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Intracardial migration of a ventriculoperitoneal shunt
  1. Fabian Hack1,
  2. Anna Oder2,
  3. Christoph Baumgartner2 and
  4. Friedrich M Lomoschitz1
  1. 1Radiology, Wiener Gesundheitsverbund Klinik Hietzing, Wien, Austria
  2. 2Neurology, Wiener Gesundheitsverbund Klinik Hietzing, Wien, Austria
  1. Correspondence to Dr Fabian Hack; fabian_hack{at}

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A man in his mid 30s was admitted to the hospital with cephalea, nausea and vomiting. Intubation was necessary after he developed severe disorder of consciousness. Medical history was unremarkable.

CT revealed massive subarachnoidal haemorrhage (Hunt & Hess 4) due to an aneurysm of the anterior communicating artery (figure 1A). Surgical clipping of the aneurysm and implantation of an external ventricular drainage on both sides was performed. One month after being hospitalised, a ventriculoperitoneal shunt was implanted without any complications.

Figure 1

CT revealed subarachnoidal haemorrhage due to an aneurysm of the anterior communicating artery (A). One month after being hospitalised a ventriculoperitoneal shunt was implanted (B).

During neurological rehabilitation a control CT scan was initiated due to persisting psychotic disorder and lack of sustained clinical improvement. CT showed dilated hydrocephalic lateral ventricles with the tip of the shunt in the left lateral ventricle (figure 1B). A presumptive diagnosis of hydrocephalus due to shunt dysfunction was made.

Chest radiograph and CT (figure 2) revealed dislocation of the distal catheter. The shunt runs through the superior vena cava (SVC), the right atrium and right ventricle into the pulmonary arteries forming a loop from right to left and back to the right pulmonary artery.

Figure 2

Chest X-ray showed intracardial dislocation of the ventriculoperitoneal shunt. The shunt runs through the superior vena cava, the right atrium and right ventricle into the pulmonary arteries forming a loop from right to left and back to the right pulmonary artery (A, B). Partial 3D reconstruction (C).3D, three dimension.

The patient was immediately transferred to the department of neurosurgery for shunt revision. The dislocated catheter was carefully removed and a new ventriculoperitoneal shunt was implanted. Follow-up CT scans after revision showed reduction of ventricular size accompanied by neurological improvement.

Implantation of ventriculoperitoneal shunts is a common therapeutic option to treat hydrocephalus. In addition to the most common complications such as infection, abdominal pseudocysts, ascites, hernia, intestinal obstruction, shunt-fracture/dislocation,1 intracardial migration of the distal catheter like in this case is rare.2

Literature reports two possible pathophysiological mechanisms for intracardial migration of ventriculoperitoneal shunts. One hypothesis in the literature is that migration into the venous system occurs to gradual erosion over time.3

In our case, the dislocation of the distal catheter was diagnosed only 2 months after implantation, so the possible mechanism in this case might be iatrogenic perforation of the SVC during the process of catheter-tunnelling in the cervicothoracic region.4 In both possible mechanisms negative pressure during inspiration and movement of the head support the process of migration. Also venous blood flow towards the heart could support the protrusion and migration of catheters over time in case of perforation during the tunnelling process.

Possible complication of intracardial migration range from arrhythmia, cardiac insufficiency, pleural effusion to pulmonary embolism.2

Independent of the exact mechanism of shunt dysfunction the resulting neurological symptoms due to raised intracranial pressure5 point to the importance of early diagnosis of shunt complications.

Learning points

  • Lack of clinical improvement after hydrocephalus can occur due to migration of the shunt.

  • Chest X-ray and chest-CT are useful in detection of a possible shunt migration.

  • Early diagnosis of shunt complications is important.

Ethics statements

Patient consent for publication



  • Contributors FH and AO contributed to patient management and design of case report; FL and CB contributed to data interpretation and revision of the article; all authors are in agreement with the content of the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.