Prognostic Factors and Treatments Efficacy in Spontaneous Spinal Epidural Hematoma

Discussion

SSEH is a rare entity with approximately 1,100 cases reported in the literature by 2021. However, most neurosurgeon or neurologist would have experienced at least 1 of these cases in their careers.⁸ In our case series, the incidence of SSEH was higher in male patients and the age profile showed a bimodal distribution, with peak incidences in the second and sixth decades of life (Figure, A). Twenty-one cases were on anticoagulants in our study. Compared with cases with normal coagulation profile, patient with coagulopathy/anticoagulated most probably will have “prolonged clotting time,” leading to a larger hematoma. Because coagulopathy/anticoagulated status is unlikely to be the direct cause of bleeding, we enrolled patients who were on anticoagulants. Age-hematoma distribution analysis showed that younger age (younger than 50 years) correlated with the cervicothoracic area, while older patients (older than 50 years) showed a bimodal distribution, with peaks at the cervicothoracic and the thoracolumbar area (Figure, C). The possible explanation would be, in both younger and older groups, the posterior internal vertebral venous plexus (IVVP) is particularly prominent at the cervicothoracic area where SSEH frequently occurs.⁹ By contrast, at the thoracolumbar area, the posterior IVVP is more prominent with more advanced age.⁶ Zhang et al. reported positive study findings, that is, spinal epidural arteriovenous fistulas, during the presurgical spinal digital subtraction angiography (DSA) in 15% of SSEH cases (6 of 40 cases).¹⁰ They also reported that, of those with negative DSA findings, 10 cases were found to have abnormal vessels dilations or expansion of the vascular bed during surgical decompression. Thus, the authors concluded that bleeding from the posterior IVVP could be the most likely source leading to SSEH.^11,12

There is no consensus on the best SSEH management approach. Patients with mild clinical conditions or significant recovery were more likely to receive conservative management. Decompressive laminectomy is recommended in patients with severe neurologic dysfunction or clinical deteriorations.¹³ The degree of preoperative neurologic deficit and the time interval between symptoms onset to surgery have been suggested as critical factor predicting patient recovery after treatment.⁴ In our study, every 1 in 3 patients were managed conservatively, which was similar to other studies (23%)¹³ in which 73%–84% of patients could recover completely after conservative management.^13,14

Patients on anticoagulants (warfarin) were found to have a worse outcome (Table 2). This observation is also in line with the findings from the previous studies.⁶ Anticoagulant therapy may contribute to larger hematoma size and poorer outcomes. However, both univariate analysis and multivariable analysis revealed that the use of either anticoagulants or platelet inhibitor in the surgery subgroup was not an independent risk factor for prognosis (Table 3). Patients taking anticoagulants/antiplatelets medications would receive plasma, cryoprecipitate, and platelet transfusion to correct the coagulopathy before the surgery. Previous study suggested that correcting the coagulation function before surgery may stop the progression of hematoma and potentially lead to improved surgical outcomes.³

Thoracic SSEH has been reported to be associated with the worst clinical outcome.^6,8 Similarly, in our study, middle and lower thoracic SSEH had worse prognosis (Table 2). The likely reason may be that there are 3 major arterial supplies to the spinal cord, which are divided into cervicothoracic (C1-T2), midthoracic (T3-T9), and thoracolumbar (T10-L2) branches. The midthoracic area seems the most vulnerable to an ischemic insult.¹⁵ Both univariate analysis and multivariable analysis showed that the lower thoracic spine location was associated with worse outcomes in the surgery group; however, the observed differences were not statistically significant (Table 3).

The severity of neurologic deficit at the time of intervention was the most important prognostic factor. Poor neurologic function on admission has been reported to be associated with the worst prognosis.^6,8,10 The results of our retrospective analysis supported this association (Table 2). It is worth noting that preservation of sphincter function increased the chances of good outcomes compared with those with complete loss of sphincter function (Table 2). In our study, both the univariate and multivariate analyses showed that severe preoperative neurologic deficit (Frankel scale grade A) was an independent predictor of poor outcome after surgical decompression (Table 3).

The development of early neurologic deficits is most likely caused by direct neural compression.¹⁶ The focal mechanical force could cause conduction blocks and damage to the myelin in the spinal cord.⁶ This direct and severe neural compression seems to be responsible for the short progression interval. Besides that direct neural compression, the impairment of the venous drainage of the spinal cord could lead to venous congestion, white matter edema, and axonal swelling.⁶ These secondary circulatory disturbances, likely to be responsible for the longer progress interval, could be relieved by direct surgical decompression or spontaneous hematoma resolution. The univariate analysis demonstrated that the progression interval was a significant prognostic factor in our study (Tables 2 and 3). These patients with a rapid progression are more prone to a poor prognosis. However, multivariate analysis failed to confirm this. One explanation could be the contributing effects of other possible confounding factors included in our regression analysis such as anticoagulants. We also noticed that anticoagulants were not associated with outcome in univariate and multivariate analyses (p = 0.06) in (Table 3).

Groen and van Alphen⁵ demonstrated that preoperative neurologic condition and preoperative time interval were correlated with the outcomes of SSEH. Mukerji and Todd⁴ recently reviewed the literature on the timing and outcome of surgery and concluded that surgery within 12 hours was associated with the best outcome, even in paraplegic patients. Several studies have suggested that early surgical decompression within 12–24 hours is the key to improve patient prognosis.^5,6,17 Our results only partially confirm the literature findings. For example, the operative interval was not always associated with postoperative outcomes. On the other hand, univariate and multivariable analyses showed that preoperative paraplegic time was an independent predictor of outcome after surgical decompression (Table 3). In this regard, the preoperative interval should be defined as the interval between emergences of severe neurologic dysfunction to surgery. As soon as patients manifest neurologic deterioration, surgery should occur at the earliest possible opportunity.

This study included the largest sample size of patients with SSEH ever studied. Adverse prognostic factors for patients with SSEH include thoracic segment, use of anticoagulation, severe neurologic deficits on admission, sphincter dysfunction, and short progression interval. Preoperative neurologic deficit and paraplegia time were strongly correlated with the prognosis in the subset of patients who underwent surgical decompression. Timely surgical decompression should be recommended for patients with moderate to severe neurologic deficits or progressive neurologic deterioration. We believe that our study findings will provide new insights and guidance for neurosurgeons to improve SSEH management.

This study is a retrospective analysis and thus bears the inherent limitations of such studies. Another main limitation was the lack of representativeness of the study cohorts to general population. Because of the rarity of SSEH and the various inclusion and exclusion bias, our data may not represent the general population. Therefore, a prospective, multicenter, controlled, parallel study is needed in the future.