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 »  Introduction
 »  Case report
 »  Discussion
 »  References

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Year : 2000  |  Volume : 48  |  Issue : 4  |  Page : 378-80

CSF ascites : a rare complication of ventriculoperitoneal shunt surgery.


Department of Neurosurgery, The Childs Trust Hospital, Chennai, 600004, India.

Correspondence Address:
Department of Neurosurgery, The Childs Trust Hospital, Chennai, 600004, India.

  »  Abstract

CSF ascites is a very rare complication of ventriculoperitoneal (VP) shunt procedure. No definite explanation has been offered for the inability of the peritoneum to absorb the CSF. Two children who underwent VP shunting for hydrocephalus, presented with ascites 3 (1/2) years and 4 months respectively, after the shunt was placed. The treatment of choice is conversion of the VP shunt to a ventriculoatrial shunt.

How to cite this article:
Chidambaram B, Balasubramaniam V. CSF ascites : a rare complication of ventriculoperitoneal shunt surgery. Neurol India 2000;48:378


How to cite this URL:
Chidambaram B, Balasubramaniam V. CSF ascites : a rare complication of ventriculoperitoneal shunt surgery. Neurol India [serial online] 2000 [cited 2020 Feb 23];48:378. Available from: http://www.neurologyindia.com/text.asp?2000/48/4/378/1495




   »   Introduction Top

CSF ascites is a rare complication of ventriculoperitoneal (VP) shunt. The peritoneum is unable to absorb the CSF, due to the sheer volume of CSF produced or due to, as of now, an unexplained pathology in the peritoneum. Two children who suffered from ascites secondary to VP shunt are presented here.


   »   Case report Top

Case 1 : A 3 month old female baby underwent a right sided ventriculoperitoneal shunt for congenital hydrocephalus in March 1989. She was born at term and had birth asphyxia. In July 1989 a left sided VP shunt was placed since the right side shunt was not working. In October 1989 shunt infection was suspected and the shunts were removed and an external ventricular drain was placed. (The shunt infection was not proved by microbiologic studies). After a course of antibiotics, a VP shunt was placed, on the right side. There were no shunt related problems till April 1992 when the shunt had to be revised twice in that month. She underwent another revision in July 1992. She was all right till January 1993 when she was admitted for evaluation of progressive ascites. Clinical examination revealed no shunt problems and no abnormality in the gastrointestinal system. There was, however, marked ascites. All the haematological investigations and liver function tests were normal. Sonographic evaluation revealed only ascites. There was no loculated collection of CSF or fluid in the abdomen. Attempts were made to treat this condition by repeated tapping, but to no avail. Analysis of the ascitic fluid revealed 810 polymorphs, 2-4 lymphocytes and 1-3 RBCs per high power field, protein content of 2.7 gm% and
sugar of 66 mg%. CSF analysis revealed 3-5 polymorphs and 1-2 RBCs per high power field, sugar of 79 mg % and protein of 246 mg%. Cultures did not grow any organism in the ascitic fluid or CSF. Investigations for tuberculosis (to explain the ascites/malabsorption) were negative.
Peritoneal biopsy was done to elucidate the cause of the non-absorption of the CSF. Histologic examination revealed, 'granulation tissue infiltrated with numerous eosinophils, plasma cells, lymphocytes and a few histiocytes. Focal areas of mesothelial (reactive) proliferation with vascular congestion' were seen. There was no evidence of tuberculous infection. It was felt by the pathologist that, 'in view of the eosinophilic infiltration the possibility of a reaction to a foreign body could be thought of'. In March 1993 the ventriculoperitoneal shunt was converted to a ventriculoatrial shunt. There has been no shunt related problems since then.
Case 2 : A 7 year old boy was admitted for headache and drowsiness of 10 days duration in April 1998. On examination he was drowsy and had bilateral optic atrophy. CT revealed an optochiasmatic glioma with hydrocephalus. In view of the hydrocephalus and drowsiness, an emergency right VP shunt was done. After an MRI he underwent craniotomy and subtotal excision of the tumour. Histology disclosed Grade II astrocytoma. He was given a course of radiotherapy. Four months later, he was readmitted for progressive ascites. Liver function tests were normal. Sonographic evaluation revealed ascites only. There was no loculated collection of fluid. CSF analysis (from a shunt tap) showed 29 WBCs and 10 RBCs/cumm, sugar of 59 mg% and protein of 2.86 mg%. No abnormality was noted on Gram's stain and the culture was sterile. Examination of the ascitic fluid revealed 16 WBCs and 15 RBCs/cumm sugar of 93 mg% and protein of 1.19 g%. The Gram's stain was unremarkable and the culture was sterile. In the light of our experience with the previous patient, the ventriculoperitoneal shunt was changed to a ventriculoatrial shunt without delay. At the time of this surgery an open peritoneal biopsy was done. The histologic examination disclosed no abnormality apart from 'perivascular round cell infiltrates'. This was interpreted as 'mild chronic inflammation'. This child, too, did not receive any antituberculous therapy. No antibiotic therapy (apart from routine surgical prophylaxis) was given. He is doing well now.


   »   Discussion Top

Ascites has been defined as 'accumulation of excess fluid within the peritoneal cavity'.[1] The commonest cause of ascites is cirrhosis of the liver, closely followed by other serious hepatic diseases.[2] In all of these, however, an underlying disease state can be found. In our patients none of the above two causes existed. It is apparent that the primary problem was in the peritoneum which just failed to absorb the CSF.
Several intra-abdominal complications of a VP shunt are known and some are so common that they do not merit any elaborate discussion here. Loculated collection of CSF, however, merits discussion. Patients may present with an intra-abdominal mass after a shunt or it may be noted during the work up for a shunt malfunction or infection. In these cases, the mesentery wraps itself around the peritoneal catheter and the CSF accumulates at that site. The mesentery prevents the collected CSF from gaining access to the rest of the peritoneal cavity. Thus a loculated collection of CSF develops. The aetiology of this condition is usually low grade sepsis or infection from microaerophilic or anaerobic organisms. All of these may be difficult to demonstrate. However, CSF ascites is a completely different problem. Here there is an excessive accumulation of CSF in the peritoneal cavity resulting from an inability of the peritoneum to absorb the CSF. This inability may be the result of the sheer excess volume of CSF produced as in a case of choroid plexus papilloma or villous hypertrophy of the choroid plexus.[3],[4]
CSF ascites may develop even several years after the shunt is placed.[5] No satisfactory explanation has been given, to date, for this condition.[6] Infection has been proposed as a causative factor.[7],[8],[9] Both the children reported here had no clinical or biochemical evidence of hepatic dysfunction. Nor did they have any evidence of peritonitis. Although the cell count and the protein content of the ascitic fluid were high, there was no infection. Long term follow up (6 years in Case 1 and 1 year in Case 2) did not reveal signs of any sepsis, shunt malfunction or hepatic dysfunction. Both the children received only the routine surgical prophylactic dose of antibiotics (Cefotaxime 100 mg/kg/day IV for two days). This effectively ruled out infection as a cause of ascites in our patients.
Clinical, biochemical or radiologic investigations did not reveal any evidence of tuberculosis in our cases. Open peritoneal biopsy was done in both to rule out abdominal/peritoneal tuberculosis, as a cause of ascites. Peritoneal biopsy is the best way to diagnose peritoneal tuberculosis.[2] An inflammatory response may result from the talc used in surgical gloves. However, in that case the reaction is 'localized and minimal'.[10] Our patients had a generalised problem. High CSF protein has also been put forth as a causative factor.[11] However, the high protein content alone cannot explain this problem because children with elevated CSF protein have had shunts placed without any untoward effect. Peritonitis, sterile or infective, may result in a state of non-absorption of CSF. None of our patients had any evidence of infection or inflammation. The eosinophilic response seen in the first patient was as a result of the presence of a foreign body in the tissue and cannot explain the problem. The second child had no eosinophilic response, yet had CSF ascites.
CSF ascites seems to be commonly related to tumours in the suprasellar region and has been reported in optic pathway gliomas and craniopharyngioma.[12],[13],[14],[15] CSF ascites has been reported in children with optic pathway gliomas (as in case 2). This has been ascribed to the high protein content which results in an altered absorptive state. A high protein content alone should not result in ascites. The authors have inserted shunts in children with CSF protein level as high as 1gm% and have not encountered any problem. Increased protein content of the shunted CSF resulting in reversed osmosis and accumulation of the ascitic fluid has also been proposed, but, if this were true, all patients with increased protein in the CSF should develop ascites, which is not the case.[11] Also, the protein content of the shunted CSF must be higher than the plasma protein concentration.
CSF ascites in addition to being a complication in its own right can lead to other complications. These include all the complications of ascites and shock.[16] Intermittent occurrence of the ascites has also been reported.[17]
The treatment of choice for VP shunt associated ascites is conversion of the shunt to a ventriculoatrial shunt, after making sure there is no infection. Endoscopic 3rd ventriculostomy, where feasible, is another alternative procedure, which can be used to manage this problem. Ventriculopleural shunting may be hazardous because pleura is also a mesothelial structure and the same problem may occur there, resulting in hydrothorax.

 

  »   References Top

1.Podolsky DK, Isselbacher K : Major complications of cirrhosis, in Fauci AS, Braunwald E, Isselbacher KJ, et al (eds): Harrisons Principles of Internal Medicine. McGraw-Hill, New York. 1998; 1710-1716.   Back to cited text no. 1    
2.Glickman RW, Isselbacher KJ: Abdominal swelling and cirrhosis, in Fauci AS, Braunwald E, Isselbacher KJ, et al (eds): Harrisons Principles of Internal Medicine. New York, McGraw-Hill, 1998: 255-257.   Back to cited text no. 2    
3.Britz GW, Kim DK, Loeser JD : Hydrocephalus secondary to diffuse villous hyperplasia of the choroid plexus. Case report and review of the literature. J Neurosurg 1996; 85 : 689-691.   Back to cited text no. 3    
4.Ray BS, Peck FC Jr : Papilloma of the choroid plexus of the lateral ventricles causing hydrocephalus in an infant. J Neurosurg 1956; 13 : 405-410.   Back to cited text no. 4    
5.Perez Pena F, Aparicio Campillo G, Lopez Asenjo JA et al : Ascites due to cerebrospinal fluid accumulation. Rev Clin Esp 1990; 187 : 128-130.   Back to cited text no. 5    
6.Weidmann MJ : Ascites from a ventriculoperitoneal shunt. J Neurosurg 1975; 43 : 233-235.   Back to cited text no. 6    
7.Bucholz RD, Pittman T : Endoscopic coagulation of the choroid plexus using the Nd:Yag laser: initial experience and proposal for management. Neurosurgery 1991; 28 : 421 426   Back to cited text no. 7    
8.Nlikawa S, Hara A, Nokura H et al : Central nervous cryptococcosis giving rise to ascites after ventriculoperitoneal shunting - a case report. No Shinkei Geka 1988; 16 : 881-885.   Back to cited text no. 8    
9.Rush DS, Walsh JW, Belin RP et al : Ventricular sepsis and abdominally related complications in children with cerebrospinal fluid shunts. Surgery1985; 97 : 420-427.   Back to cited text no. 9    
10.Dayal Y, DeLellis RA : Gastro instestinal tract - peritoneum, In Robbins Pathologic Basis of Disease.EB Cotran RS, Kumar V, Robbins SL (eds) Saunders, Philadelphia. 1989; 905-909.   Back to cited text no. 10    
11.Tang TT, Whelan HT, Meyer GA et al : Optic chiasma glioma associated with inappropriate secretion of antidiuretic hormone, cerebral ischaemia, nonobstructive hydrocephalus and chronic ascites following ventriculoperitoneal shunting. Child's Nerv Syst 1991; 7 : 458-461.   Back to cited text no. 11    
12.Adegbite AB, Khan M : Role of protein content in CSF ascites following ventriculoperitoneal shunting. J Neurosurg 1982; 57 : 423-425.   Back to cited text no. 12    
13.Shuper A, Horev G, Michovitz S et al : Optic chiasm glioma electrolyte abnormalities, nonobstructive hydrocephalus and ascites. Med Pediatr Oncol1997; 29 : 33-35.   Back to cited text no. 13    
14.West GA, Berger MS, Geyer JR : Childhood optic pathway tumours associated with ascites following ventriculoperitoneal shunt placement. Pediair Neurosurg 1994; 21 : 254-258.   Back to cited text no. 14    
15.Yount RA, Glazier MC, Mealey J Jr et al : Cerebrospinal fluid ascites complicating ventriculoperitoneal shunting. Report of four cases. J Neurosurg 1984; 61: 180-183.   Back to cited text no. 15    
16.Gairi Tahull JM, Costa Clara JM, Garcia-Tornell Florensa S et al : Ventriculo-peritoneal shunt, hypovolemic shock and cerebrospinal fluid ascites. An Esp Pedialr 1984; 21 : 147152.   Back to cited text no. 16    
17.Ohaegbulam SC : Cerebrospinal fluid ascites complicating a ventriculoperitoneal shunt. Int Surg1980; 65 : 455-457.   Back to cited text no. 17    

 

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