Abstract
Introduction and importance:
Abdominal cerebrospinal fluid pseudocysts (APCs) are a rare complication of ventriculoperitoneal (VP) shunts, occurring in 1–4.5% of cases and potentially causing abdominal symptoms, bowel obstruction, or shunt malfunction. We present a case of a VP shunt–associated pseudocyst leading to mechanical small bowel obstruction.
Presentation of case:
A 40-year-old woman with a long-standing VP shunt presented with abdominal pain, vomiting, and obstipation. CT imaging showed a large pseudocyst encasing the shunt tip and causing mechanical ileus. Emergency surgery revealed adhesion-related small-bowel obstruction, requiring partial cystectomy and ileal resection. cerebrospinal fluid (CSF) cultures grew Cutibacterium acnes, prompting complete shunt removal, external ventricular drainage, and later placement of a ventriculoatrial shunt. She recovered with conservative management of minor postoperative complications.
Clinical discussion:
APCs may form due to impaired CSF absorption, inflammation, or low-grade infection. In this patient, a chronic shunt infection likely contributed to cyst development and bowel obstruction. Management typically requires cyst drainage or resection, and revision of the distal catheter, with complete shunt removal necessary when infection is present. Early diagnosis and multidisciplinary management are essential to prevent morbidity.
Conclusion:
VP shunt–associated pseudocysts, though rare, can cause acute abdominal emergencies. Prompt imaging, surgical intervention, and appropriate treatment of shunt infection are critical for optimal outcomes.
Keywords: hydrocephalus, intestinal obstruction, postoperative complications, pseudocyst, ventriculoperitoneal shunt
Introduction and importance
Ventriculoperitoneal (VP) shunting, first described by Kausch in 1905, remains the standard treatment for hydrocephalus following major advances in shunt and valve technology[1,2]. Despite its widespread use, VP shunting is associated with complications in 20–50% of cases, including infection, obstruction, disconnection, peritonitis, ascites, shunt malfunction, intestinal perforation, and abdominal cerebrospinal fluid pseudocyst (APC) formation[3]. APCs are rare, occurring in approximately 1–4.5% of cases[4]. They are characterized by the accumulation of cerebrospinal fluid (CSF) within a fibrous, non-epithelial-lined cavity resulting from impaired peritoneal CSF absorption. Clinical presentation may include abdominal pain, distension, nausea, vomiting, constipation, fever, and symptoms of shunt dysfunction[5]. The cyst wall may result from a sterile inflammatory process or low-grade infection, and management typically involves cyst excision and relocation of the distal catheter[6].
Here, we report a case of mechanical small-bowel obstruction caused by a VP shunt–associated pseudocyst, complicated by shunt infection and requiring multistage surgical and neurosurgical management.
HIGHLIGHTS
Rare cause of bowel obstruction: A VP shunt–associated pseudocyst led to a mechanical small-bowel obstruction requiring cyst and bowel resection.
A low-grade infection was identified: Cutibacterium acnes was cultured from shunt hardware, supporting chronic infection as a driver of pseudocyst formation.
Management validated the diagnosis: Symptoms resolved after shunt explantation, targeted antibiotics, and conversion to a ventriculoatrial shunt.
This case report has been reported in line with the Surgical CAse REport checklist[7].
Case presentation
A 40-year-old woman with congenital hydrocephalus and spina bifida following meningomyelocele repair in childhood presented with a 2 week history of progressive nausea, vomiting, diffuse abdominal pain, abdominal distension, and obstipation. She was VP shunt–dependent and had undergone multiple childhood revisions, although detailed records were unavailable. In 2001, the shunt valve was revised to a medium-low-pressure Sophysa valve, while the distal catheter was retained because distal drainage was adequate.
Her medical history included arterial hypertension, a VP shunt infection with Staphylococcus epidermidis sepsis in 2011, which was successfully treated with antibiotics, and the resection of left lower abdominal cysts in 2012 and 2017. These cysts were reportedly associated with the left adnexa without confirmed continuity with the shunt system. Histopathology revealed a peritoneal cyst and an endometrioma in 2012, and peritoneal inclusion cysts in 2017. Baseline neurological status included mild chronic spastic paraparesis with preserved cognition. She denied smoking, alcohol abuse, and illicit drug use; her family history was noncontributory. Home medications included lisinopril, fesoterodine, and tamsulosin.
On admission, the patient was febrile but hemodynamically stable. Physical examination showed abdominal distension, diffuse lower abdominal tenderness, and reduced bowel sounds, without peritonitis or a palpable mass. Neurological examination revealed a Glasgow Coma Scale score of 15, intact cranial nerves, baseline mild spastic paraparesis, and no new focal deficits or signs of acute shunt malfunction.
Abdominal computed tomography (CT) demonstrated a high-grade mechanical ileus with a large fluid collection surrounding the distal VP shunt tip, consistent with an abdominal CSF pseudocyst (Fig. 1a and b). Cranial CT showed stable shunt positioning without hydrocephalus or shunt dysfunction (Fig. 1c). Laboratory investigations revealed elevated inflammatory markers, including a C-reactive protein level of 59.7 mg/L and a leukocyte count of 12.9 × 109/L.
Figure 1.

Initial abdominal computed tomography (CT) demonstrating ventriculoperitoneal (VP)-shunt-associated complications: (A) Sagittal view and (B) axial (transverse) view showing a large intra-abdominal fluid collection (asterisk) around the tip of the VP shunt catheter, suggestive of a pseudocyst or abscess. (C) Axial unenhanced computed tomography showing intraventricular location of the VP shunt with no evidence of VP shunt dysfunction. These findings support an abdominal rather than intracranial cause of the patient’s presentation.
Given the acute abdomen and radiological evidence of high-grade mechanical ileus, emergency diagnostic laparoscopy was converted to midline laparotomy because of extensive adhesions. A large inflammatory pseudocyst containing 2000 mL of clear fluid surrounded the distal VP shunt catheter and extended from the ligament of Treitz to the lower abdomen (Fig. 2). Dense adhesions between the pseudocyst and adjacent ileal loops caused high-grade mechanical small bowel obstruction. Following detection of bacteria in CSF from the burr-hole reservoir, the VP shunt was explanted. Extensive adhesiolysis was required; because the distal ileum was densely incorporated into the cyst wall and could not be safely separated, approximately 20 cm of ileum were resected with primary end-to-end ileo-ileostomy. Intraoperative samples and CSF were obtained. The patient required intensive care for three postoperative days.
Figure 2.

Intraoperative findings during emergency laparotomy. The image demonstrates an abdominal cerebrospinal fluid pseudocyst adherent to adjacent ileal loops and surrounding the distal VP shunt catheter. Adhesions between the pseudocyst and small bowel contributed to a mechanical bowel obstruction and necessitated a partial cystectomy with ileal resection.
CSF obtained from the burr-hole reservoir grew Cutibacterium acnes, which was confirmed by cultures of the sonicated catheter, whereas intra-abdominal fluid and blood cultures remained negative. The VP shunt was explanted, and a right trigonal external ventricular drain (EVD) was inserted. Empiric intravenous ceftriaxone (2 g twice daily) was initiated on admission. After microbiological identification of C. acnes, vancomycin was added for 1 week following an interdisciplinary consultation with infectious disease specialists, given the device-associated infection and the known susceptibility profile of C. acnes to beta-lactam antibiotics and vancomycin.
The postoperative course was complicated by partial ileus managed conservatively and localized intra-abdominal collections at the resection site (Fig. 3a,b). On postoperative day (POD) 12, 10 mL of purulent fluid was drained percutaneously; cultures remained sterile.
Figure 3.

Postoperative abdominal CT after VP-shunt explantation: Rim-enhancing fluid collections consistent with postoperative abscesses or pseudocysts are visible: (A) one measuring 31 × 25 mm in the right mid-abdomen (interenteric) and (B) another measuring 40 × 30 mm in the left mid-abdomen (interenteric, adjacent to the inner abdominal wall). These collections prompted image-guided percutaneous drainage during postoperative management.
On POD 13, EVD obstruction necessitated placement of a stereotactically navigated right-frontal ventriculoatrial (VA) shunt with a Certas Plus valve, as the peritoneal cavity was no longer suitable for CSF diversion. Revision of the proximal catheter was required the following day because of malposition seen on postoperative CT. Ceftriaxone therapy was continued until POD 24. Follow-up CT demonstrated near-complete resolution of the intra-abdominal collections. An incidental segmental pulmonary embolism was treated with anticoagulation. The patient remained neurologically stable and was transferred for rehabilitation on POD 20.
Two months later, she re-presented with exposure of the right frontoparietal VA shunt reservoir. The VA shunt was explanted and a new EVD was inserted. Catheter cultures grew Corynebacterium tuberculostearicum and C. acnes, whereas repeated CSF cultures remained sterile. Intravenous meropenem and vancomycin were administered.
Given severe aqueductal stenosis, multiple prior shunt revisions, and an unsuitable peritoneal cavity, an endoscopic third ventriculostomy (ETV) was subsequently performed without complications. Temporary CSF leakage from the EVD insertion site was managed conservatively, and the EVD was removed 7 days later.
The patient was discharged to a rehabilitation facility in good neurological condition. At six-month follow-up, she remained neurologically stable without recurrent symptoms. MRI demonstrated a patent ventriculostomy, and CT of the abdomen and thorax showed no evidence of infection or pulmonary embolism.
The patient described the prolonged hospitalization and staged procedures as physically and emotionally demanding but expressed relief after symptom resolution and satisfaction with the multidisciplinary treatment and rehabilitation process (Table 1).
Table 1.
Timeline of clinical course and interventions.
| Day/event | Clinical course |
|---|---|
| 2 weeks before admission | Nausea, vomiting, abdominal pain, obstipation |
| Day 0 | Admission and CT imaging showing pseudocyst and mechanical ileus |
| Day 0 | Emergency laparoscopy converted to laparotomy with partial cystectomy and ileal resection |
| Day 1 | CSF cultures positive for Cutibacterium acnes |
| Day 1 | VP shunt explantation and EVD placement |
| POD 12 | Percutaneous drainage of postoperative intra-abdominal fluid collection |
| POD 13 | EVD obstruction |
| Conversion to ventriculoatrial shunt | |
| POD 20 | Transfer to neurorehabilitation |
| POD 24 | Resolution of abdominal collections; incidental pulmonary embolism diagnosed and anticoagulation initiated |
| 2 months later | Re-presentation with exposed VA shunt reservoir and suspected shunt infection prompting VA shunt explantation and EVD insertion |
| Catheter cultures positive for Corynebacterium tuberculostearicum and Cutibacterium acnes | |
| ETV performed | |
| 6-month follow-up | Neurologically stable without recurrent abdominal symptoms, hydrocephalus, infection, or pulmonary embolism |
CSF, cerebrospinal fluid; CT, computed tomography; ETV, endoscopic third ventriculostomy; EVD, external ventricular drain; POD, postoperative day; VA, ventriculoatrial; VP, ventriculoperitoneal.
Discussion
APCs are a rare complication of VP shunting, with an incompletely understood pathophysiology. Proposed risk factors include low-grade shunt infection, multiple revisions, distal catheter dysfunction, impaired CSF absorption, elevated CSF protein levels, and prior abdominal surgery[8]. In the present case, chronic Cutibacterium acnes infection, together with multiple previous abdominal operations, likely contributed to pseudocyst formation and subsequent adhesive small bowel obstruction.
Infection is the second most common cause of VP shunt failure after mechanical obstruction, occurring in 8–15% of cases[9]. Risk factors include young age, postoperative CSF leak, intraventricular hemorrhage, and previous shunt infection[9,10]. Although most shunt infections occur shortly after implantation, delayed infections may develop and are frequently associated with pseudocyst formation or peritoneal inflammation[11]. Clinical manifestations are often nonspecific and may include fever, nausea, vomiting, and headache[12]. In our patient, C. acnes was isolated from CSF and catheter cultures, and ventricular CSF demonstrated pleocytosis, supporting the diagnosis of chronic shunt infection. Aspiration of CSF via the shunt reservoir remains an important diagnostic tool with a high pathogen detection rate when infection is suspected[13,14].
The standard treatment for shunt infection consists of complete hardware removal and intravenous antibiotic therapy[15]. Prevention remains important and includes perioperative antibiotics, strict sterile technique, antibiotic-impregnated catheters, and minimizing operative time[16].
VP shunt infections may contribute to APC formation through chronic inflammation and adhesion formation[17]. APCs occur in approximately 1–4.5% of VP-shunted patients[4] and often present years after shunt placement or revision. Interestingly, while infection may contribute to their development, most pseudocyst cases have negative CSF cultures at diagnosis[18].
Symptoms typically include abdominal pain, distension, nausea, and signs of shunt dysfunction. Ultrasound and CT scans are the preferred imaging tools for diagnosis[19]. Management depends on the presence of infection and generally includes shunt externalization, cyst excision, and revision of CSF diversion. In our case, emergency surgery was required because of acute mechanical small bowel obstruction caused by dense adhesions between the pseudocyst and adjacent ileal loops.
Recurrence remains a concern, with reported rates of 20–24%. Relocation of the distal catheter outside the peritoneal cavity appears to reduce the risk of recurrence [20].
Although VP shunt–associated abdominal pseudocysts with bowel obstruction have previously been reported, including by Kashyap et al[17], our case was distinguished by severe adhesion-related mechanical ileus requiring bowel resection, culture-confirmed chronic Cutibacterium acnes infection, and staged neurosurgical management culminating in successful ETV. Furthermore, the patient experienced postoperative intra-abdominal collections, EVD obstruction, and subsequent shunt exposure requiring additional intervention. This case highlights the interplay among chronic low-grade shunt infection, pseudocyst formation, and progressive adhesive bowel disease.
Weaknesses and limitations
Because this is a single case report, causality between chronic shunt infection and pseudocyst formation cannot be established. The patient’s extensive abdominal surgical history likely contributed to adhesion formation and represents a potential confounding factor. Interpretation is further limited by the retrospective nature of the analysis and by incomplete historical operative records.
Strengths
This case describes a rare VP shunt–associated pseudocyst causing a mechanical bowel obstruction requiring bowel resection. It highlights the value of multidisciplinary collaboration, microbiological evaluation, and staged neurosurgical and abdominal management of complex shunt-related complications.
Conclusion
VP shunt–associated APCs, although rare, may cause severe complications, including mechanical bowel obstruction and shunt infection. APCs should be considered in VP shunt–dependent patients presenting with acute abdominal symptoms. Prompt diagnosis, multidisciplinary management, shunt removal, and targeted antimicrobial therapy are essential to reduce morbidity and achieve favorable outcomes.
Footnotes
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
Contributor Information
Adisa Poljo, Email: adisa.poljo@clarunis.ch.
Gabriel F. Hess, Email: gabriel.hess@clarunis.ch.
Severina Leu, Email: Severina.Leu@usb.ch.
Beat P. Müller, Email: beat.mueller@clarunis.ch.
Jennifer M. Klasen, Email: jennifer.klasen@clarunis.ch.
Ethical approval
This study did not require approval by an Institutional Review Board (IRB) in accordance with the regulations of our local ethics committee.
However, all procedures performed in this study involving human participants were in accordance with the ethical standards of the institutional and/or national research committees and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards.
Consent
The patient has provided informed consent for this case report to be published, and all identifying information has been removed.
Sources of funding
This research received no external funding.
Author contributions
All authors contributed to the study conception and design. Adisa Poljo wrote the main manuscript text and prepared Figures 1–3. All authors contributed to the review and editing of the manuscript and approved the final version.
Conflicts of interest disclosure
The authors declare no conflicts of interest concerning the materials or methods used in this case report or the findings of this study.
Research registration unique identifying number (UIN)
Not applicable.
Guarantor
Jennifer M. Klasen.
Provenance and peer review
Not commissioned; externally peer reviewed.
Data availability statement
Data supporting this case report can be obtained from the corresponding author on reasonable request; however, no personal or identifiable patient data will be disclosed.
Acknowledgements
Not applicable.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
Data supporting this case report can be obtained from the corresponding author on reasonable request; however, no personal or identifiable patient data will be disclosed.
