Our case represents a classic presentation of DPOSEH with initially favorable recovery followed by delayed neurological deterioration. Our patient exhibited acute neurological decline on postoperative day 5, featuring deep back pain at the incision site, new-onset flaccid paraparesis (muscle strength ∼1/5), saddle anesthesia, and bowel/bladder dysfunction. This constellation of symptoms constitutes the characteristic triad of cauda equina compression (10), with onset beyond 72 h confirming its delayed nature. MRI confirmed the diagnosis, revealing a hyperintense epidural mass from L4 to L5 causing significant compression on fat-suppressed T2-weighted imaging. Surgical exploration directly corroborated the MRI findings. The procedure revealed the presence of several substantial compressive clots within the epidural space.

The risk of bleeding in MISS is often underestimated compared to open procedures. While extensive decompressions and instrumented fusions are traditionally considered to predispose to epidural bleeding due to a larger raw surface area and greater venous disruption (10), data paradoxically indicate a higher incidence of symptomatic POSEH following MISS (11–14). A meta-analysis found the pooled incidence to be approximately five times higher with minimally invasive approaches (∼1.94%) than with traditional open surgeries (∼0.42%) (11). Considering the characteristics of OSE, a plausible explanation for this paradox is that continuous irrigation and limited visualization make minute bleeding points difficult to detect. The most likely scenario is that a small venous bleed persisted postoperatively at a very slow rate. A tiny laceration or oozing point in the epidural venous plexus might have been present. Over several days, this slow accumulation of blood could form a substantial hematoma (15).

Inadequate postoperative drainage is a possible contributing factor to the delayed hematoma in this case. Insufficient drainage is a recognized risk factor for hematoma formation, as unevacuated residual bleeding can accumulate within the closed surgical space and eventually form a significant hematoma (16). For reference, the average drain output after single-level discectomy is approximately 72 mL over three days (17). Our patient's output of 25 mL on the first postoperative day was slightly below this average and ceased completely by day 2, which does not preclude the possibility of inadequate postoperative drainage. Interestingly, the role of surgical drains in prevention remains debated, some studies associate premature removal or omission of drains in extensive surgeries with a higher risk of hematoma (18–20), while others find their use does not significantly reduce the incidence (21, 22). In practice, many surgeons leave a drain for 24–48 h in most cases and ensure it remains functional. The drain should not be removed too early if output is significant.

In the present case, the patient's age of 69 years is a likely contributing factor to the bleeding. Advanced age, typically defined as over 60 years, is another significant risk factor (23). Age-related anatomical and physiological changes, such as reduced epidural space compliance, spinal stenosis, and a higher incidence of comorbidities like hypertension, can all promote bleeding.

Another possible contributing factor involves the patient's early ambulation and constipation, both of which could induce a Valsalva maneuver and increase intra-abdominal pressure. This is a potential risk factor because the valveless, thin-walled epidural venous plexus is highly sensitive to pressure fluctuations (24). A sudden rise in intra-abdominal or intrathoracic pressure can transmit directly into this plexus, potentially rupturing fragile veins or dislodging an initial thrombus, leading to renewed bleeding and hematoma enlargement even days after surgery.

Alternatively, a venous congestion vicious cycle may have contributed. The established epidural hematoma compresses the venous plexus, impeding venous outflow. The resulting venous congestion raises local venous pressure further in a vicious cycle, promoting more bleeding into the epidural space. Epidural veins are thin-walled and bleed easily when distended, making continued or intermittent bleeding around the clot possible, which rapidly enlarges the hematoma (25).

The timing of emergent surgical decompression is critical for optimizing neurological outcomes. In this case, the unavoidable delays from analgesic observation, urgent MRI confirmation, and preoperative consent discussions contributed to a postponed intervention, which is a significant factor in the patient's residual neurogenic bladder and moderate lower limb weakness. Earlier decompression is associated with improved neurological recovery (26, 27), with the ideal “golden window” being within 6 h of symptom onset to offer the best chance for complete functional restoration (8). One study found that patients decompressed within 6 h of deficit onset improved by an average of 2 Frankel grades, compared to only ∼1 grade for those decompressed later (7). Conversely, full recovery is rare after 72 h of ongoing compression (28). Therefore, decompression should occur as soon as humanly possible once the diagnosis is made.

By the time decompression was performed, the cauda equina had likely been under pressure for several hours, with overt sphincter dysfunction already present, potentially leading to irreversible axonal degeneration or neuronal cell death (16). In patients with postoperative spinal epidural hematomas, those with milder deficits often recover fully, whereas those presenting with complete paralysis or loss of sphincter function have a higher likelihood of permanent deficit (9, 15). One study reported that among patients with delayed spinal epidural hematomas, some had persistent neurological deficits postoperatively; in their series, 2 of 7 patients did not fully recover (15). Similarly, a comparative study documented a few cases with “poor” neurological outcome despite hematoma evacuation (9). These data indicate that the extensive neural damage already present at the time of intervention limits the potential for complete functional recovery.

Additionally, one study suggests a potential reperfusion mechanism underlying this process (15). Following hematoma evacuation, reperfusion may paradoxically induce further inflammation or free-radical damage, which compounds the initial metabolic insult and explains incomplete neurological recovery despite surgical decompression.

Patient-related factors significantly influence the risk of postoperative spinal epidural hematoma (POSEH). Major risk factors include coagulation disorders or anticoagulation therapy (reported in approximately 44% of cases (10, 28). Furthermore, postoperative hypertension is a well-recognized risk factor, with studies showing an association between acute blood pressure spikes and hematoma formation (29, 30). Other comorbidities, including hepatic or renal dysfunction, chronic alcohol use, and hematologic disorders such as thrombocytopenia, can further increase the risk (26, 29, 30). Some evidence also suggests that diabetes mellitus and obesity may be associated with a higher incidence of POSEH, possibly due to more extensive degenerative disease and altered healing processes (30).

Surgical factors also contribute to the risk of POSEH. Larger and more invasive procedures inherently carry a higher risk due to greater tissue dissection and longer operative duration, which can lead to increased blood loss and more opportunity for bleeding to accumulate. One study identified operating on more than five spinal levels and intraoperative blood loss exceeding 1 L as significant risk factors for epidural hematoma (23). Prior surgery at the same level is also considered a predisposing condition, as epidural scar tissue may reduce the space available for tamponade and increase vascular fragility during dissection (28). Additionally, incidental durotomy with cerebrospinal fluid (CSF) leakage is a recognized risk factor in some series (16). A CSF leak can lower intrathecal pressure, potentially leading to intracranial hypotension and engorgement of the epidural veins, thereby promoting bleeding.

It is noteworthy that while a clear link to the aforementioned risk factors was not established in the present case, the literature unequivocally confirms their existence. These factors remain essential considerations for surgeons and warrant vigilant clinical awareness.

The presence of a symptomatic POSEH is a surgical emergency. Urgent surgical decompression usually involves reopening the prior incision, performing a laminectomy, or expanding the existing one if needed, and evacuating the clot to relieve pressure on the neural elements. Any active bleeding sources are cauterized or controlled, and the wound is thoroughly hemostatic before reclosure.

There are several reports of conservative management. The administration of high-dose corticosteroids represents a controversial non-surgical option in the management of spinal epidural hematomas. The consensus is that this is rare and only appropriate in highly selected cases. Ghaly and Cuenca reported rapid symptomatic improvement after intravenous methylprednisolone in cervical and thoracic cases, respectively (31, 32). Lin et al. (33) documented one successful and one failed dexamethasone trial in traumatic cervical hematomas, underscoring the unpredictability of this approach. Importantly, non-operative management is only feasible when neurological deficits are minimal and stable. However, given that our patient presented with significant neurological deficits, emergent surgical intervention was the only reasonable course of action.