was selected as a threshold, compared with the trauma subdural hematoma guidelines threshold of 10mm, there were two reasons. First, a part of the patients were non-traumatic chronic subdural hematomas; second, according to our clinical experience, when the thickness of hematoma is between 10mm and 20mm, some patients had no obvious clinical manifestations and did not require surgical treatment. According to the results, there was no significant relationship between hematoma thickness and CSDH recurrence or postoperative AIH.
Our results showed that anticoagulant drug use is an independent risk factor for CSDH recurrence. Antiplatelet drugs did not increase the CSDH recurrence rate following BHD. Similarly, a recent systematic study showed that anticoagulant drugs increased re-bleeding on the operation side of CSDH, but antiplatelet therapy did not. However, this result is controversial as in other studies, antiplatelets or anticoagulants were not associated with CSDH recurrence.[16, 36, 41] The authors speculated that the reason for this finding may be that the patients were not adequately anticoagulated, especially in the non-recurrence group. At present, only one study has reported that anticoagulants or antiplatelet drugs do not increase the incidence of postoperative AIH. Similar to our results, we suspect that it may be the result offset caused by insufficient sample size. Therefore, a large sample clinical trial is necessary to verify this result.
Atorvastatin is another management option, which may be used alone or in conjunction with surgery. Several studies have shown that CSDH is caused by impaired angiogenesis in the neomembrane and localized inflammation, and that atorvastatin improves angiogenesis and reduces the inflammatory response.[42, 43] A randomized control study showed that the oral administration of atorvastatin is safe and effective in treating CSDH, and promotes the resolution of hematoma. A prospective study showed that atorvastatin administration may decrease the risks of CSDH recurrence. However, in our study, atorvastatin did not reduce the rate of CSDH recurrence, nor did it reduce the incidence of postoperative AIH. We suspect that different research methods may lead to varying results.
In our study, intraoperative saline irrigation was based on the surgeon’s preference. Some studies have shown that intraoperative saline irrigation of the hematoma cavity does not improve the incidence of postoperative AIH and CSDH recurrence.[25, 46] According to our results, intraoperative irrigation does not reduce the risk of CSDH recurrence, however, it does reduce the incidence of postoperative AIH. We speculate that BHD for CSDH without irrigation significantly reduces intracranial pressure for a short period of time. The abrupt decrease in intracranial pressure may cause further damage to the intracranial blood vessels and lead to acute intracranial bleeding.
Our study had some limitations. First, our study is a retrospective design, which usually produces a risk of bias. Based on our data and personal communication with neurosurgeons in each participating department, neurosurgeons not only choose the surgical method based on symptoms and hematoma size, but also according to their preferences. For example, the use of a single burr hole, the 1.5-2cm craniotomy and whether to irrigate is based on neurosurgeon preference. However, according to literature reports and our results, the selection of these surgical methods did not result in significant differences postoperative complications in total and recurrence rates. Second, in the multivariate model, although ideally more stringent criteria for variable inclusion in the model would be applied in lieu of p<0.1. However, it may lead to too few variables and too many confounding factors, which will have a greater impact on the results.