Introduction
Hydrocephalus is defined as an active distension of the ventricular system of the brain resulting from inadequate passage of cerebrospinal fluid from its point of production within the cerebral ventricles to its point of absorption into the systemic circulation.1 Patients with hydrocephalus need cerebrospinal fluid diversion to normalize their intracranial pressure and its attendant adverse effects on the brain.2 Ventriculoperitoneal (VP) shunt is the mainstay of surgical treatment of hydrocephalus despite advances in endoscopic surgery.3 The failure of VP shunts is attributed to several different factors, one being failure due to the disconnection of abdominal tubing with subsequent migration of the tubing, the most common site being further inside the peritoneal cavity.4 there are three different anatomical patterns of migration based on catheter extension and organs involved: internal, when the catheter invades any viscus inside the thoracic, abdominal, or pelvic cavity; external, when the catheter penetrates through the body wall either incompletely (subcutaneously) or completely (outside the body); and compound, when the catheter penetrates a hollow viscus and protrudes through a pre-existing anatomical orifice.5 The colon is the most involved site of visceral perforation by VPS catheter, and extrusion through the rectum is reported in less than 0.1 %–2.5 % of the cases. Trans anal migration is even a rarer complication occurring in 0.1–0.7 % of the patients6
In this report, we present a case of transanal migration of a VP shunt, which was managed laparoscopically.
Case Summary
A 15-year-old male patient with a history of suboccipital craniotomy and gross total resection (GTR) of a World Health Organization (WHO) Grade IV medulloblastoma 11 months prior and right sided VP shunt placement for unresolved hydrocephalus post-operatively, presented to the emergency department with a 1-day history of global headache and projectile vomiting, accompanied by trans anal protrusion of a ventriculoperitoneal (VP) shunt during defecation over the preceding 9 months. This shunt system underwent three subsequent surgical revisions within the first 2 postoperative months due to mechanical malfunctions.
On physical examination, the patient was severely malnourished and cachectic. Neurological examination revealed signs consistent with increased intracranial pressure, but no focal deficits or neck stiffness. Abdominal examination demonstrated a soft, non-distended abdomen without guarding or rebound tenderness; however, the distal catheter of the VP shunt was visibly extruding through the anal sphincter. Initial laboratory investigations revealed mild hyponatremia (131 mEq/L) and a slightly elevated C-reactive protein (CRP) (14 mg/L). The complete blood count (CBC), renal function tests, and liver function panels were within normal reference ranges.
A shunt-preserving, minimally invasive method was first chosen due to the patient’s severe malnutrition and history of multiple shunt procedures. The patient was brought to the operating theater for primary repair of the colorectal perforation site, shunt shortening, and diagnostic laparoscopy. Intraoperatively, dense, severe intraperitoneal adhesions were encountered along the upper border of the rectum, and the track of the shunt catheter was identified within these adhesions. Using a laparoscopic approach, the shunt catheter was intraperitoneally shortened by transecting the tube. The disconnected, contaminated distal portion of the catheter was then pulled down and completely retrieved through the anus. The remaining proximal portion of the shunt catheter was carefully inspected intraperitoneally, and no macroscopic leaks or structural damage were observed. The pelvic adhesions surrounding the rectal perforation site were extensively lysed, and the abdominal wall wounds were closed in anatomical layers. The patient tolerated the procedure well, woke up without new neurological deficits, and remained hemodynamically stable.
Intraoperative CSF obtained from the shunt valve was sent for culture, and empirical intravenous meropenem and vancomycin were initiated. Culture grew Gram-negative bacilli resistant to ampicillin and trimethoprim/sulfamethoxazole, and targeted meropenem and vancomycin therapy was continued.
The patient had localized abdominal pain on the third postoperative day. A complex echogenic fluid collection in the right lower quadrant surrounding the distal shunt tip was seen during an abdominal ultrasound, which strongly suggested the presence of an intraperitoneal abscess. The patient was immediately brought back to the operating room due to the localized intra-abdominal infection and the shunt-sparing strategy’s failure. To act as an external ventricular drain (EVD) for ongoing hydrocephalus treatment and CSF cleaning, the contaminated VP shunt system was exteriorized proximally. To enable continuous purulent evacuation, a distal drainage tube was surgically inserted into the right lower quadrant abscess cavity at the same time.
Discussion
Shunt remains the most common procedure done for hydrocephalus. Shunts can be VP, theco-peritoneal, ventriculoatrial, or ventriculopleural.7 The major disadvantage of VPS is the fact that it constitutes a foreign body and is prone to complications such as infection of different parts of the central nervous system. The draining abdominal tips may also cause complications like paralytic ileus in the early postoperative period and intestinal obstruction secondary to adhesion formation in a later period. Some other abdominal complications may occur, like blockade due to fibrous encasement or kinking, expulsion through the abdominal wound, or migration (both cranial or caudal) into various abdominal organs.8,9 A VP shunt anal protrusion is a rare condition. The first case of anal extrusion of distal VPS was reported by Wilson and Bertrand in 1966. A total of 210 cases of transanal migration are reported in the literature.6 Most cases appear months after surgery, and interestingly, >40% of patients are asymptomatic, with diagnosis based only on visualization of the prolapsed catheter from the anus.10 Protrusion of the distal VPS catheter per rectum can occur without producing peritonitis11
The etiology of VPS bowel perforation is largely unknown. Potential causative factors include longer catheter length, a sharp/heavy catheter tip, fibrous adhesions, chronic inflammatory processes from steady pressure that cause boring of the catheter through the visceral wall, silicon allergy, malnutrition, and young age at the shunt placement.12,13 In adults, for whom cases are reported much less frequently than in children, potential risk factors include conditions that compromise the integrity of the bowel wall, such as diverticulosis, chronic constipation, chronic inflammation, or previous abdominal surgery, as well as steroid use.14 Upon bowel perforation, certain factors have been postulated to be responsible for the migration of the distal end of the catheter, such as intestinal peristalsis, continuous water-hammer effect of CSF-transmitted arterial pulsations, and intermittent rise in the intra-abdominal pressure.3 In our patient, malnutrition and multiple abdominal surgeries might have contributed to the bowel perforation.
Bowel perforation from a VP shunt, although uncommon, carries an overall mortality rate of 15%. This rate increases to 22% with the presence of a CNS infection and 33% with an intrabdominal infection. Given the high morbidity and mortality, early detection and treatment are essential.15 Neurological symptoms of raised intracranial pressure, such as headache, nausea, vomiting, impaired gait, nuchal rigidity, seizures, and others, in combination with abdominal pain, abdominal distention, abdominal wall rigidity, or local irritation, are the signs and symptoms of shunt migration.16
While a physical examination showing the VP catheter protruding is often diagnostic, various imaging modalities can be used as supplemental tools. Abdominal X-rays, CT scans, and endoscopy have all been described as helpful adjuncts in the diagnosis.15 During the presentation of our patient, he already had an extruding VP shunt through the anal canal, thus imaging modalities were not used for diagnosis.
Traditionally, laparotomy was necessary for both peritoneal shunt placement and subsequent shunt revisions. The advent of laparoscopy has afforded a minimally invasive approach that has resulted in decreased patient morbidity related to shunt placement.4 Takeshi Morinaga et al developed an algorithm for handling peritonitis related to a ventriculoperitoneal shunt, where laparoscopic irrigation, drainage, and reconstruction can be used in patients where the use of laparoscopy is possible. Laparoscopic surgery has several advantages over laparotomy when retrieving distal shunt tubes. Intra-abdominal irrigation really helps in eliminating bacterial contamination, mostly when dealing with severe peritonitis resulting from gastrointestinal perforation. Using laparoscopy for this task is very convenient since the system is already supplied with a highly functional irrigation device that can effectively remove contaminants by flushing them with a high flow of sterile solution, not only at the local level but also in the entire abdomen. Laparoscopy is also beneficial in that, through this method, only minimal damage is done to the peritoneum. This would be very helpful in preventing adhesive peritonitis, a condition that would hinder the functioning of the water-absorbing shunt catheter. Laparoscopy has been rising in popularity as a standard method to access the peritoneal cavity since it is quicker, more hygienic, and offers a minimal traumatic experience, although there is no infection involved.13 Although there were some initial reservations about insufflating the abdomen with CO2 to a certain pressure, as it is necessary for laparoscopic surgery, laparoscopy for the abdomen when a VP shunt is present has been reported to be feasible and, in fact, should be the preferred approach16
The VP shunt’s distal end must never be pulled back into the peritoneal cavity, as this might cause contamination throughout the tract.10 The primary concern for catheter perforation into a hollow viscus is for ascending infection and meningitis caused by enteric organisms. Most, but not all, reports describe obtaining CSF cultures and a prolonged course of broad-spectrum intravenous antibiotics to manage or prevent this feared complication, even without overt neurological symptoms or signs on exam, given the high reported mortality.14 In our patient culture, taken from the removed distal tube showed growth for gram-negative bacteria. The patient was treated with Vancomycin and Meropenem post-op.
Conclusion
Transanal migration of a ventriculoperitoneal (VP) shunt catheter remains an exceedingly rare, life-threatening complication of hydrocephalus management, typically arising from delayed bowel perforation. While a minimally invasive, laparoscopic shunt-preserving approach can be considered to reduce surgical trauma, particularly in severely malnourished or cachectic patients with a history of multiple revisions, the high risk of ascending microbial contamination and subsequent intra-abdominal abscess formation often necessitates eventual shunt exteriorization and systemic antimicrobial therapy. This case underscores the paramount importance of early clinical recognition, vigilant postoperative monitoring via cross-sectional or ultrasound imaging, and the need for a low threshold to transition to definitive shunt removal or exteriorization when localized intraperitoneal infection occurs.