# Spinal Subarachnoid Hematoma After Spinal Anesthesia: A Case Report and Literature-Aligned Review

## TL;DR

A rare spinal subarachnoid hematoma case highlights diagnostic challenges and the urgency of treatment after spinal anesthesia.

## Contribution

This case report clarifies the clinical and diagnostic nuances of spinal subarachnoid hematoma following spinal anesthesia.

## Key findings

- MRI limitations in differentiating hematoma compartments were confirmed during surgery.
- Neurological deficits persisted despite timely decompression and guideline-compliant care.
- SSH likely requires both significant bleeding and restricted cerebrospinal fluid circulation for clot formation.

## Abstract

Spinal subarachnoid hematoma (SSH) is an infrequent but potentially devastating complication of spinal anesthesia (SA). Diagnosis may be challenging due to early nonspecific symptoms and the limited ability of magnetic resonance imaging (MRI) to reliably differentiate subarachnoid from subdural or epidural bleeding, making timely recognition critical. We report a 72‑year‑old woman who underwent uneventful SA for orthopedic surgery and initially recovered without complications. On postoperative day 2, she developed acute dorsolumbar pain progressing rapidly to complete bilateral lower‑limb paralysis and hypoesthesia below T12. MRI suggested a large posterior epidural hematoma extending from T9 to L2 with an inferior component interpreted as a subdural hematoma at L3-L4. Pharmacologic thromboprophylaxis had been initiated 24 hours after surgery in accordance with current European Society of Anaesthesiology and Intensive Care (ESAIC)/European Society of Regional Anaesthesia (ESRA) guidelines.

Urgent surgical decompression was performed approximately six hours after symptom onset. Intraoperatively, however, the hematoma was identified as an extensive SSH from T10 to L2, confirming a diagnosis that MRI had been unable to establish. A T10-L2 laminectomy with evacuation of the hematoma was completed successfully. Despite prompt recognition, guideline‑compliant anticoagulation timing, and rapid surgical intervention, the patient developed permanent neurological deficits.

This case illustrates how SSH likely requires the coexistence of substantial bleeding and anatomical conditions that restrict cerebrospinal fluid circulation, enabling clot formation within the subarachnoid space. Typical clinical presentation includes acute back pain followed by rapidly progressive motor, sensory, and sphincter dysfunction. Prognosis is strongly influenced by the severity of initial neurological impairment and the urgency of decompression, with optimal outcomes associated with surgery performed within 6-12 hours of deficit onset.

Given its rarity and potential for catastrophic outcomes even with protocol‑driven care, SSH must remain an important differential diagnosis in patients presenting with neurological deterioration after SA. This case reinforces the need for vigilant postoperative monitoring, immediate imaging when red‑flag symptoms arise, awareness of MRI limitations in compartmental differentiation, and timely multidisciplinary intervention.