Surgical Management of Concurrent Cranial and Spinal Subdural Hematomas Causing Confusion and Lower-Extremity Weakness: A Case Report and Literature Review

Introduction

Cranial subdural hematomas (CSDH) overlying the brain are one of the most common pathologies managed by neurosurgeons. Chronic CSDH specifically have an incidence of 1.7–20.6 per 100 000 persons per year and occur more commonly in older adults [1]. Although many can be managed conservatively, dissipating slowly over time without evacuation, burr hole craniotomy is a mainstay of guideline treatment, with 10–20% recurrence rates [1], with adjunctive middle meningeal artery embolization as a safe method for reducing recurrence rates [2]. Spinal subdural hematomas (SSDH) are significantly less common and have fewer standardized guidelines for intervention [3–5]. Similar to CSDH, SSDH can arise from trauma, coagulopathy, vascular anomalies, or iatrogenic causes. In cases with concurrent cranial involvement, spinal subdural hematomas can result from gravity-dependent craniocaudal migration over time [6–8]. The principles of surgical management, however, remain the same. SSDH, whether acute or chronic, are typically managed conservatively unless they are large, fail to resolve, or cause neurologic deficits. We present the case of a man with a rare disease process in which both cranial and spinal subdural hematomas were discovered simultaneously without a clear history of trauma, malignancy, or hematologic etiology. Less than 15 cases of true concurrent cranial and spinal subdural hematomas have been reported in the last 2 decades, and there is wide variation in the treatments prescribed. This report describes the case of a 40-year-old man presenting with confusion and weakness of the lower limbs due to concurrent intracranial and spinal hematomas. We discuss surgical management of these 2 symptomatic hemorrhages, as well as reasonable alternatives, why they were not chosen, possible etiologies, and other management approaches described in the literature for similar situations.

Case Report

A 40-year-old man with a history of uncontrolled acquired immunodeficiency syndrome (AIDS) (CD4 count = 4), hepatitis C, ongoing substance use disorder (methamphetamines, cocaine, phencyclidine), prior exploratory laparotomy for penetrating abdominal injury, and deep vein thrombosis (DVT) presented to our hospital after 1 week of progressive low back pain, radiating to the upper back and bilateral posterior lower extremities, resulting in ambulatory difficulty. He also reported subacute onset of bowel and bladder incontinence during this same time frame. He denied recent trauma or falls, and was not taking any anticoagulation at the time despite a history of DVT. A neurologic exam demonstrated proximal symmetric lower-extremity weakness. Initial evaluation was limited by agitation, prompting a non-contrasted CT scan of his head in addition to lumbar spine imaging. CT head demonstrated a large 2.0-cm holohemispheric chronic CSDH causing a 1.6-cm of midline shift (Figure 1A, 1B). MRI of the lumbar spine showed a significant SSDH from L2 to S1, causing severe compression of the cauda equina, with dentate ligaments and dorsal septum separating subdural space in the classic “inverted Mercedes-Benz sign” (Figures 2A, 2B, 3). The patient elected to leave the hospital after initial evaluation and returned the following day, undergoing tandem surgery within 72 h of initial presentation.

He underwent a right craniotomy for subdural hematoma evacuation, immediately followed by same-day L2–5 laminectomy for subdural hematoma evacuation. Both hemorrhages were dark and liquid, indicating their chronic nature. Evacuation of the spinal subdural hematoma revealed the intact arachnoid layer underneath, which quickly re-expanded. The spinal dura was closed primarily with Prolene sutures. Cranial and lumbar surgical drains were left in place. The patient tolerated both operations well. Postoperative imaging was obtained, showing resolution of the CSDH (Figure 4) and SSDH (Figure 5A, 5B), and appropriate re-expansion of the brain and cauda equina (Figures 4, 5).

He remained in the intensive care unit, briefly requiring pressors, with concern for possible meningitis. A lumbar puncture above the operative levels was performed under fluoroscopy, with cerebrospinal fluid cultures showing no growth. Blood cultures and laboratory test results for opportunistic infections were negative as well. After 2 days without fevers and with final negative culture results, the patient was discharged to a rehabilitation facility without clinical complications.

Discussion

The purpose of this report was to highlight the safety, feasibility, and time-sensitive management of concurrent cranial and spinal SDH (CSDH and SDH) in the acute setting. Spinal subdural hematomas are rare, and concurrent cranial and spinal SDH are even less common, occurring in 1–2% of patients with cranial SDH [3–5]. SSDH, like its cranial counterpart, can be acute, subacute, or chronic depending on how quickly it is discovered. Many are traumatic in nature, often preceded by ground-level falls or intentional assault [6–9]. Others are iatrogenic, often from administration of spinal anesthesia via epidural injections [10–12]. Coagulopathies, both inherited and medication-related, are yet another large contributor to spontaneous bleeding into the subdural compartment of the spine [13–15]. Even COVID-19 coagulopathy has been a suggested diathesis for unprovoked SSDH on multiple occasions when laboratory test results and history were unrevealing [16,17]. The remaining 30–40% of SSDH are idiopathic, with no clear etiology despite a thorough workup [18,19].

Our patient had an idiopathic SSDH with concurrent CSDH, both symptomatic and facilitating their simultaneous diagnosis. In other reported cases, one hemorrhage may be reported days to weeks after the other, sometimes necessitating staged interventions, as one subdural presents itself only after treatment of the other is completed [8,9,20]. A recent review of concurrent CSDH and SSDH cases excluded these reports, including only those in which the bleeds are diagnosed within 48 h of each other, to ensure they are truly simultaneous [7]. Our patient was diagnosed with CSDH and SSDH on the same day with head CT and lumbar MRI, then underwent tandem surgical intervention within 72 h after initial presentation.

Although numerous cases of concurrent CSDH and SSDH have been reported, definitive evidence for the underlying mechanism remains limited [4–7]. Proposed mechanisms generally fall into 2 categories: migration and simultaneous insult. Migration theory posits that a subdural hematoma forms in 1 compartment, typically cranial, and tracks caudally within the subdural space. In contrast, simultaneous insult theory suggests that both cranial and spinal SDH arise spontaneously in their respective compartments. In this example, gravity favors a cranial-to-caudal direction. The simultaneous insult theory states that the pathologies are truly concurrent in that they occurred in 2 different locations via the same mechanism. For example, imagine a situation in which someone is struck on the head and the lower back during an assault, tearing bridging veins of the brain and disrupting those of the spinal cord. Alternatively, a severe coagulopathy has somehow led to bleeding from the brain and spine in the same instance. This obviates the need for migration. Both theories potentiate simultaneous CSDH and SSDH, but by different means. In an attempt to differentiate between the 2, a recent publication described the use of histology for this purpose. Our patient had severe dementia, and samples of both CSDH and SSDH were sent to pathology to study the staging of membranous formation in each [21]. If the hematomas were in the same stage of coagulation, encapsulation, or dissolution, then that might suggest simultaneous insult. On the contrary, if the CSDH was further along in its progression than the SSDH sample, this could suggest craniospinal migration of blood. Their results made the former scenario more likely.

Treatment of concomitant CSDH and SSDH lacks standardization due to its low incidence. Many are treated conservatively, whereas others are treated with a hybrid approach. One may be evacuated surgically and the other non-surgically, depending on the etiology, level of neurologic deficit, and chronicity of the hemorrhage [7,18,22,23]. Craniotomy or burr hole evacuation are options for chronic CSDH, whereas craniotomy or craniectomy are necessary for acute SDH. When surgical intervention is warranted for SSDH, lumbar puncture and laminectomy have been utilized, depending on the extent and chronicity of the hemorrhage, as well as the urgency demanded by the clinical presentation. Our patient had a CSDH that met radiographic criteria for evacuation, and his SSDH was compressing his cauda equina to the point of unrelenting back and radicular pain, bilateral leg weakness, and urinary symptoms. As such, he underwent craniotomy and laminectomy for removal of both compressive hemorrhages. Burr holes or twist drill craniotomy with subdural drain placement were considered as reasonable alternatives for a chronic CSDH, but these options limit the ability to address membrane formation, a common component of chronic CSDH. Studies also show similar outcomes at 6 months across methods [24].

Laminectomy was chosen over lumbar puncture and drainage to maximize decompression, maximize the extent of evacuation, directly visualize any unforeseen SSDH etiology, and prevent inadvertent introduction of blood into the subarachnoid space. An L2–5 decompressive laminectomy was performed without fusion. The possibility of needing future operations including posterior spinal fusion was discussed with the patient preoperatively. However, given his young age and good bone quality, laminectomy alone was deemed sufficient with the understanding of the risk of post-laminectomy syndrome. This approach aligns with literature supporting decompressive laminectomy alone in patients with progressive neurologic decline, as spinal instability is uncommon in the absence of preexisting instability or prior resection [25].

Of the 12 truly concurrent CSDH and SSDH cases reported in the last 2 decades, excluding the present case, only 2 required operative intervention for both [7]. This case report contributes to the limited but growing body of evidence supporting urgent dual decompression as a safe and effective approach in select patient populations.

Conclusions

We present a rare case of concurrent cranial and spinal subdural hematomas, demonstrating the safety and feasibility of urgent dual decompression in the setting of rapidly declining neurological status. Concurrent SDH are usually caused by simultaneous trauma or craniocaudal migration; in this case, migration was the likely mechanism. Early and aggressive surgical management of both lesions can lead to rapid neurologic and radiographic improvement, supporting dual surgical intervention as a viable option in select patients despite limited guidelines. Of the 12 cases of concomitant cranial and spinal SDH reported in the last 20 years, this is the third in which both hematomas were evacuated, and the first in which craniotomy and laminectomy were successfully performed in tandem.