|Year : 2014 | Volume
| Issue : 6 | Page : 277-279
Silent bowel perforation cause by migration of ventriculoperitoneal shunt masquerading as acute enteritis
Hsiao-Kuei Chang1, Shih-Hung Tsai2, Yu-Long Chen2, Yuan-Pin Hsu2
1 Department of Emergency Medicine, Taichung Armed Forces General Hospital, Taichung, Taiwan, Republic of China
2 Department of Emergency Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China
|Date of Web Publication||19-Dec-2014|
Dr. Yuan-Pin Hsu
Department of Emergency Medicine, Tri-Service General Hospital, National Defense Medical Center, No. 325, Sec. 2, Cheng-Gong Road, Neihu District, Taipei City 11490, Taiwan
Republic of China
Source of Support: None, Conflict of Interest: None
Ventriculoperitoneal (VP) shunt is an established method of diverting cerebrospinal fluid for the management of hydrocephalus. The procedure is associated with various complications. Bowel perforation caused by migration of VP shunt is rare but serious complication. Because most of the patients are asymptomatic, and the occurrence of such complication is fatal due to ascending meningitis, early diagnosis, and rapid treatment is important in these patients. The diagnosis of such complication is based on direct visual of the protruding tube from the anus or abdominal computed tomography. Colon perforation due to shunt catheter migration may initially but not essentially present as meningitis after shunt infection, abdominal symptoms, seizure, and fever. However, colon perforation may rarely resemble the symptoms of acute gastroenteritis (abdominal pain, vomiting and/or diarrhea) before the prolapse of shunt catheter from the rectum. Here, we report a 75-year-old man underwent VP shunt for hydrocephalus presented with "watery diarrhea" masqueraded as acute gastroenteritis and further diagnosed as migration of VP shunt from the colon, via digital examination and further disclosed by computed tomography.
Keywords: Bowel perforation, ventriculoperitoneal shunt, acute enteritis
|How to cite this article:|
Chang HK, Tsai SH, Chen YL, Hsu YP. Silent bowel perforation cause by migration of ventriculoperitoneal shunt masquerading as acute enteritis. J Med Sci 2014;34:277-9
|How to cite this URL:|
Chang HK, Tsai SH, Chen YL, Hsu YP. Silent bowel perforation cause by migration of ventriculoperitoneal shunt masquerading as acute enteritis. J Med Sci [serial online] 2014 [cited 2020 Jul 5];34:277-9. Available from: http://www.jmedscindmc.com/text.asp?2014/34/6/277/147274
| Introduction|| |
Ventriculoperitoneal (VP) shunt surgery is the standard treatment for hydrocephalus since 100 years ago, which allows the drainage of cerebrospinal fluid (CSF) via a catheter into the peritoneal cavity. In addition to the most common shunt complications - obstruction and infection - VP shunts have been associated with a variety of abdominal complications, which affect 10-30% of patients.  Bowel perforation after VP shunting is extremely uncommon and accounts <0.1% of all abdominal complications. Over 50% of these patients are asymptomatic, however, the mortality rate associated with it is as high as 15%. 
| Case Report|| |
A 75-year-old man had undergone revision of VP shunt for normal hydrocephalus 2 months ago. He presented to the emergency department (ED) with frequent passage of "watery" diarrhea, of 1-week duration. Initially, he went to the local clinic and took some antidiarrheal agent under impression of acute enteritis, but the symptom persisted. When he arrived in our ED, his body temperature was 36.1°C, his blood pressure was 115/68 mm Hg, his pulse rate was 88 beats/min, and his respiratory rate was 20 breaths/min. The abdominal examinations were normal. Our laboratory examination showed a white cell count of 5400/μL, with neutrophils at 56.2%, lymphocytes at 32.3%, hemoglobin at 12.4 g/dl, hematocrit at 36.5%, platelets at 162 × 10 3 /μl, C-reactive protein at 0.1 mg/dl, aspartate aminotransferase at 18 U/L, alanine aminotransferase at 13 U/L, blood urea nitrogen at 22 mg/dl, creatinine at 1.4 mg/dl. Stool examination revealed normal. The "stool" looked clear and low volume. The stool made the underwear wet. The patient stated he had wet underwear needed to the frequency change in a day during the previous 1-week. The general appearance of anal orifice is normal. The digital examination revealed a foreign body sensation of the finger. The foreign body was pulled out. It disclosed a yellowish plastic tube [Figure 1]. Abdominal computed tomography revealed VP shunt migrated from the colon distal to the anus [Figure 2], which was consistent with the digital examination finding. The patient was treated with revision of VP shunt and broad spectrum antibiotics. As a result, he discharged under stable condition 2-week later.
|Figure 1: The digital examination revealed a foreign body sensation of the finger. The foreign body was pulled out. It disclosed a yellowish plastic tube|
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|Figure 2: Abdominal computed tomography revealed ventriculoperitoneal shunt migrated into the colon|
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| Discussion|| |
Hydrocephalus is a pathological state of CSF accumulation, which leads to the dilatation of the cerebral ventricles. The management of hydrocephalus includes the drainage of CSF through a subcutaneous catheter into an absorption site that is most frequently the peritoneum.
Several complications including disconnection and/or occlusion of the tube, shunt infection, intestinal obstruction, migration of the shunt, and perforation of the internal organs have been reported in association with the VP shunt.
Among the internal organ perforations, bowel is the most common site of perforation by a VP shunt catheter and is a rare but serious complication occurring in <1% of cases with mortality of up to 15%.  The exact pathophysiology of bowel perforation is still a matter of debate; adherence of the tip of the VP catheter to the bowel wall and subsequent local inﬂammation and erosion,  encasing ﬁbrosis around the tube, , and silicone allergy leading to a foreign body-like reaction  have been regarded as the possible mechanisms of bowel perforation. Furthermore, younger age , and myelomeningocele  may be contributing factors to developing perforation; the latter gives rise to weakness in the bowel wall due to the defective innervations. In the present case, adhesions along with ﬁbrosis were seen between the peritoneal tube and the colon near the perforating site.
Although the incidence of bowel perforation due to VP catheter is low, the mortality rate is high. Therefore, early diagnosis is important, but it may be difficult because nearly half of these cases are asymptomatic. The most frequent finding is VP catheter dislodgement through the anus,  therefore, this extrusion seems like a chance for early diagnosis of bowel perforation. In contrast, colon perforation may rarely resemble the symptoms of acute gastroenteritis (abdominal pain, vomiting, and/or diarrhea) before the prolapse of shunt catheter from the rectum. Associated diarrhea may occur because of the CSF drainage via the catheter into the colon. Thereby, nausea and vomiting may be among the neurological symptoms of hyponatremia because of excessive CSF loss. In our present case, the patient presented with the symptoms of acute gastroenteritis without any apparent peritoneal signs, the "watery" diarrhea (clear and low volume "stool") may be the only hint, than digital examination was performed. Diagnosis was made according to shunt catheter protruding from the anus during digital examination.
Ruling out of central nervous system (CNS), and intra-abdominal infection by retrograde spread is the initial step in the management of bowel perforation. The removal of the shunt catheter along with short-term external ventriculostomy and intravenous antibiotics has been used as a treatment of VP shunt-related colonic perforation. The protruding catheter can be removed by pulling it through the anus, surgical removal, or endoscopic removal, based on the clinical state of the patient. Surgical intervention is indicated for cases in which clinical ﬁndings of peritonitis or CNS infection are signiﬁcant. In contrast, if there is no retrograde infection, endoscopic removal of the catheter may be considered in case of a more proximal location of the distal tip or a resistance while pulling the catheter. In nonsurgical options of removal, the perforation site is believed to be plugged due to the presence of a ﬁbrous sheath around the shunt tract. ,, In the present case, the penetration site of the VP catheter was established by preoperative colonoscopy to localize the minimal laparotomy incision.
| Conclusion|| |
Ventriculoperitoneal shunt-related colonic perforation is a rare but fatal complication. Our present case exhibited that clinical suspicion of bowel perforation should be focused on any patient with a VP shunt presenting with prolonged diarrhea of unknown etiology, abdominal symptoms, and gastroenteritis.
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[Figure 1], [Figure 2]