Spinal subarachnoid hematoma following lumbar puncture in a patient without coagulopathy: a case report

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Kosin Med J. 2025;40(2):145-149

Publication date (electronic) : 2025 June 19

doi : https://doi.org/10.7180/kmj.25.110

Kyung Ryeol Lee

Department of Radiology, Jeju National University College of Medicine, Jeju, Korea

Corresponding Author: Kyung Ryeol Lee, MD Department of Radiology, Jeju National University College of Medicine, 102 Jejudaehang-ro, Jeju 63243, Korea Tel: +82-64-717-1373 Fax: +82-64-717-1377 Email: we1977@jejunu.ac.kr

Received 2025 April 25; Revised 2025 June 8; Accepted 2025 June 11.

Abstract

Introduction

Spinal subarachnoid hematoma (SSAH) is a rare complication of lumbar puncture (LP), attributed to blood dilution by the cerebrospinal fluid (CSF), which typically prevents clot formation [1]. Consequently, SSAH is uncommon in the absence of vascular malformation or coagulopathy [2,3]. This case report examines the clinical presentation, progression, diagnosis via magnetic resonance imaging (MRI) and treatment of SSAH in a patient without vascular anomalies or coagulopathy.

Case

A 41-year-old male patient underwent perianal abscess surgery under spinal anesthesia and subsequently developed severe headache, prompting him to visit an external hospital. A second LP was performed for CSF analysis, revealing bloody CSF with 11 white blood cells (WBC)/μL and 9,000 red blood cells (RBC)/mm³. There is no record of the exact level at which the LP was performed at the outside hospital, but as it was a blind LP, it is presumed to have been at the L3–4 or L4–5 level. Pain management with nonsteroidal anti-inflammatory drugs and morphine was initiated, and he was transferred to our institution for further evaluation. Upon hospital arrival, the patient reported persistent headache and neck stiffness, with low-grade fever, but no abnormal neurologic signs, sensory deficits, or motor impairments.

CSF analysis at our institution showed bloody CSF with an opening pressure of 31 mmH₂O, protein of 114 mg/dL, glucose of 31 mg/dL, 150 WBC/μL, and 26,000 RBC/mm³. Suspecting bacterial meningitis based on the clinical symptoms and CSF findings, the neurology team initiated treatment with steroids and antibiotics (dexamethasone, ceftriaxone, and vancomycin). However, persistent headache and new-onset back pain prompted brain and whole spine MRI. Brain MRI findings were normal, but spinal MRI revealed a subarachnoid hematoma (SAH) filling the thecal sac from L3 to S1, displacing the cauda equina. The hematoma exhibited high signal intensity on T1-weighted imaging and low signal intensity on T2-weighted imaging in both axial and sagittal images, consistent with an early subacute hematoma (Fig. 1). Its intrathecal location within the CSF-filled thecal sac distinguishes it from epidural hematomas (EDHs) (extradural location) and subdural hematomas (SDHs) (between dura and arachnoid), highlighting the importance of precise MRI localization for diagnosis and management. Blood tests performed upon admission revealed a platelet count of 311×10³/μL, a prothrombin time of 12.8 seconds, and an international normalized ratio of 1.04, all of which were within normal limits. Additionally, there was no history of anticoagulant use. The patient continued the previous treatment regimen, and the fever was resolved. On hospitalization day 11, follow-up CSF analysis showed xanthochromic CSF (indicative of subarachnoid hemorrhage) with a pressure of 140 mmH₂O, protein of 98 mg/dL, glucose of 21 mg/dL, 104 WBC/μL, and 30 RBC/mm³. Consultation with infectious disease specialists revealed no causative organism in CSF culture, suggesting viral or other nonbacterial meningitis. Antibiotics were discontinued, and observation was recommended.

Fig. 1.

Sagittal T1-weighted (A) and T2-weighted (B) images of the lumbar spine, and axial T1-weighted (C) and T2-weighted (D) images of the lumbar spine show early subacute subarachnoid hematoma. Axial T1- and T2-weighted images (C, D) obtained at the L5 vertebral level demonstrate a subarachnoid hematoma filling the subarachnoid space, resulting in displacement of the cauda equina (white arrow) to the periphery. Epidural fat signal (yellow arrow) and dural demarcation (red arrow) are preserved.

Despite persistent headache, serum C-reactive protein levels normalized, and CSF parameters improved, leading to discharge with outpatient follow-up. After 1 month, the patient reported resolution of headache and back pain, and MRI confirmed complete resolution of the SSAH (Fig. 2).

Fig. 2.

Sagittal T1-weighted (A) and T2-weighted (B) images of the lumbar spine obtained approximately 1 month after conservative management show resolution of the subarachnoid hematoma.

Discussion

Among spinal hematomas, SAH is less common than EDH or SDH. Known etiologies of SSAH include trauma, vascular malformations or aneurysms, coagulopathies, neoplasms, autoimmune diseases, and spontaneous hemorrhage [4,5]. Although coagulopathy is a frequent predisposing factor, iatrogenic SSAH in the absence of coagulopathy is rare and typically linked to LP for diagnostic or anesthetic purposes [6].

In 1966, Plotkin et al. [7] introduced the concept of SSAH. Kreppel et al. [4] estimated that SSAH account for less than 1% of all spinal hematomas, based on a meta-analysis of 613 patients, highlighting their rarity compared to EDH and SDH subtypes. Similarly, Domenicucci et al. [2] analyzed 69 cases of SSAH and found that LP accounted for 44.9% of these cases, although such events represent less than 10% of all spinal hematomas, with their occurrence was rarer in patients without coagulopathy. Following a LP, bleeding may occur either at the site of needle insertion or slightly distant location from the puncture site in any of the epidural, subdural, or subarachnoid spaces [2,8]. LP may result in vascular injury by damaging blood vessels during needle insertion or withdrawal, leading to complications such as traumatic tap, hemorrhage, or, rarely, spinal cord infarction. The needle can puncture the epidural venous plexus or other blood vessels, introducing blood into the CSF. During LP, the subarachnoid space, a vascular-rich area, is susceptible to bleeding because of vascular injury. Masdeu et al. [8] proposed that traumatic LP lacerates radial vessels, a mechanism confirmed by autopsy, leading to clot formation and subsequent neurologic symptoms as the clot compresses the spinal cord or cauda equina. Fine needles (e.g., 27G or 29G) are presumed to reduce vessel trauma, suggesting that needle size and shape influence SSAH risk [8,9]. Therefore, the choice of needle characteristics is crucial in mitigating the risk of SSAH. In patients with spinal stenosis, impaired CSF flow may hinder dilution, increasing the risk of clot formation [10]. Massive bleeding, spondylolisthesis, or arachnoiditis may further elevate SSAH risk by disrupting normal CSF dynamics [2]. Additionally, reambulation after transient postpuncture bleeding may reactivate the hemorrhage [8]. Bloody CSF from a traumatic tap, often due to epidural venous plexus perforation, rarely causes hematomas or neurologic complications [6].

The symptoms of SSAH range from mild low back pain to radiating pain or, paraplegia in severe cases [4]. Post-LP headache typically prompts consideration of post-dural puncture headache, drug-related headache, intracranial hypertension, meningitis, cerebral venous thrombosis, or brain abscess [11]. Concomitant back pain warrants suspicion of rare complications such as SDH or SSAH [6].

Rapid diagnosis via MRI is critical, enabling precise localization of the hematoma (epidural, subdural, subarachnoid, intramedullary, or combined) and guiding management for optimal outcomes [12]. Hematoma signal characteristics evolve over time: hyperacute SSAH appears isointense on T1 and hyperintense on T2 due to oxyhemoglobin, whereas early subacute SSAH, as in this case, shows high T1 and low T2 signal intensity (Table 1). SSAH typically spreads longitudinally due to CSF motion, often exhibiting fluid levels within the distal thecal sac, with preserved epidural fat and dural boundaries [13]. MRI also facilitates assessment of cauda equina or spinal cord compression, informing surgical decisions.

Table 1.

MRI signal characteristics of hematomas across temporal stages

SSAH on MRI must be differentiated from EDH, SDH, and arachnoid cyst. An EDH appears as an extradural mass compressing the thecal sac. Loss of the normal epidural fat signal in the posterior epidural space is a useful locational sign, confirming its extradural position. An SDH presents as a collection of blood between the dura and arachnoid. An SDH large enough to obliterate the spinal canal may increase difficulty in differentiating it from a SAH, as the typical intrathecal distribution of the latter becomes less distinct. An arachnoid cyst is a benign, CSF-filled lesion with T2 hyperintensity matching CSF, lacking the T1 hyperintensity typical of a subacute hematoma and showing no contrast enhancement. Accurate differentiation relies on MRI signal characteristics, anatomical localization, and assessment of surrounding structures [13,14].

Xanthochromia, the yellow discoloration of CSF supernatant after centrifugation, is a key diagnostic marker for SSAH. It typically appears between 12 hours and 2 weeks post-hemorrhage due to hemoglobin breakdown, aiding in differentiating true SSAH from a traumatic LP. In traumatic LP, fresh blood introduced during the procedure does not produce xanthochromia, whereas SSAH results in time-dependent blood degradation, leading to xanthochromia. Performing LP at least 12 hours after symptom onset increases the likelihood of detecting xanthochromia, thus supporting SSAH diagnosis. However, visual inspection for xanthochromia has low sensitivity (approximately 47%, as cited in related studies), and a negative result cannot rule out SSAH, necessitating imaging such as noncontrast computed tomography or MRI for confirmation [15].

Treatment options include surgical decompression and hematoma evacuation to alleviate symptoms and prevent severe neurologic sequelae, or conservative management with steroids in less severe cases. However, it should be noted that despite surgical decompression and aggressive rehabilitation, SSAH may result in permanent neurological deficits [5]. Therefore, if symptoms are suspected, it is critical to accurately diagnose the condition using imaging studies, including MRI, and to initiate prompt treatment. Kreppel et al. [4] suggested that surgical treatment can relieve neurological compression in emergencies and enable rapid symptom improvement, although it increases the risk of complications, such as infection or rebleeding. Conservative treatment is considered an effective approach for low-risk patients with a lower risk of complications, although it has the potential for delayed complications or persistent neurological damage [4]. In this case, mild cauda equina compression without paraplegia prompted conservative management, with follow-up MRI confirming SSAH resolution, highlighting successful nonsurgical treatment.

SSAH following LP is a rare complication; however, timely MRI diagnosis and appropriate surgical or conservative management can achieve favorable outcomes without severe sequelae. This case highlights the importance of vigilance for SSAH in patients presenting with headache and back pain after LP, even in the absence of coagulopathy.

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