Contemporaneously diagnosed lumbosacral spinal subdural hematoma and cranial subdural hematoma with cerebral contusions following isolated head trauma: a case report and review of the literature

Introduction

Intraspinal hemorrhages are rare, with the majority manifesting as spinal epidural hemorrhages (EDHs). Etiology includes coagulopathies, iatrogenic procedures, and rarely, direct spinal trauma in predisposing conditions such as ankylosing spondylitis. Spinal subdural hematomas (SSDHs) are extremely rare, accounting for 4% of all spinal hemorrhages (1), and can be a rare cause of conus medullary or cauda equina syndrome (2). The exact pathophysiology of SSDH remains unresolved. Most SSDHs are in the lumbosacral spine (3). Concomitant intracranial hemorrhage with SSDH is even rarer (4). A recent review identified 43 cases of concurrent cranial subdural hematoma (CSDH) and SSDH in the current literature, 22 of them posttraumatic (5). Few reports exist on spontaneous SSDH with cranial subarachnoid hemorrhage (SAH) (6-9). However, concurrent SSDH with intracerebral hemorrhage (ICH) is extremely rare, with one case report of spontaneous SSDH with ICH (10) and another case of SSDH occurring after surgical evacuation of traumatic CSDH and cerebral contusions (3).

Here, we reported the first case of concurrent SSDH with CSDH and cerebral contusions following isolated head trauma, whereby all pathologies were contemporaneously diagnosed in magnetic resonance imaging (MRI) of the neuroaxis and completely managed conservatively. Furthermore, we conducted a review of all hitherto published cases of concomitant CSDH and SSDH in literature. Finally, we discussed currently proposed pathomechanisms for SSDH with simultaneous intracranial hemorrhage, management strategies, and prognosis. We present this case in accordance with the CARE reporting checklist (available at https://jss.amegroups.com/article/view/10.21037/jss-24-120/rc).

Case presentation

A previously healthy 19-year-old man presented to our emergency department with transient symptoms of increased intracranial pressure, i.e., cephalgia, nausea, and vomiting, accompanied by persistent lumbar pain with bilateral radiculopathy. He reported sustaining head trauma 1 week prior during a brawl. He explicitly negated additional trauma to the spine. Cranial computed tomography (CT) scan performed immediately after the attack at another institution was normal. Hence, the patient was discharged. Due to the development of the aforementioned symptoms, cranial and lumbar MRI was ordered by his general practitioner.

Initial cranial MRI revealed bitemporal and right frontal cerebral contusions with subacute left temporal and parietooccipital SDHs without mass effect or herniation signs (Figure 1A,1B). Magnetic resonance time-of-flight (MR-TOF) angiography excluded vascular malformations. At the time of presentation, the patient complained of debilitating back and leg pain accompanied by mild headaches without vomiting. A transient hearing impairment in the left ear resolved completely. Examination revealed no neurologic deficit, a solitary right chin bruise, without external bruises of the trunk and spine. Blood workup was normal without coagulopathy.

Figure 1 Cranial MRI axial images, 1 week (A,B), 9 days (C,D), and 3 months (E,F) after isolated head trauma. (A,B) Initial MRI showed bitemporal and right frontal cerebral contusions with subacute left temporal SDH (indicated by red arrows) and parietooccipital SDH, which are bright in both T1 (A) and T2 (B) sequences, without mass effect or herniation signs. (C,D) Follow-up MRI 3 days after initial presentation showed no progressive bleeding of left temporal SDH (indicated by red arrows) in T1 (C) and no progression of cerebral edema in T2 FLAIR (D) sequences. (E,F) Follow-up MRI 3 months after conservative management of intracranial hematomas showed complete resolution of the hematomas in both T1 (E) and T2 (F) sequences. FLAIR, fluid attenuated inversion recovery; MRI, magnetic resonance imaging; SDH, subdural hematoma.

A follow-up cranial MRI 3 days later showed no rebleeding of the intracranial hematomas and no progression of cerebral edema (Figure 1C,1D). A neurosurgical consult recommended conservative management of the traumatic brain injury. Follow-up cranial MRI 3 weeks after discharge revealed a complete resolution of the intracranial hematomas (Figure 1E,1F).

Initial lumbar MRI detected a subacute, lumbosacral SSDH posterior to the L5 vertebral body with moderate mass effect (Figure 2A,2B). A follow-up MRI of the total spine showed no progression of the lumbosacral SSDH (Figure 2C,2D). Considering the stable course of the SSDH, lack of neurologic deficits, and young age, conservative management of the SSDH was favored over surgical treatment with hematoma evacuation via laminectomy. Should the patient develop neurologic symptoms or the SSDH show progression in follow-up MRI, a surgical option was considered a viable alternative in the future. Due to his young age and low-risk profile for cortisone-related complications, high-dose dexamethasone therapy could be safely initiated for 3 days. A case of a similarly young patient with SSDH was recently reported to have favorable clinical outcomes after conservative therapy with methylprednisolone (11). Similarly, our patient developed no complications from steroid therapy. He was discharged from our institution with substantial pain relief and without symptoms of intracranial hypertension. Follow-up spine MRI 3 weeks after discharge demonstrated a complete resolution of the SSDH (Figure 2E,2F). The patient remains pain-free without deficits.

Figure 2 Lumbar MRI images, 1 week (A,B), 9 days (C,D), and 3 months (E,F) after isolated head trauma without spinal trauma. Sagittal images: (A,C,E); axial images: (B,D,F). (A,B) Initial MRI sagittal images showed a subacute, lumbosacral SSDH posterior to the L5 vertebral body with moderate mass effect, which was bright in T1 [(A) right image; (B) lower image] and dark in T2 [(A) left image; (B) upper image] sequences. A positive “inverted Mercedes-Benz sign” in axial sequences (B,D) confirmed the diagnosis. (C,D) Follow-up MRI 3 days after initial presentation showed a stable SSDH, which was now bright in both T1 [(C) right image; (D) lower image] and T2 [(C) left image; (D) upper image] sequences. (E,F) Follow-up MRI 3 months after conservative management of lumbosacral SSDH showed complete resolution of SSDH in both T1 [(E) right image; (F) lower image] and T2 [(E) left image; (F) upper image] sequences. MRI, magnetic resonance imaging; SSDH, spinal subdural hematoma.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Literature review

A literature review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines by searching the PubMed database on 01 August 2024 for case reports and series with concurrent CSDH and SSDH, using the MeSH terms for ‘spinal subdural hematoma’ AND ‘intracranial subdural hematoma’. The search yielded 26 results. In our screening process, we included only cases with contemporaneous diagnosis of CSDH and SSDH within a narrow diagnostic timeframe of ≤48 hours. Journal articles in languages other than English and German were excluded. After screening, 12 cases including our current case were sought for retrieval. We extracted the following data from each case: authors, year of publication, age in years, sex, etiology, history of trauma, symptoms, MRI findings, pathomechanisms suggested by authors, treatment, follow-up time in months, and status at follow-up.

Since 2005, 12 cases of concomitant CSDH and SSDH were published in the literature (12-22), including the current case (Case 12, Table 1). Only one patient was female (15); the majority was overwhelmingly male. The mean age of these patients was 41.5 years (range, 11–70 years); 3 including the current case (25.0%) were ≤20 years old (19,22). In 5 patients (41.7%), anticoagulation (12,15,17) and bleeding disorders (18,22) were identified as etiologies. Cranial trauma was reported in 6 patients (13,15,17,19,20) including ours (50.0%), while the rest had no history of trauma. Headaches were present in 9 cases (66.7%), whereas 10 patients (83.3%) reported lumbago and/or radiculopathy. Both cranial and spinal symptoms were present in 9 patients (66.7%). In 9 cases (66.7%), craniospinal migration of CSDH was suggested as the possible pathomechanism for the coexistence of CSDH and SSDH. Five cases (41.7%) were treated surgically with evacuation of CSDH (14,16-18,20) and 2 cases of SSDH (16.6%) had surgical evacuation (13,15). However, in 5 patients (41.7%) conservative management of both pathologies was chosen, either due to lack of neurologic deficits in a young patient (19,21,22) such as in our case, or due to comorbidities in an older patient (12). In most cases, the prognosis is good regardless of treatment strategy. All 5 patients including ours who were treated conservatively for both CSDH and SSDH showed complete resolution of symptoms and MRI findings at follow-up (12,19,21,22). Only one patient had a surgical complication (persisting CSDH requiring re-craniotomy) (18).

Spinal hemorrhage, a rarity itself, is more likely to be EDH than SDH (1). We considered EDH as a differential diagnosis in our case. However, an interdisciplinary neuroradiological consensus arrived at the diagnosis of SSDH. In the initial MRI (7 days post-head trauma; Figure 2A,2B), the subacute SSDH was hyperintense in T1 and hypointense in T2, which eventually became hyperintense in both T1 and T2 (9 days post-head trauma; Figure 2C,2D). A positive “inverted Mercedes-Benz sign” in axial T1 and T2 sequence (23-25) confirmed the diagnosis (Figure 2B,2D). Other differentials include spinal abscess/empyema and intradural-extramedullary mass. However, lab results and history were negative for inflammatory markers and malignant tumors in our young, afebrile patient.

Simultaneous coexistence of CSDH and SSDH is rare, demonstrated by the 12 cases in our review. 22 cases of concurrent, post-traumatic SSDH and CSDH with a diagnostic timeframe >48 hours were studied in a recent review (5). In most traumatic cases, SSDH was discovered at a later stage after diagnosis of CSDH; or conversely, CSDH was revealed in a much later workup after the discovery of SSDH. To our knowledge, this is the first review of all published cases of contemporaneously diagnosed CSDH and SSDH within a narrow diagnostic timeframe of ≤48 hours. A prospective study of 168 CSDH patients showed only 2 with concomitant lumbar SSDH, suggesting a very low incidence (1.2%) of CSDH patients harboring an occult SSDH (26). A review of 58 traumatic SSDH cases revealed 30 (51.7%) with concurrent CSDH (3). This advocates for lower thresholds for ordering cranial imaging in patients with confirmed traumatic SSDH, even with a negative history of head trauma. In our review, 50.0% of patients with concurrent CSDH and SSDH had no previous cranial trauma.

To our knowledge, coexisting SSDH with CSDH and cerebral contusions have not been previously reported. Porter et al. reported a 41-year-old patient presenting with lumbosacral SSDH 11 days after surgical evacuation of traumatic CSDH with cerebral contusions secondary to head trauma. In their case, SSDH was similarly managed conservatively (3). Our case is the first report of contemporaneous diagnosis of SSDH and CSDH with cerebral contusions in craniospinal MRI, whereby all pathologies were managed conservatively. Since the initial cranial CT excluded intracranial hemorrhages, SSDH and CSDH, in our case, are presumed to have developed in the same timeframe of 1 week. Our case demonstrates that SSDH can occur concurrently with all types of intracranial hemorrhage, not just CSDH.

The exact pathomechanism of SSDH has not been elucidated. Three major theories exist in current literature. The most widely accepted explanation is the gravitational migration of CSDH along the neuroaxis to produce a satellite SSDH inferiorly (3,27,28), with a mean hematoma migration time of 12.5±15.1 days (3). Indeed, two-thirds of the cases reviewed here proposed the craniospinal migration theory as an explanation for coexisting CSDH and SSDH. Both pathologies were diagnosed simultaneously in our case. Currently, predictors for which CSDH will produce a secondary SSDH have remained elusive. An alternative explanation in the literature is the fortuitous coincidence of traumatic CSDH and SSDH rather than a causational relationship between both (20,24,26). This theory does not apply to our case since our patient explicitly denied direct spinal trauma, additionally to confirmed head trauma, and showed no signs of spinal injuries in examination or imaging. A similar case report of a 45-year-old patient who sustained cerebral edema albeit without intracranial hemorrhage after isolated cranial trauma, was found to harbor a SSDH in MRI after developing back pain (29). However, the cases in our review did not explicitly negate a history of spinal trauma. A third theory of bidirectional hematoma migration of SSAH origin is supported by some cases of SSDH with subsequent cranial SAH (CSAH) (6,7).

The current consensus in literature mandates the management of traumatic SSDH according to presence of neurologic deficits. Porter et al. found that 55.2% of traumatic SSDHs were surgically evacuated due to the presence of neurologic deficits (3,4,24,30). In our review, only 2 SSDHs (16.7%) were managed surgically (13,15). Both cases were in their mid-50s with extensive thoracolumbar SSDH involving >6 vertebral segments; one patient presented with conus medullary syndrome (15). Porter et al. demonstrated that patients without deficits managed conservatively had favorable outcomes (3). Our review corroborated these findings, where all 5 patients managed completely conservatively (12,19,21,22), including ours, displayed complete resolution of symptoms and MRI findings at follow-up. Back pain and radiculopathy portend a good prognosis (3).

Most SSDHs are located posterolaterally (31). In our case, SSDH was anterior to the dura and posterior to the L5 vertebral body, thus producing indentation of the dura and asymptomatic compression of cauda fibers. The latter was similarly displayed by cases in the review which were managed surgically (13,15). Nevertheless, our patient’s hitherto optimal outcome at the last follow-up confirms that conservative management is a safe and effective alternative to surgical evacuation in patients with similar features in MRI.

In our review, we demonstrated that CSDH and SSDH can occur simultaneously, i.e., within a diagnostic timeframe of ≤48 hours. Despite the small sample size, recommendations for diagnostic and treatment management of these concurrent pathologies could be derived from the review. Due to a relatively high incidence of occult CSDH in confirmed traumatic SSDH cases (51.7%) (3) and 50% of patients in our review with negative history of cranial trauma, diagnosis of SSDH in spinal MRI should raise suspicion for a concurrent CSDH even in the absence of head trauma. We recommend additional cranial imaging to rule out CSDH. Conversely, there is a relatively low incidence of CSDH patients harboring occult SSDH (1.2%) (26), therefore it is not recommended to routinely rule out SSDH with additional imaging. However, CSDH patients with accompanying spinal symptoms should undergo spinal MRI to detect concurrent SSDH, even in cases of isolated cranial trauma.

CSDH patients in our review who were treated surgically were older (age range, 40–70 years) with risk factors for rebleeding e.g., anticoagulation and coagulopathy (18,20). Conservative management of CSDH is reasonable option in younger patients without risk factors. Surgical evacuation of SSDH is recommended in older patients with extensive involvement of >6 vertebral segments and compression of neural structures, as well as in patients with severe neurologic deficits. Younger patients without neurologic deficits can be effectively treated with conservative management, e.g., with cortisone therapy in patients with low-risk profiles. Other conservative measures reported previously include hematoma aspiration via lumbar puncture (14,20).

Conclusions

We presented the first case of contemporaneously diagnosed SSDH and CSDH with cerebral contusions after head trauma without spinal trauma. Our case demonstrates that SSDH can occur after isolated head trauma with all types of intracranial hemorrhage (SDH, ICH, contusions). Furthermore, we conducted the first literature review of all cases reporting concurrent CSDH and SSDH, which were both diagnosed within a narrow timeframe of ≤48 hours. We advocate for lower thresholds for ordering cranial imaging upon MRI evidence of SSDH after spinal trauma to facilitate swift detection of occult CSDH, even in the absence of cranial trauma or symptoms. Conversely, CSDH patients may harbor occult SSDH, albeit at a lower incidence. Thus, the development of back pain with or without neurological deficits following isolated head trauma should also prompt spinal imaging. Our case report and review reinforce the effectiveness of conservative management in SSDH patients with only back pain and radiculopathy without deficits, especially in younger patients. Older patients with extensive SSDH compressing neural structures and causing severe neurologic deficits should be treated surgically with hematoma evacuation. Regardless of management strategies chosen, the prognosis of both CSDH and SSDH is generally good with very low complication rates.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://jss.amegroups.com/article/view/10.21037/jss-24-120/rc

Peer Review File: Available at https://jss.amegroups.com/article/view/10.21037/jss-24-120/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jss.amegroups.com/article/view/10.21037/jss-24-120/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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