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Abdominal Complications of VP Shunts

 

Ventriculoperitoneal shunting procedure for the measuring of hydrocephalus. The beginning of the 20th century brought about the use of the peritoneal cavity as an absorptive surface for shunted cerebrospinal fluid. Since these early clinical trials, numerous reports of various complications from the presence of a catheter in the peritoneal cavity have appeared in the literature. Improvements in surgical techniques in the development of lesser reactive shunt tubing have been helpful adjuncts in reducing the incidence of abdominal complications. Nonetheless abdominal complications still occur and can potentially create diagnostic and therapeutic indecision.

Ventriculitis from shunt infection is a well documented complication of VP shunts and frequently occurs in the early postoperative period secondary to wound infection or intraoperative contamination. The occurrance of a viscus perforation by the abdominal portion of a VP shunt is often a prolonged clinical phenomenon, which usually does not lead to acute peritonitis. The catheter may gravitate transmurally into the bowel lumen over a prolonged period while being surrounded by fibrous encasement at the enterotomy without subsequent peritoneal infection.

While acute viscus perforation due to catheter irritation may also occur leading to peritonitis, this is the exception rather than the rule. Noninteric viscus perforations have been sporadically reported. These include urinary bladder, vagina, gall bladder, and scrotum, with one case that seemed to be testicular torsion in a newborn. Rare case reports include intestinal volvulus around the shunt catheter. A frequent and important consideration of VP shunt patients, primarily infants and children, is the increased incidence of inguinal hernia. Important etiologic factors that have been documented include patent processus vaginalis in children up to the age of two as well as the presence of increased intrabdominal pressure.

Another complication as is evidenced by this case is the formation of loculated intraperitoneal CSF. Although the pathophysiologic mechanism is unclear, proposed explanations are related to chronic, low grade inflammatory responses with fibrous encapsulation of the irritated area. The irritable focus may be the catheter itself, infected CSF, or sterile xanthochromic CSF . The CSF draining into these fibrous loculations produce large intraabdominal, fluid filled pseudocysts that may become symptomatic from gastrointestinal or genitourinary compromise.

Diagnosis of intraabdominal complications may be difficult. Although an acute abdomen may appear to be exclusively an intraabdominal problem, patients with VP shunts need thorough physical examinations with special attention to neurologic status and shunt function, as well as careful abdominal examination to exclude intraperitoneal pathology. If neurologic symptoms prevail, then a plain film should be performed. If the scan shows a functional shunt, then cranial CT should follow to determine if there is new or progressive intracranial pathology.

If the scan shows a shunt malfunction, then delineation of the cranial or abdominal portion of the catheter causing it needs to be identified. Stagnation of the radiotrace in the catheter after a one hour scan suggests proximal shunt dysfunction. If abdominal complications are present, then intraabdominal scanning may determine the source of the problem. If abdominal symptoms are present, than plain films of the abdomen may reveal a mass, obstruction, or displacement of the bowel gas pattern. Plain films also may helpful in identifying the intraperitoneal position of the catheter.

If a mass is palpable of physical exam or suggested by plain film, abdominal ultrasonography can be useful in delineating mass composition, size, location, and possible catheter encasement. If no mass is apparent and obstruction is suggested, then abdominal CT is recommended. If no abnormalities are defined on physical exam or x-ray , then a radionuclide scan of the shunt is indicated to determine if the shunt is functional and if fluid accumulation, such a pseudocyst or ascites, is present or if a viscus perforation has occurred.

Once preoperative diagnosis has been made, correction can be done by a formal or minilaparotomy. If the shunt is infected, then externalization and antibiotic therapy is suggested. If no infection is present, many surgeons reposition the catheter by direct visualization. If there are fibrous adhesions or if there is concern about possible infectious sequellae, using a ventriculopleural or ventriculovenous shunt is recommended.

A high index of suspicion, optimum preoperative assessment, and early defendive surgical procedure will improve the management of patients with shunt abnormalities and should provide a more rapid recovery minimize long term complications inpatients as a result of VP shunting.