|Year : 2018 | Volume
| Issue : 2 | Page : 153-159
Delayed intra-abdominal complications of ventriculoperitoneal shunts
Mihir Shah, Bhuwan Giri, Tony R Capizzani, Matthew L Moorman
Department of General Surgery, Cleveland Clinic, Cleveland, OH, USA
|Date of Submission||14-Dec-2017|
|Date of Acceptance||27-Feb-2018|
|Date of Web Publication||30-Aug-2018|
Dr. Matthew L Moorman
Department of Trauma and Acute Care Surgery, OhioHealth Grant Medical Center, Columbus, OH
Source of Support: None, Conflict of Interest: None
Acute perioperative abdominal complications of ventriculoperitoneal shunt placement are generally well understood and managed by general surgeons. Delayed complications occur at nontrivial rates and can masquerade as a variety of typical diagnoses such as adhesive bowel obstruction. In some rare cases, the presentation is quite unusual with the shunt protruding from the anus or urethral meatus. Preexisting neurologic conditions often make the history and examination less reliable. Diagnostic and treatment delay can have devastating effects. The variability of these delayed presentations and problems does not allow for evaluation protocols, and the care of these patients must be individualized. General surgery principles continue to apply and, combined with a high index of suspicion, will lead the surgeon to the appropriate diagnosis and treatment options. The barrier is a failure to consider the shunt as the source of the problem when its placement was not recent. A review of the literature and presentation of an unusual case highlight several of the common delayed presentations, diagnoses, and management options.
The following core competencies are addressed in this article: Patient Care, Medical Knowledge, System-based Practice.
Keywords: Bowel perforation, ventriculoperitoneal shunt delayed complication, intra-abdominal complication
|How to cite this article:|
Shah M, Giri B, Capizzani TR, Moorman ML. Delayed intra-abdominal complications of ventriculoperitoneal shunts. Int J Acad Med 2018;4:153-9
|How to cite this URL:|
Shah M, Giri B, Capizzani TR, Moorman ML. Delayed intra-abdominal complications of ventriculoperitoneal shunts. Int J Acad Med [serial online] 2018 [cited 2019 Oct 16];4:153-9. Available from: http://www.ijam-web.org/text.asp?2018/4/2/153/240145
| Introduction|| |
Ventriculoperitoneal (VP) shunts are commonly used to drain excess cerebrospinal fluid (CSF) and normalize intracranial pressure in patients with hydrocephalus. In adults, this procedure has a complication rate as high as 25%–29% in the 1st year.,, Long-term, shunt revision is necessary in 45%–59% of patients in all age groups. Intra-abdominal complications account for 25% of all VP shunt (VPS) complications., VPS revisions are responsible for nearly half of all shunt-related procedures in the United States.
Late complications are usually defined as those occurring after 30 days and include infection, loculated CSF ascites (CSF pseudocyst), visceral perforation, and simple mechanical failure of the device.,, Several studies quote complication rates as high as 52% by 10 years with adults experiencing comparatively lower rates of shunt complications compared to both neonates and children., Multiple case reports describe alarmed caregivers and patients presenting with the shunt catheter protruding through oral, anal, vaginal, or urethral orifice secondary to visceral perforation.,,,
Intra-operative and early post-postoperative complications in the abdomen tend to focus on bowel injury and are well described.,, The approach to the acute complication of an inadvertent bowel perforation is generally not in debate. Acute wound and shunt infections will be seen in approximately 5% of patients. This mimics the rate of clean surgical incisional infections. Early failure of the device and subsequent insufficient drainage can occur in a wide range of cases (up to about 20%, depending on series). These mechanical failure modes vary between kinked catheter, detachment from the valve, defective valve, and unknown or unreported causes.,,
Delayed complications are more difficult and patients may present with a range of symptoms which may not obviously implicate their shunt. The diagnosis of undifferentiated abdominal pain, small bowel obstruction, peritonitis, or even sepsis can lead to their admission to a general surgery service. Early identification of a possible VPS issue is critical in preventing the progression to a life-threatening problem. The presence of the shunt often causes confusion regarding the best way forward and ultimately delays definitive patient care. Consequences of these delays can be significant. Prompt appropriate multidisciplinary management of these intra-abdominal problems is important.
Our acute care surgery (ACS) service has participated in the care of several unique cases of delayed intra-abdominal VPS complications. Basic tenants of general abdominal surgery have been successfully applied. We present a review of the literature and our experiences.
| Review of Common Delayed Complications|| |
Delayed gastrointestinal (GI) perforation by a VPS occurs in <1% of cases. Mortality is reported as high as 15%–18%.,, A review by Hai et al. estimated the most common site to be the large bowel followed by the stomach, rectum, and small bowel. The duration from VPS surgery to detection of bowel perforation was on average 4.8 months in children younger than 1 year and 24.8 months in older patients.
The mechanism of delayed visceral perforation by peritoneal catheters is unclear. Simple bowel injury on insertion is typically implicated first. This is indeed likely for an immediate or very early complication which results in typical symptoms such as peritonitis. Those which present more subtly and, in some cases, months or years later are difficult to correlate with such an obvious etiology.
Various conclusions from autopsy findings and case reports allude to a number of other factors. Focal fibrosis around the peritoneal catheter may anchor it to adjacent bowel resulting in mechanical irritation and eventual perforation. Transmural migration through the bowel wall likely occurs over a prolonged period of time. The area becomes surrounded by fibrous material at the enterotomy site which limits the spillage of succus and resultant peritonitis. This may explain the absence of abdominal findings in these patients. Sharp and rigid tips of distal catheters, coiled spring catheter, long intra-abdominal length of distal shunts, and allergy to silicon tubes have all been hypothesized to be contributive although all types of catheters have been associated with complications of perforation. Children with congenital hydrocephalus and meningomyelocele are believed to have weak bowel innervation leading to increased susceptibility to perforation. These patients will present with highly variable signs and symptoms. Despite their intra-abdominal pathology, some will have a benign abdomen and only demonstrate neurologic signs of VPS failure or infection. In a report by Yousfi et al., clinical peritonitis was documented in 15% of all reported cases of VPS associated with bowel perforation.
Pneumoperitoneum and extravasation of enteric contrast on imaging are not common with delayed gut perforations. Pneumocephalus may be an incidental finding. Several intra-abdominal complications have been found incidentally on abdominal computed tomography (CT) examinations done during the workup of what appeared as a simple shunt infection. Gastric perforation by a shunt seems to more frequently cause typical abdominal symptoms (e.g., pain, nausea, vomiting, and fever).,
In a nontrivial number of patients, a first sign of enteric perforation will be the sight of the VPS exiting through a natural orifice of the body. Normal gut motility likely explains anal extrusion of the shunt distal end. Less easily explained is retrograde migration out of the mouth. Abdominal X-rays, shunt-o-grams, abdominal CT scans, and endoscopy are useful to localize the site of perforation. Radiographic shunt-o-gram consists of visualization of the ventricular system with the injection of a small quantity of nonionic contrast. Forward flow of contrast material and CSF is confirmed by serial filming over a period of 15 min. Although typically used in the pediatric population, Bartynski et al. suggest the time limit of 12 min to demonstrate spontaneous flow and a functioning unit. Its advantage is that it can help isolate the components responsible for malfunction as well as obtain CSF for culture to exclude shunt infection. Systemic infection is however an absolute contraindication to this procedure.
Confirmed or suspected VPS violation of the GI tract requires CSF Gram's stain and culture to rule out concomitant intracranial infection. Empiric broad-spectrum antibiotics should be considered while awaiting final culture results. Gram-negative and anaerobic meningitis in these patients is concerning for bowel perforation.
Surgery to remove the VPS from the bowel is necessary. Open or laparoscopic technique may be used based on local expertise and comfort. Decisions on exteriorizing the shunt or its complete revision are best individualized to each case and require discussion between at least the general surgeon and neurosurgeon. The gut perforations associated with these cases will generally be very small and may be closed primarily after debriding the inflamed edges of the defect. Basic surgical principles of bowel perforation may be applied. Following the logic that the etiology of this complication is underlying ulcer disease, Helicobacter pylori should be evaluated for stomach and duodenal perforation and treated accordingly. Gastric perforations may be associated with underlying malignancy, and their repair should include full-thickness pathology specimen., Postoperative care can mimic that done for typical peptic ulcer perforation of the upper GI tract.
Perforations which occur in the distal small bowel should prompt a search for an inflammatory etiology such as Meckel's diverticulum. Primary repair remains appropriate in cases with minimal or no peritoneal soiling. This logic is sound for the remainder of the lower GI tract as well. Special concern is always warranted for left-sided colon, and rectal perforations and trauma surgery principles may be applied in this region. Again, no spillage of stool allows for low-risk primary closure of small perforations. Diversion of the fecal stream is necessary only for high-risk repairs. End colostomy is typically not necessary.
In the absence of peritoneal contamination, antimicrobials may be discontinued within 24 h of surgery. Empiric coverage until negative CSF cultures are confirmed is often the chosen course.
Thoracic migration of a VPS catheter can be through any hiatus in the diaphragm or through an inflammatory diaphragmatic perforation similar to that described for the GI tract. Diaphragmatic perforation has been associated with appendicitis, cholecystitis, and other inflammatory conditions in the peritoneum. Supradiaphragmatic migration may result from any traumatic diaphragmatic injury, including inadvertent entry into the pleural space during catheter placement, most commonly in the supraclavicular fossa during the distal tunneling of catheter. Negative pleural space pressure can draw the entire shunt into the chest. Once in the pleural cavity, CSF collection can lead to pleural effusion and respiratory distress. Bronchial perforation, pneumothorax, and pneumonia have also been described. Patients may present with shortness of breath, pleuritic chest pain, or abdominal discomfort and have been reported to do so as late as 1 year after shunt placement.,
In most cases, no lung injury is seen, and the shunt may be simply returned to the abdominal cavity through laparoscopy. Closure of the diaphragmatic defect may be necessary based on type of injury or other finding. Pleural CSF fluid collections may require tube or video-assisted thoracostomy. Due to the high-risk nature of VPS infections, CSF and pleural fluid cultures will likely be obtained, and patients typically begun on broad-spectrum antibiotics. Without organ perforation, no infectious etiology exists. Findings at surgery along with negative Gram's stain and culture should prompt discontinuation of antibiotics.
Cerebrospinal fluid pseudocyst
Intra-abdominal CSF pseudocyst occurs in up to 4.5% of VPS patients. Children tend to present with headache, nausea, distension, and possibly a palpable abdominal mass. Abdominal symptoms (89.9% in children and 83.6% in adults) are more common than neurological symptoms (38.6% of children and 34.6% of the adults). The shunt tip may or may not be involved within the cyst cavity itself. Some may simply form as result of unabsorbed CSF in the abdomen, often predisposed with significant adhesions [Figure 1].
|Figure 1: Intra-abdominal cerebrospinal fluid pseudocyst causing small bowel obstruction in an adult|
Click here to view
Risk factors for pseudocyst formation are multiple shunt revisions, intra-abdominal shunt infection, and increased CSF protein content contributing to a sterile inflammatory response., All of these lead to excess adhesion formation and subsequent loculation of fluid. These conditions are often asymptomatic but may present as typical small bowel obstructions.
Rarely, they may present as cysts within solid organs such as the liver or spleen. These too may be asymptomatic and discovered incidentally. In a report of 15 patients with hepatic CSF pseudocysts, only 6 presented with signs of shunt malfunction while 14 had pain and abdominal distension. Elevated liver enzymes were seen in most patients and ultrasonography can be used to confirm the diagnosis. CSF cysts show smooth echo-free space with or without septation. The catheter tip is displaced with a “rail road” sign within the cyst due to double echo of the shunt. Abdominal CT is more accurate in large cysts which deform the normal abdominal architecture and helps differentiate between other etiologies such as abdominal abscess, appendicitis, and diverticulitis.
No consensus exists regarding the optimal management of CSF pseudocysts in the abdominal cavity or its solid organs. Multiple approaches are described including simply repositioning the catheter to another location in the abdomen, placing the distal catheter in another body compartment (e.g., atrium and pleura), or temporarily exteriorizing the catheter and replacing in the abdomen at a later time. Treatment algorithms are typically based on the suspicion of an infection and presence of bowel obstruction.,
Bowel obstruction thought to be associated with CSF fluid collection likely requires surgical drainage. A fluid sample and distal VP catheter tip culture should be obtained at surgery. Typical of patients with VPS are significant adhesions making percutaneous drainage problematic. That said, minimally invasive removal of CSF collection may relieve obstructive symptoms albeit temporarily. Some authors recommend excision of the cyst wall with repositioning of the catheter in an uninvolved area of the peritoneal cavity. This can be done laparoscopically or through laparotomy. A more involved approach may be to convert the catheter to a ventriculopleural or caval device. This should likely be reserved for repeated VP failures and uninfected patients., In the presence of obvious infection, exteriorization, antibiotic duration, and timing of revision are typically left to the neurosurgeon.
First described in 1974, bladder perforation by a VPS has been reported in around 24 patients to date. One reason why bladder perforations are relatively rare is attributed to the fact that the catheter has to pass through the peritoneum before perforating the bladder. In a review of cases with bladder perforation reported in the literature, 6 out of 21 cases described had bladder augmentation surgery for noncompliant or small capacity bladder. Two of the earliest cases described had patients who presented with abdominal pain, fever, and erythema of skin in the suprapubic region. Other symptoms described in reports include shunt malfunction, urinary retention, dysuria, hematuria, pyuria, or protrusion of the catheter through the urethra. The average duration to bladder perforation from last date of revised shunt ranged from 6 months to 11 years with a mean duration of 4 years.
Although optimal management is controversial, removal of the shunt is the cornerstone of treatment. Initial broad-spectrum intravenous antibiotics are administered after appropriate CSF and distal tip cultures have been sent. Combined neurosurgical and urology support is required in the operating room. Continuous drainage of the bladder by a urethral catheter is also advised by most authors as a safeguard. A less invasive approach to removing the shunt would be pulling out the distal tube gently through the urethra as the shunt material is usually soft and injuries due to knots are negligible. Alternatively, the bladder can be approached anteriorly through an extraperitoneal cystostomy to identify the site of perforation and repair the defect following removal of the catheter.
In patients with previous bladder augmentation, the rate of perforation is estimated to be around 5%–10% and can be a life-threatening event. Management consists of prophylactic externalization of the shunt followed by revision of the shunt.
| Case Report|| |
A 62-year-old man was admitted to the hospital by his neurosurgeon due to edema, erythema, and tenderness along the right side of his neck and supraclavicular region 9 years after placement of right-sided parietal VPS. Concern for shunt infection resulted in a workup which included CT scan of the head, chest, abdomen, and pelvis in addition to shunt fluid analysis. These images were interpreted as having a loop of the VPS within the gastric lumen [Figure 2]. The shunt fluid was described as green, had no bacteria on Gram's stain, and was sent for culture. These findings prompted broad-spectrum antibiotics and a consult to our ACS service which typically assists the neurosurgery team with VPS placement procedures. The ACS team had no previous contact with this individual.
|Figure 2: Ventriculoperitoneal shunt perforating the pylorus in an adult|
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The patient was advised to undergo removal and revision of his VPS, to which he consented. At surgery, the VPS catheter entered the abdominal cavity in the typical position, left subcostal, midclavicular. It was completely encased with thin omental adhesions in a meandering path. Its tip was lying in the midabdomen and appeared to be working normally. The catheter was found to enter and exit the gut lumen at the pylorus with entrance and exit defects separated by about 5 mm [Figure 3]. These defects were only large enough to accommodate the catheter, and there was no active leak of succus. Approximately 2 feet of the catheter had been pulled into the gut lumen resulting in much less than typical remaining free in the abdominal cavity. The cranial end of the catheter was undisturbed.
|Figure 3: Ventriculoperitoneal shunt perforating the pylorus in an adult|
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The two perforations were sharply resected en bloc resulting in a 1 cm defect. This tissue was sent for pathologic analysis, and the defect was closed primarily similar to an acute perforation. Omental patch reinforcement was used as well. A closed-suction drain was left in the upper abdomen at closure.
The neurosurgery team elected to exteriorize the shunt temporarily. It was returned to the abdominal cavity in approximately 1 week after a 7-day course of antibiotics. In the interim, the final pathology was positive for H. pylori and showed only inflammatory mucosa in the area of perforation. The patient has had no further difficulties.
| Discussion|| |
General surgeons are typically familiar with acute postoperative VPS complications. These problems typically do not pose a diagnostic or treatment dilemma. However, many VPS complications occur in a delayed fashion. In our practice, these outnumber the acute complications and are more difficult to diagnose and manage. General surgeons will often become involved with these patients as their presentations can be generalized abdominal pain, distension, ileus, or obstruction. Managing the intra-abdominal portion of a delayed VPS complication should be in every general surgeon's skill set.
Any patient with abdominal complaints should have a detailed neurological examination as the initial effort to determine shunt efficacy. These patients typically have a lengthy healthcare history which provides a baseline for comparison which to compare. This is equally true for neuroimaging studies (e.g., CT brain) which should be obtained if there is any question of shunt problems. In addition, examination of the entire tract of the catheter in the subcutaneous tissue may indicate both mechanical problems (e.g., kinking and coiling) and infection (e.g., cellulitis of the tract).
Abdominal complaints should be evaluated, as with any other patient, with detailed history and examination first. This will lead to a differential diagnosis which can be further pursued with basic laboratories and possible imaging. Simple X-rays (e.g., upright chest and abdomen) may reveal pneumoperitoneum which can obviate the need for further testing and radiation exposure. In many cases, contrast-enhanced CT of the abdomen and pelvis will be diagnostic.
The most challenging of these cases involves the violation of another organ or body cavity by the VPS. Migration through the diaphragm, into the gut, or into the genitourinary system can cause angst among the inexperienced surgeon. The basic principles of general surgery apply and when managed in concert with a neurosurgeon will lead to a successful outcome. Deviation from these tenants often leads to additional complications, and efforts should be made to avoid unnecessary delays in definitive surgical care.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Chumas P, Tyagi A, Livingston J. Hydrocephalus – What's new? Arch Dis Child Fetal Neonatal Ed 2001;85:F149-54.
Lam CH, Villemure JG. Comparison between ventriculoatrial and ventriculoperitoneal shunting in the adult population. Br J Neurosurg 1997;11:43-8.
Brasey DL, Fankhauser H, de Tribolet N. Normal-pressure hydrocephalus in adults. Analysis of results and complications following ventriculo-cardiac derivation. Schweiz Med Wochenschr 1988;118:919-23.
Wu Y, Green NL, Wrensch MR, Zhao S, Gupta N. Ventriculoperitoneal shunt complications in California: 1990 to 2000. Neurosurgery 2007;61:557-62.
Sells CJ, Loeser JD. Peritonitis following perforation of the bowel: A rare complication of a ventriculoperitoneal shunt. J Pediatr 1973;83:823-4.
Park CK, Wang KC, Seo JK, Cho BK. Transoral protrusion of a peritoneal catheter: A case report and literature review. Childs Nerv Syst 2000;16:184-9.
Martinez Hernández-Magro P, Barrera Román C, Villanueva Sáenz E, Zavala MJ. Colonic perforation as a complication of ventriculoperitoneal shunt: A case report. Tech Coloproctol 2006;10:353-5.
Chung JJ, Yu JS, Kim JH, Nam SJ, Kim MJ. Intraabdominal complications secondary to ventriculoperitoneal shunts: CT findings and review of the literature. AJR Am J Roentgenol 2009;193:1311-7.
Lazareff JA, Peacock W, Holly L, Ver Halen J, Wong A, Olmstead C, et al.
Multiple shunt failures: An analysis of relevant factors. Childs Nerv Syst 1998;14:271-5.
Snow RB, Lavyne MH, Fraser RA. Colonic perforation by ventriculoperitoneal shunts. Surg Neurol 1986;25:173-7.
Yilmaz MB, Egemen E, Tonge M, Kaymaz M. Transoral protrusion of a peritoneal catheter due to gastric perforation 10 years after a ventriculoperitoneal shunting: Case report and review of the literature. Turk Neurosurg 2013;23:285-8.
Sathyanarayana S, Wylen EL, Baskaya MK, Nanda A. Spontaneous bowel perforation after ventriculoperitoneal shunt surgery: Case report and a review of 45 cases. Surg Neurol 2000;54:388-96.
Nishijima M, Endoh S, Ohyama H, Higuchi H. Gastric perforation by a ventriculoperitoneal shunt. Neurosurgery 1982;10:754-6.
Hai A, Rab AZ, Ghani I, Huda MF, Quadir AQ. Perforation into gut by ventriculoperitoneal shunts: A report of two cases and review of the literature. J Indian Assoc Pediatr Surg 2011;16:31-3.
] [Full text]
Masuoka J, Mineta T, Kohata T, Tabuchi K. Peritoneal shunt tube migration into the stomach – Case report. Neurol Med Chir (Tokyo) 2005;45:543-6.
Yousfi MM, Jackson NS, Abbas M, Zimmerman RS, Fleischer DE. Bowel perforation complicating ventriculoperitoneal shunt: Creport and review. Gastrointest Endosc 2003;58:144-8.
Ramana Murthy KV, Jayaram Reddy S, Prasad DV. Perforation of the distal end of the ventriculoperitoneal shunt into the bladder with calculus formation. Pediatr Neurosurg 2009;45:53-5.
Ghritlaharey RK, Budhwani KS, Shrivastava DK, Gupta G, Kushwaha AS, Chanchlani R, et al.
Trans-anal protrusion of ventriculo-peritoneal shunt catheter with silent bowel perforation: Report of ten cases in children. Pediatr Surg Int 2007;23:575-80.
Matsuoka H, Takegami T, Maruyama D, Hamasaki T, Kakita K, Mineura K, et al.
Transanal prolapse of a ventriculoperitoneal shunt catheter – Case report. Neurol Med Chir (Tokyo) 2008;48:526-8.
Zhou F, Chen G, Zhang J. Bowel perforation secondary to ventriculoperitoneal shunt: Case report and clinical analysis. J Int Med Res 2007;35:926-9.
Shetty PG, Fatterpekar GM, Sahani DV, Shroff MM. Pneumocephalus secondary to colonic perforation by ventriculoperitoneal shunt catheter. Br J Radiol 1999;72:704-5.
Bartynski WS, Valliappan S, Uselman JH, Spearman MP. The adult radiographic shuntogram. AJNR Am J Neuroradiol 2000;21:721-6.
Doh JW, Bae HG, Lee KS, Yun IG, Byun BJ. Hydrothorax from intrathoracic migration of a ventriculoperitoneal shunt catheter. Surg Neurol 1995;43:340-3.
Akyüz M, Uçar T, Göksu E. A thoracic complication of ventriculoperitoneal shunt: Symptomatic hydrothorax from intrathoracic migration of a ventriculoperitoneal shunt catheter. Br J Neurosurg 2004;18:171-3.
Sanders DY, Summers R, DeRouen L. Symptomatic pleural collection of cerebrospinal fluid caused by a ventriculopleural shunt. South Med J 1997;90:345-6.
Sekiguchi H, Suzuki J, Wetjen NM, Mullon JJ. Recurrent cerebrospinal fluid (CSF) pleural effusions caused by ventriculoperitoneal (VP) shunt: A case with a successful treatment with endoscopic third ventriculostomy. Clin Neurol Neurosurg 2013;115:1190-3.
Rainov N, Schobess A, Heidecke V, Burkert W. Abdominal CSF pseudocysts in patients with ventriculo-peritoneal shunts. Report of fourteen cases and review of the literature. Acta Neurochir (Wien) 1994;127:73-8.
Dabdoub CB, Dabdoub CF, Chavez M, Villarroel J, Ferrufino JL, Coimbra A, et al.
Abdominal cerebrospinal fluid pseudocyst: A comparative analysis between children and adults. Childs Nerv Syst 2014;30:579-89.
Ghritlaharey RK, Budhwani KS, Shrivastava DK, Srivastava J. Ventriculoperitoneal shunt complications needing shunt revision in children: A review of 5 years of experience with 48 revisions. Afr J Paediatr Surg 2012;9:32-9.
] [Full text]
Yuh SJ, Vassilyadi M. Management of abdominal pseudocyst in shunt-dependent hydrocephalus. Surg Neurol Int 2012;3:146.
] [Full text]
Kolić Z, Kukuljan M, Bonifačić D, Vukas D. CSF liver pseudocyst as a complication of a ventriculoperitoneal shunt. Wien Klin Wochenschr 2010;122:641-4.
Dabdoub CB, Fontoura EA, Santos EA, Romero PC, Diniz CA. Hepatic cerebrospinal fluid pseudocyst: A rare complication of ventriculoperitoneal shunt. Surg Neurol Int 2013;4:162.
] [Full text]
Ghritlaharey RK, Budhwani KS, Shrivastava DK, Jain AJ, Gupta G, Kushwaha AS. CSF pseudocysts peritoneal cavity following VP shunt surgery: Report of three cases in children and review of the literature. J Indian Assoc Pediatr Surg 2006;11:4.
Anderson CM, Sorrells DL, Kerby JD. Intra-abdominal pseudocysts as a complication of ventriculoperitoneal shunts: A case report and review of the literature. Curr Surg 2003;60:338-40.
Mobley LW 3rd
, Doran SE, Hellbusch LC. Abdominal pseudocyst: Predisposing factors and treatment algorithm. Pediatr Neurosurg 2005;41:77-83.
Silen W. Cope's Early Diagnosis of the Acute Abdomen. 22nd
ed. New York: Oxford University Press; 2010.
[Figure 1], [Figure 2], [Figure 3]