Unusual Spinal Epidural and Paraspinal Venous Engorgement Secondary to Hepatosplenic Schistosomiasis: A Rare Cause of Severe Low Back Pain

ABSTRACT

Severe low back pain from spinal epidural and paraspinal venous engorgement secondary to hepatosplenic schistosomiasis is rare. MRI revealed dilated epidural veins and neural foraminal narrowing. The patient was managed conservatively with analgesia and carvedilol for portal hypertension and subsequently experienced complete resolution of back pain.

Key Clinical Message

Epidural and paraspinal venous engorgement secondary to hepatosplenic schistosomiasis is a rare but important cause of severe low back pain that mimics spinal pathology. Clinicians should suspect it in patients with portal hypertension and atypical MRI findings. Recognition of this vascular mimic on contrast‐enhanced MRI may prevent misdiagnosis and unnecessary surgical intervention.

1. Introduction

The spinal epidural venous plexus is a valveless venous network that communicates extensively with systemic and segmental veins, making it highly susceptible to hemodynamic changes and venous congestion. Dilatation of this plexus is an uncommon but increasingly recognized entity that may present with low back pain, radiculopathy, or even mimic space‐occupying spinal lesions on imaging. Various underlying conditions have been implicated, including inferior vena cava obstruction, thrombosis, pregnancy, and other causes of increased venous pressure, all of which may lead to epidural and paraspinal venous engorgement and neural compression [1, 2, 3].

Several case reports have highlighted the clinical significance of this phenomenon. Engorgement of the epidural venous plexus has been shown to produce symptoms resembling lumbar disc herniation or spinal stenosis, often leading to diagnostic confusion. Paksoy and Gormus described patients with inferior vena cava obstruction presenting with radiculopathy and back pain due to epidural and paravertebral venous dilation. Similarly, Hanley et al. reported lumbar epidural varices as a rare but important cause of nerve root compression, while Donmez emphasized the need to identify underlying systemic causes of venous engorgement to avoid unnecessary surgical intervention [4, 5].

Schistosomiasis remains a major neglected tropical disease in endemic regions such as Ethiopia, with the hepatosplenic form characterized by periportal fibrosis and subsequent portal hypertension. This condition leads to the development of extensive collateral venous pathways as a compensatory mechanism to bypass increased portal resistance [6, 7].

However, involvement of the spinal epidural and paraspinal venous systems as part of these collateral pathways is exceedingly rare and poorly described in the literature. Here, we present a unique case of hepatosplenic schistosomiasis manifesting as extensive epidural and paraspinal venous engorgement causing severe low back pain, highlighting an unusual extra‐abdominal consequence of portal hypertension.

2. Case Presentation /Examination

A 27‐year‐old Ethiopian male presented with a two‐month history of progressive lower back pain, which had acutely worsened over the preceding 2 days. The pain was associated with tingling sensations in both lower extremities. There was no history of trauma, headache, fever, loss of consciousness, abnormal body movements, or bowel/bladder dysfunction.

Six years prior, he had been diagnosed with hepatosplenic schistosomiasis after presenting with abdominal distension. At that time, stool examination was positive for Schistosoma mansoni , while urine examination was negative. Abdominal ultrasound demonstrated periportal fibrosis, and he was treated with praziquantel for 3 days. He remained clinically stable until the onset of his current symptoms. He had no history of upper gastrointestinal bleeding, behavioral changes, or chronic medical conditions such as hypertension, diabetes mellitus, or cardiac disease.

On examination, his vital signs were: blood pressure 125/70 mmHg, pulse rate 110 beats per minute, respiratory rate 22 breaths per minute, temperature 36.9°C, and oxygen saturation 94% on room air. Abdominal examination revealed splenomegaly measuring 6 cm below the left costal margin and hepatomegaly 2 cm below the right costal margin. There was no clinical evidence of ascites. No stigmata of chronic liver disease, such as clubbing or palmar erythema, were observed. Neurological examination of the lower extremities revealed normal motor strength (5/5) bilaterally, preserved and symmetrical deep tendon reflexes, and intact sensation to light touch and pinprick. There was no objective motor or sensory deficit. The straight‐leg‐raising test was positive bilaterally. There was no vertebral tenderness or visible spinal deformity. The remainder of the systemic examination was unremarkable.

2.1. Investigations and Diagnostic Workup

Laboratory investigations showed a white blood cell count of 7.6 × 10³/μL, hemoglobin of 13.4 g/dL, and platelet count of 125 × 10³/μL. On current evaluation, both stool and urine examinations were negative for schistosomiasis. Abdominal ultrasound demonstrated hyperechoic periportal bands consistent with Symmers' periportal fibrosis. Further evaluation included contrast‐enhanced computed tomography (CT) of the whole spine (Figure 1) and magnetic resonance imaging (MRI) of the entire spine.

FIGURE 1.

Sagittal CT slice of the entire spine (A) and axial CT slice (B) from the same patient, obtained during the current admission, demonstrates dilated and tortuous paraspinal vein extending from the L2 level and draining into the external iliac veins. Additionally, dilated and tortuous extradural vein noted, traversing the neural foramina to communicate with the paraspinal venous system (black arrow and red circles).

On post‐contrast MRI, there were bilateral dilated and tortuous paraspinal veins extending from the L2 level and draining into the respective external iliac veins. Additionally, dilated and tortuous veins were noted within the extradural space, traversing the neural foramina and draining into the paraspinal venous system. These abnormal venous structures caused narrowing of the neural foramina with obliteration of the perineural fat at the L2/L3 and L3/L4 levels (Figure 2). Upper gastrointestinal endoscopy revealed two columns of small esophageal varices located 22 cm from the incisors, without red wale signs, mucosal abnormalities, or active bleeding.

FIGURE 2.

Post‐contrast MRI of the lumbar spine in the same patient during admission. (A) Coronal and (B–D) axial sequences demonstrate abnormal venous morphology. Bilateral dilated and tortuous paraspinal veins are seen originating from the L2 level. Additionally, prominent tortuous extradural veins traverse the neural foramina (green arrows) and communicate with the paraspinal venous system. The resulting mass effect causes concentric narrowing of the neural foramina at L2/L3 and L3/L4, with complete obliteration of the adjacent perineural fat (green arrows and green circles). (Red arrow in A; orange arrow in B indicates the level of neural foraminal stenosis and perineural fat effacement).

A diagnosis of hepatosplenic schistosomiasis with portal hypertension and extensive collateral venous formation, including epidural and paraspinal venous plexus engorgement, was made.

2.2. Differential Diagnosis

The differential diagnosis in this case primarily includes lumbar disc herniation or spinal stenosis, spinal epidural abscess or neoplasm, and epidural venous plexus engorgement secondary to inferior vena cava (IVC) obstruction or thrombosis [1, 2, 3]. Lumbar disc herniation is the most common cause of low back pain and radiculopathy and is frequently the initial clinical consideration [8]; however, it is typically characterized on MRI by focal disc protrusion or degenerative changes, which were absent in this patient. Instead, imaging demonstrated serpiginous, enhancing vascular structures, making a discogenic etiology unlikely. Similarly, spinal epidural abscess or tumor may present with severe back pain and contrast‐enhancing epidural lesions, but these are usually associated with systemic features such as fever, inflammatory markers, or a discrete mass lesion—none of which were observed in this case [1].

Epidural venous plexus engorgement due to IVC obstruction represents a well‐established vascular mimic of spinal pathology and has been reported to cause back pain and radiculopathy through nerve root compression by dilated venous channels. Such cases often closely resemble disc herniation or epidural masses on imaging and may even lead to unnecessary surgical intervention if unrecognized. However, the absence of radiologic or clinical evidence of caval obstruction, together with the presence of portal hypertension from hepatosplenic schistosomiasis, supports portal‐hypertension–related collateralization as the more likely mechanism in this patient [1, 2, 3, 4, 5].

Importantly, epidural venous abnormalities are increasingly recognized as rare but significant mimickers of common spinal conditions, including disc herniation, abscess, tumor, hematoma, and cystic lesions. In this patient, the combination of bilateral, symmetrical venous dilatation, characteristic MRI features, and underlying portal hypertension strongly favors epidural and paraspinal venous engorgement secondary to hepatosplenic schistosomiasis rather than other more common spinal pathologies.

2.3. Treatment and Follow‐Up

The patient was managed conservatively. Carvedilol 6.25 mg orally once daily was initiated for primary prophylaxis of variceal bleeding in the setting of portal hypertension. His severe back pain was initially treated with intravenous morphine 4 mg twice daily, followed by oral analgesics after clinical improvement. No surgical decompression, endovascular intervention, anticoagulation, or additional spinal intervention was performed. He improved clinically after 3 days of inpatient management and was discharged with oral analgesics and follow‐up advice.

At one‐month follow‐up, the patient reported complete resolution of back pain and had returned to his normal daily activities without limitation.

3. Discussion

Epidural venous plexus engorgement is an uncommon but well‐documented vascular mimic of spinal pathology, often presenting with low back pain, radiculopathy, or even cauda equina syndrome [1, 2]. Reported cases most frequently arise secondary to impaired venous return, particularly due to inferior vena cava (IVC) thrombosis, congenital agenesis, or pelvic venous obstruction. In such scenarios, MRI typically demonstrates dilated, tortuous epidural and paraspinal veins that may enhance with contrast and compress adjacent neural structures, closely resembling disc herniation or epidural masses. For instance, Wong et al. described a case of IVC thrombosis presenting as a contrast‐enhancing epidural lesion causing cauda equina syndrome, initially misdiagnosed as an abscess, while Donmez reported epidural venous engorgement secondary to IVC anomalies presenting with back pain. These cases highlight that venous congestion can mimic surgical spinal pathology and lead to unnecessary interventions if not recognized early [1, 2, 3, 4, 5].

The underlying mechanism linking systemic venous hypertension to spinal venous engorgement is best explained by the valveless vertebral venous system, commonly referred to as Batson's plexus [8, 9]. This extensive network provides a low‐resistance pathway connecting pelvic, abdominal, and thoracic venous systems with the spinal epidural veins. In conditions of increased venous pressure or obstruction, such as IVC thrombosis or portal hypertension, blood is diverted through this plexus, resulting in dilatation of epidural and paraspinal veins. Importantly, Batson's plexus functions as an alternative route for venous return when normal pathways are compromised, explaining the development of spinal venous congestion in systemic venous hypertension states [10, 11].

While prior literature predominantly describes epidural venous engorgement in the context of caval obstruction or pelvic venous compression, its association with portal hypertension is exceedingly rare. Hepatosplenic schistosomiasis is a well‐known cause of non‐cirrhotic portal hypertension, characterized by periportal fibrosis and the formation of extensive portosystemic collaterals [6, 8]. However, these collateral pathways are typically confined to the gastrointestinal and abdominal regions, such as esophageal varices and splenorenal shunts. Extension of these collateral pathways into the spinal epidural venous system, as demonstrated in this case, has been scarcely reported and represents a unique manifestation of altered venous hemodynamics. These findings raise the possibility that portal hypertension, similar to caval obstruction, may utilize the vertebral venous plexus as an alternative collateral pathway.

Comparison with previously published cases further underscores the uniqueness of this report. Unlike IVC‐related cases, which often present with acute neurological deficits including motor weakness or sphincter dysfunction, our patient presented predominantly with severe back pain without neurological compromise. Additionally, most reported cases required anticoagulation, endovascular intervention, or even surgical decompression; our patient improved with conservative symptomatic management and medical management of portal hypertension, without surgical or endovascular intervention. Similar reversible cases have been described in conditions such as pelvic venous compression, where treatment of the underlying cause led to resolution of epidural venous dilatation, supporting the concept that these vascular changes are dynamic and potentially reversible [12].

Clinically, this case is important for several reasons. First, it expands the spectrum of complications associated with hepatosplenic schistosomiasis by demonstrating a rare extra‐abdominal manifestation of portal hypertension. Second, it reinforces the need to consider vascular etiologies in patients presenting with atypical spinal imaging findings, particularly in endemic regions where schistosomiasis is prevalent. Third, accurate recognition of this entity can prevent misdiagnosis and avoid unnecessary surgical interventions, as epidural venous engorgement is a known mimic of disc herniation, tumors, and abscesses. Finally, this case highlights the broader physiological significance of Batson's plexus as a dynamic collateral system capable of redistributing venous flow in response to systemic hemodynamic alterations.

4. Limitations

This case has several limitations that should be acknowledged. First, it represents a single‐patient observation, which limits generalizability and prevents establishing a definitive causal relationship between portal hypertension and spinal venous engorgement. Second, although imaging findings strongly support a vascular etiology, no direct hemodynamic or venographic studies were performed to conclusively demonstrate the pathway of collateral flow through the vertebral venous system. Third, unlike many reported cases of spinal schistosomiasis where histopathological confirmation is obtained, no tissue diagnosis was available in this case, as diagnosis relied on clinical and radiologic correlation. Finally, the absence of long‐term follow‐up limits assessment of recurrence or persistence of venous changes, which may be dynamic and influenced by underlying venous pressure alterations.

5. Conclusion

Spinal epidural and paraspinal venous engorgement should be suspected in patients with severe low back pain and atypical MRI findings, particularly when no disc pathology or mass is identified. This is especially relevant in individuals with conditions causing venous hypertension, such as portal hypertension, where the valveless vertebral venous system allows rapid transmission of increased pressure to spinal veins. MRI with contrast is essential for accurate diagnosis and to avoid misinterpretation as surgical pathology. Management should be directed toward the underlying venous disorder and associated portal hypertension, with symptomatic treatment as appropriate. In selected patients without neurological compromise, conservative management may result in clinical improvement. Urgent intervention is only required if neurological deficits or red flag signs develop.

5.1. Learning Points

• Epidural venous plexus engorgement is a recognized but underdiagnosed cause of back pain and radiculopathy that can closely mimic disc herniation or epidural mass on MRI; the presence of serpiginous enhancing structures should raise suspicion of a vascular etiology rather than primary spinal disease.

• Because the vertebral venous system is valveless, conditions causing increased intra‐abdominal or systemic venous pressure (e.g., portal hypertension, IVC obstruction) can lead to spinal venous congestion via Batson's plexus, emphasizing the need for a whole‐body diagnostic approach.

• Many reported cases initially mimic surgical emergencies but resolve with treatment of the underlying cause; recognizing this entity and correlating with clinical context can prevent misdiagnosis and unwarranted invasive interventions.

5.2. Patient Perspective

“I had severe back pain for two months that made it hard to walk or sleep, and I was very worried something was seriously wrong with my spine. After the MRI and further tests, doctors explained that my previous schistosomiasis and associated increased venous pressure were related to the changes around my spine. After receiving treatment for my pain and being started on medication for the portal hypertension, my symptoms gradually improved, and I returned to my normal activities.”

Author Contributions

Endalew Dessie Birara: methodology, validation, visualization, writing – review and editing, writing – original draft, funding acquisition, investigation, conceptualization, software, formal analysis, project administration, data curation. Yonas Damtew Bejiga: conceptualization, investigation, funding acquisition, writing – original draft, writing – review and editing, visualization, validation, methodology. Rediet Girmaye: conceptualization, methodology, validation, investigation, funding acquisition, visualization, writing – original draft, writing – review and editing. Elias Getahun Bayu: conceptualization, investigation, methodology, validation, visualization, writing – review and editing, writing – original draft. Hosea Manyazewal Anberber: methodology, validation, visualization, writing – review and editing, writing – original draft, funding acquisition, investigation, conceptualization. Alefe Aklewok Tadesse: methodology, validation, visualization, writing – review and editing, writing – original draft, funding acquisition, investigation, conceptualization. Habtamu Ferede Kidanu: conceptualization, investigation, writing – review and editing, visualization, writing – original draft. Ragasa Getachew Bayisa: conceptualization, investigation, funding acquisition, methodology, validation, visualization, writing – review and editing, writing – original draft. Tamirat Godebo Woyimo: conceptualization, investigation, funding acquisition, writing – original draft, visualization, writing – review and editing, validation, methodology, software, formal analysis, project administration, resources, data curation, supervision.

Funding

The authors have nothing to report.

Ethics Statement

Ethical approval was waived as per institutional policy for single case reports.

Consent

Written informed consent was obtained from the patient for publication of this case report and any accompanying images.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.