Untreated hydrocephalus has a poor natural history, with a death rate of 20% to 25% and severe physical and mental disabilities in survivors. 1,2 This has been significantly altered by cerebrospinal fluid (CSF) shunting. Unfortunately, treatment with CSF shunts is associated with multiple complications. 3 The rate of shunt malfunction in the first year of placement is 40% and thereafter it is about 10% per year. The cumulative risk of infection approaches 20% per patient, although the risk of infection per procedure is only 5% to 8%. 4 The technologic advances in shunt valve designs and materials have had only a marginal impact on the rate of complications. Despite significant advances in our understanding of the pathophysiology of hydrocephalus, the gold standard for treatment remains CSF diversion shunts. Third ventriculostomy has become popular in recent years for the management of obstructive hydrocephalus, but many questions remain about its permanence. Choroid plexectomy 5,6 aimed at arresting hydrocephalus by reducing CSF production and pharmacotherapy, 7 with similar intentions, have had limited success in selected patients.
Hydrocephalus is not a diagnosis that stands alone: it is usually a symptom of infection, intraventricular hemorrhage, congenital malformation, or tumor. As such, the term “hydrocephalus” should be linked to the cause whenever possible. This helps to clarify the physician's thinking with regard to the separation of communicating versus obstructive hydrocephalus. It also allows the physician to assess whether the neurologic deficits seen are consistent with the diagnosis or whether other diagnoses, such as vascular lesions or chronic meningitis from tuberculous infection, need to be entertained.
It is easy to identify patients who would benefit from CSF diversion if the presentation includes clear evidence of increased intracranial pressure (ICP), manifested as severe headaches with projectile vomiting, diplopia, upward gaze paresis, and a dilated ventricular system on radiologic imaging. The most difficult is the evaluation of a child with macrocephaly and normal development. Computed tomography scanning shows increased extraaxial collections, with a normal or mildly enlarged ventricle. This entity, sometimes referred to as benign extraaxial collections of infancy, may be a stage of transient communicating hydrocephalus that may resolve in a period of 12 to 18 months with a normal outcome. 8–10 It is a clinical and not an imaging diagnosis, although some radiologists read films as this entity. It must be distinguished from true communicating hydrocephalus. If the child is developing normally, close observation with neurodevelopmental examination and head circumference measurements are adequate. If the child is neurologically abnormal, then a radionuclide cisternogram plays a role in the evaluating the contribution of abnormal fluid dynamics. It has been used to identify patients with communicating hydrocephalus. 11 A high lumbar pressure, poor 4-hour urinary excretion (normal 50%, borderline 30–40%, definitely abnormal <30%), persistence of ventricular filling at 24 hours, and poor flow over convexity are highly suggestive of communicating hydrocephalus and an indication for CSF diversion. 12
Whenever an extraaxial collection is seen, it is important to distinguish it from a subdural collection, which is frequently associated with nonaccidental trauma from increased subarachnoid spaces in a child. A chronic subdural hematoma by extension to the midline along the convexity may impair the CSF absorption at the arachnoid villi, resulting in secondary communicating hydrocephalus with an increase in the ventricular size and subarachnoid space. The increased signal on T2-weighted image in the subdural space can be separated from the CSF signal in the secondarily enlarged subarachnoid space. 13
No treatment other than CSF diversion has been effective in management of this form of hydrocephalus. Lumbar CSF diversion avoids the potential of brain injury by the ventricular catheter. Lumbar shunts have a lower risk of obstruction and infection 14 but are more prone to malfunction from mechanical failures, 15 and the development of hindbrain herniation over a period of time has been well documented. 16,17 Evaluating a lumbar shunt for function is more cumbersome than a ventricular shunt. We reserve lumbar shunts for patients with communicating hydrocephalus or small slit ventricles and patients who have had multiple ventricular shunt malfunctions.
Three basic types of proximal catheter designs are available: simple with multiple perforations (Codman, Raynham, MA; PS Medical, Goletta, CA), simple flanged (Heyer-Schulte, Plainsboro, NJ), and Anti-Blok (Phoenix BioMed, Valley Forge, PA) with receded perforations. The last two have been designed to minimize the ability of choroid plexus to grow into the perforations, but there have been no results of controlled studies suggesting that these two designs are in any way superior to simple perforations. The flanged catheter would appear to get stuck by the choroid plexus wrapping itself around the flanges, thus making catheter removal difficult 18; however, in our experience this has not always been the case.
Placement of the proximal catheter has generated considerable controversy in the literature. 18–22 More recently, endoscopic placement of the proximal catheter into the frontal horn, away from the choroid plexus, has been advocated to minimize proximal malfunction. 23–25 Again, no controlled study has been performed to assess whether placement of the proximal catheter into the frontal or occipital horn is superior to placement in the body of the lateral ventricle. Often catheters that are grossly malpositioned may continue to work, whereas those that are well positioned may fail. It may be reasonable to attempt placement of the catheter in the most dilated part of the ventricle. The choice of the site, frontal or parietal, may be made on the basis of the above, although some studies have suggested a higher incidence of seizure with catheters placed using a frontal bur hole. 19 Frontal placement may be technically easier for surgeons who do few shunts. A study to evaluate endoscopic placement of shunt is in the analysis phase.
It is now standard practice to use intraluminal coagulation of the choroid plexus, using a stylet and low-voltage diathermy to dislodge a stuck ventricular catheter at the time of shunt revision. 26–28 One should remain vigilant for the presence of a fishmouth catheter placed endoscopically, which would allow the stylet to pass through the catheter and result in inadvertent coagulation of the neural tissue. Massive intraventricular hemorrhage may occur if the choroid plexus is torn while forcefully removing the catheter. Caution is advised when using diathermy for malpositioned proximal catheters that are near the hypothalamus, internal capsule, or a major vascular structure, because injury may occur from the spread of heat during coagulation. Delayed subarachnoid hemorrhage from rupture of pseudoaneurysm resulting from diathermy of a catheter close to anterior cerebral artery has been reported. 29 If the ventricular catheter is severely stuck, sometimes it is advisable to leave it in position but occlude it by a ligature and clip. This may become necessary because sometimes an occluded catheter may become unstuck over time and begin to function partially, resulting in the formation of a subgaleal CSF collection.
Replacing a new catheter into the ventricle in patients with small or slit ventricles is sometimes challenging. In most instances, after removal of the old catheter, the new catheter can be gently passed into the ventricle through the same tract. Frameless stereotaxis is now available and may offer an alternative to cumbersome and time-consuming frame-based stereotactic catheter placement. 24 This technology is likely to reduce significantly the risk of inadvertent neurologic injury from catheter passes in patients with slit ventricles.
Several studies have suggested the development of silicone allergy in some patients with ventricular shunts. 30–34 It is unclear whether this represents a true immunologic reaction or a nonspecific foreign body-type granulomatous reaction. 35 In patients with suspected or documented silicone allergy, the use of polyurethane 31 or more recently CO2 extracted silicone catheters has been postulated but not proven to offer some advantage in reducing the risk of recurrent malfunctions.
There is no evidence to suggest that one type of valve is superior to another, and several valve designs are available on the market (Table 1). A recent multicenter study evaluating three basic types of valves failed to confirm the utility of flow-control or antisiphon valves in children and infants compared with differential pressure valves. 36 Further, over a period of time the ventricle tended to become small, irrespective of the type of valve used. The same study showed that the risk of proximal malfunction in a patient with flow-control valves was 6.5% compared with 42% to 46% with the other two valves, although the overall rates of malfunction and shunt survival were not statistically different. The design of the flow-control valves with a narrow orifice makes it sensitive to malfunction. 37 Certainly, revising a valve has a lower rate of complications and a decreased risk of neurologic injury compared with revising the proximal catheter, especially in patients with slit ventricles. Our experience has also suggested that many patients do not tolerate flow-control valves, and despite a radiologically functioning shunt have high ICP from underdrainage through the valve. In patients with limited pressure-volume compensatory reserve, there can be an excessive increase in ICP during cardiovascular fluctuations, especially at night; this can be responsible for nighttime or early-morning headaches in patients with flow-control devices. 38 Self-adjusting diaphragm valves such as the Orbis-Sigma (NMT, Duluth, GA) on bench testing have proved to be inaccurate and unstable at perfusion rates of 20 to 30 mL/hr, which is the most important physiologic range, leading to prevalve pressures rapidly changing between 5 and 45 cm water. During long-term perfusion, these may resemble ICP waves. 38
Diaphragm-based antisiphon devices are prone to obstruction from encapsulation; this has been shown in experimental animals and often encountered in patients who have had recurrent malfunctions. 39 Some patients are more prone to develop heavy scarring around the shunt system. Again, there is no evidence that using an open system has any advantage over using a closed system, although theoretically malfunctions in an open system would result only in loss of antisiphon function, without obstruction to CSF flow. In the open system, the flow through the valve stops only after the ICP has become negative in the upright position. This is more physiologic than with a closed system, in which the flow stops once the pressure reaches zero. In the multicenter shunt study, the incidence of overdrainage was 7.8% in the closed-system group and 2.6% in the standard valve group. The results suggests that diaphragm-based antisiphon devices may not be superior to differential pressure valves in reducing overdrainage. 36
There is also controversy over the best site for placement of the antisiphon device. 40–45 The classic position is at the level of the skull base; however, bench testing suggest a marked tendency to overdrain if the closed device were below the level of the proximal catheter. 41 These factors may be minor when considered in light of the excessive sensitivity of the closed device to external pressure from scar or when the patient is lying on the device. 37
Standard differential pressure valves are available in different pressure ranges. It is unclear whether using a low-, medium-, or high-pressure valve makes a difference in the ambulatory patient because in the upright position, irrespective of the rating, the hydrostatic column converts all differential pressure valves into “negative”-pressure valves. 46 This also limits the utility of programmable valves, unless they are used in combination with an antisiphon mechanism. Further, the rating of the valve may not match the specifications given by the manufacturer. 38 Slit valves tend to be the most inaccurate in their performance, followed by ball and spring valves. Diaphragm valves proved to be the most stable in long-term tests. Most valves, like the slit valves, ball and spring, and diaphragm valves, offer lower resistance (<2.5 mm Hg/mL/min) than the normal physiologic CSF outflow of 6 to 10 mm Hg/mL/min. Connecting a standard distal tubing of 110 cm increases the overall resistance to 50% to 80% of the physiologic value. 38
A gravity-compensating accessory is used in conjunction with the differential pressure valve to limit overdrainage. 47 It is similar to the horizontal/vertical valve used in lumbar shunts but constructed to fit in-line with a ventriculoperitoneal shunt. There have been no studies assessing its utility, but in individual cases we have found it effective. Experimental evidence suggests that motion and vibration 37 make the mechanism of these devices ineffective, although clinical studies are lacking. The position of the gravity-compensating device is critical for its functioning. Slight angulation of the device to the vertical can cause underdrainage in the horizontal position and overdrainage in the vertical position.
Distal shunt malfunction is reported to occur in 12% to 34% of shunts. 20,22,48 Three types of distal catheters have been used: closed-ended with side slits, open-ended with side slits, and open-ended. A higher incidence of distal catheter obstruction has been noted in catheters with side slits, whether closed-ended or open-ended. 22,49 Omental ingrowth is responsible for the peritoneal catheter obstruction; the distal slits may act as collection points for the debris and provide a channel for trapping the omentum. It is unclear whether using open-ended distal catheters increases the likelihood of small ventricle malfunction. Use of extended-length catheters (110–120 cm) is not associated with an increase in the complication rate and eliminates the need to lengthen the peritoneal catheter for the patient's growth. 50 However, care must be taken to identify patients who may have enough length of tubing in the abdomen but may underdrain because of a narrow and taut segment of tubing from subcutaneous tethering as a result of scarring and calcification.
It is difficult to justify use of the atrial over the peritoneal site for distal absorption. 51–54 Data on 887 patients suggested that atrial shunts have a higher rate of malfunction, although the results of some studies have not shown a significant difference. However, when the same information was stratified by age, shunt type, and time period, there was no significant difference in shunt durability. 51 Cardiopulmonary complications such as irreversible pulmonary hypertension, endocarditis, and glomerulonephritis are some of the more serious complications that may occur with atrial shunts. 52 Alternative sites such as the pleura may result in significant negative pressures in the shunt system. 55 Poor absorption from the pleura may result in large pleural effusions in small children. 55 The gallbladder has also been effectively used in patients in whom peritoneal, atrial, or pleural sites have been exhausted. 56,57 Potential complications of these shunts, notably biliary ventriculitis and biliary meningitis, have been reported. 58,59 A ventriculofemoral shunt in a patient in whom there is difficult access to the atrium from the subclavian or jugular route has been used at some centers. 54 Transdiaphragmatic placement of the distal catheter in the suprahepatic space was successful in one patient with poor peritoneal access as a result of scarring. 60
The subcutaneous location of the distal catheters makes them susceptible to degradation from the foreign body reaction mounted by the body. 61 Scarring around the catheter, calcification, and stress fractures are long-term consequences of this reaction. 62,63 Unless there is some surface degradation, adhesions to the subcutaneous tissues do not occur. 61 Evidence suggests that the barium used in the silicone catheters is probably not an important factor in promoting calcification and degradation, 64 and using barium-free catheters makes it difficult to evaluate a shunt system on radiologic imaging.
To improve the existing shunt systems, it is important to understand the factors that reduce shunt survival. Although the location of the proximal catheter has not been clearly shown to influence shunt survival, 21,22 the presence of a small amount of fluid around the proximal catheter is associated with longer shunt survival. In a study that assessed shunts during an 11-year period, statistically significant differences were noted in shunt survival in patients with tumor versus posthemorrhagic and aqueductal stenosis. Shunts in babies and children were found to survive for a shorter period than in adults. Shunts after multiple revisions survived for a shorter period, and additional shunts placed for isolated ventricles had a shorter survival. 49,65,66 Chronic inflammatory changes of granular ependymitis, often seen at endoscopic shunt placement in patients with multiple revisions, probably contribute to recurrent malfunction and progressive shortening of the interval between revisions as the number of surgeries increase (Fig. 1). 66
The nature of the valve clearly influences the risk of proximal catheter malfunction: it is much lower with flow-control valves. 36,67 Overdrainage from the differential pressure valves pulls choroid plexus toward the proximal catheter and may promote malfunction. 68 However, the increased rate of valve malfunction in flow-control devices balances out this advantage. 36 The development of valves with better dynamics and of methods to reduce choroidal migration and proliferation may help reduce the high rate of shunt malfunctions.
Third ventriculostomy has been recommended during the past few decades for patients with obstructive hydrocephalus. However, there have been no prospective studies showing a statistically improved cure rate. A retrospective analysis of ventriculographic versus endoscopic third ventriculostomy in 213 patients showed the superiority of the endoscopic procedure compared with the ventriculographic procedure in terms of reduced risk and improved survival. 69 Despite the theoretical advantages, the results of several reports and our experience suggest that third ventriculostomy may not be effective in controlling increased ICP. 69,70 Early failures in a radiologically proven case of obstructive hydrocephalus may relate to the multifactorial etiology of hydrocephalus; associated absorption defects, obliteration of the subarachnoid space from longstanding ventricular dilatation, and an unidentified infectious cause of aqueductal stenosis may be responsible. Later failures may relate to gliotic scarring over the ventriculostomy, which has been visually confirmed by endoscope in some patients. It is unclear whether the ventriculostomy closes from scarring or whether it is a secondary response to lack of flow through the ventriculostomy resulting from poor absorption and therefore a lack of gradient between the ventricle and the subarachnoid space. In a small prospective study comparing the shunt failure rate with the failure rate of third ventriculostomy, no statistical difference was found between the two after removing the confounding variables. 71,72 Likewise, no controlled study has compared laser, blunt, or sharp fenestration of the floor or demonstrated the utility of balloon dilatation of the fenestration. The success rate of third ventriculostomy of 49% to 100%, as reported in the literature, may not truly represent the efficacy of the procedure. 71,72 It is difficult to evaluate after third ventriculostomy and to define success in the absence of a documented reduction in ICP or improvement in the results of neuropsychological tests. This is because the ventricles may not reduce in size, and to-and-fro motions through the patent fenestration may still be observed on magnetic resonance imaging cine-flow sequences, even though the patient may be symptomatic.
In the absence of clear evidence from the literature, we continue to advocate third ventriculostomy as the first procedure in patients with obstructive hydrocephalus. However, in early or late failures, we prefer shunting to a repeat fenestration.
About 30% to 40% of shunts malfunction in the first year of placement, and 80% of malfunctions are proximal malfunctions. Although most patients with a malfunctioning shunt have the classic features of increased ICP, headache, and vomiting, in 20% there are no signs of increased ICP. 73 Instead, these patients have subtle change in behavior, a decline in school performance, gait disturbances, and incontinence. Some patients may show aggravation in the signs and symptoms of Chiari malformation or syringomyelia. Parents are often more sensitive to these subtle changes: in a study comparing the accuracy of referral source in diagnosing shunt malfunction, parents were more likely to be correct about the diagnosis compared with a hospital or general practitioner. 74
On examination, a tense fontanelle, split sutures, and swelling at the shunt site strongly suggest a malfunctioning shunt. Shunt pumping has a positive predictive value of only 20%. 75 A shunt valve that fails to fill in 10 minutes strongly suggests shunt malfunction. Radiologic assessment may demonstrate a fracture or dislocation. The presence of double-backing of the distal catheter, wherein the distal catheter tip loops out of the peritoneum through the same spot that it enters it, is diagnostic of distal malfunction. 76 A shunt tap gives useful information about the proximal and distal shunt system. Absence of spontaneous flow and a poor drip rate indicate proximal malfunction; a high opening pressure suggests distal malfunction. 77 Increased size of the ventricles on computed tomography confirms a malfunctioning shunt, but many patients with longstanding shunt have altered brain compliance and may not show dilation of the ventricles at presentation (Fig. 2). In children, similar symptoms that occur in common illnesses such as otitis media and gastroenteritis of viral fevers often confound the diagnosis. Radiologic assessment of shunt flow using radionuclide or iodide contrast injected into the shunt may help. 78–83 Unfortunately, although some studies have shown an accuracy of 99% with combined pressure and radionuclide evaluation, 79,80 others have shown a 25% to 40% incidence of deceptive patency when evaluated by radionuclide cisternography. 82,83 This could stem from an inadequately functioning shunt, intermittent malfunction, or the presence of an isolated ventricle. Similar problems are encountered with iodide contrast-based shuntograms or shunt injection tests. In the absence of normative data with regard to adequate flow in the shunt, which may vary significantly with the patient, the time of day, and the activity, 84 the use of Doppler-based flow devices or magnetic resonance imaging-based flow systems becomes irrelevant for an individual patient. Lumbar infusion tests and shunt infusion tests to assess the outflow resistance through the shunt are cumbersome and require a laboratory-based set-up; this may not be possible in an emergency department setting. 85–87 Infusion through a reservoir to assess outflow resistance through the shunt suggests a cutoff of less than 12 Hg/mL/min as reliable for distinguishing patients with a clinically suspected high probability of malfunction from those with a low probability of shunt malfunction. 87 However, this is the group of patients who may not really need the test, and patients who have a questionable malfunction on clinical grounds often have equivocal results on the infusion study.
In patients with normal or decreased brain compliance, ICP is the only accurate guide to shunt function other than symptoms. 88 Again, the ability to measure ICP through the valve tap becomes unreliable with a partial proximal malfunction. A similar problem may be encountered with in-line telemetric ICP monitors. 89,90 In addition, telemetric transducers may develop a significant drift over time. In difficult cases, the only way to resolve the issue may be to explore the shunt, measure ICP through a lumbar puncture if the patient has communicating hydrocephalus, or place an ICP monitor. For patients who have a very compliant brain, ventricular dilation on the computed tomography scan easily confirms inadequate shunt function.
1. Foltz EL, Shurtleff DB. Five-year comparative study of hydrocephalus
in children with and without operation (113 cases). J Neurosurg 1963; 20:1064–79.
2. Laurence KM, Coates S. Further thoughts on the natural history of hydrocephalus
. Dev Med Child Neurol
3. Walters BC, Hoffman HJ, Hendrick EB, Humphrey RP. Cerebrospinal fluid shunt infection. J Neurosurg 1984; 60:1014–21.
4. Epstein F. How to keep shunts functioning, or “the impossible dream.” Clin Neurosurg 1985; 32:608–31.
5. Weiss MH, Nulsen FE, Kaufmann B. Selective radionecrosis of the choroid plexus for control of experimental hydrocephalus
. J Neurosurg 1972; 36:270.
6. Pople IK, Ettles D. The role of endoscopic choroid plexus coagulation in the mangement of hydrocephalus
. Neurosurgery 1995; 36:638.
7. Greitz D, Dreitz T, Hindmarsh T. A new view on the CSF circulation with the potential for pharmacological treatment of childhood hydrocephalus
. Acta Pediatr 1997; 86:125–32.
8. Pettit RE, Kilroy AW, Allen JH. Macrocephaly with head growth parallel to normal growth pattern. Neurological, developmental and computerized tomography findings in full-term infants. Arch Neurol 1980; 37:518–21.
9. Ment LR, Duncan CC, Geehr JR. Benign enlargement of the subarachnoid spaces in the infant. J Neurosurg 1981; 54:504–8.
10. Andersson H, Elfverson J, Svendsen P. External hydrocephalus
in infants. Child Brain 1984; 11:398–402.
11. Robertson Jr, WC Gomez MR. External hydrocephalus
. Early finding in congenital communicating hydrocephalus
. Arch Neurol 1978; 35:541–4.
12. Velardi F, Hoffman H, Ash JM, et al. The value of CSF flow studies in infants with communicating hydrocephalus
. Child Nerv Syst 1986; 2:139–43.
13. Aoki N. Extracerebral fluid collection in infancy. The role of magnetic resonance imaging in differentiation between subdural effusion and enlarged subarachnoid spaces. J Neurosurg 1994; 81:20–3.
14. Aoki N. Lumboperitoneal shunt: clinical applications, complications, and comparison with ventriculoperitoneal shunt. Neurosurgery 1990; 26:998–1003.
15. Selman WR, Spetzler RF, Wilson CB, Grollmus JW. Percutaneous lumboperitoneal shunt: review of 130 cases. Neurosurgery 1980; 6:255–7.
16. Chumas PD, Armstrong DC, Drake JM, et al. Tonsillar herniation: the rule rather than exception after lumboperitoneal shunting in pediatric population. J Neurosurg 1993; 78:568–73.
17. Payner TD, Prenger E, Berger TS, Crone KR. Acquired Chiari malformation: incidence, diagnosis, and management. Neurosurgery 1994; 34:429–34.
18. Ausman J. Shunts: which one, and why. Surg Neurol 1998; 49:8–13.
19. Albright AL, Haines SJ, Taylor FH. Function of parietal and frontal shunts in childhood hydrocephalus
. J Neurosurg 1988; 69:883.
20. Sainte-Rosa C, Hoffman HJ, Hirsch JF. Shunt failure. Concepts Pediatr Neurosurg 1989; 9:7.
21. Bierbrauer KS, Storrs BB, McLone DG, et al. Prospective randomized study of shunt function and infection as a function of shunt placement. Pediatr Neurosurg 1990; 16:287.
22. Sainte-Rosa C, Piatt JH, Renier D, et al. Mechanical complications in shunts. Pediatr Neurosurg 1991; 17:2–9.
23. Yamamoto M, Oka K, Nagasaka S, Tomonaga M. Ventriculoscope-guided ventriculoperitoneal shunt and shunt revision. Technical note. Acta Neurochir 1994; 129:85–8.
24. Pang D, Grabb PA. Accurate placement of coronal ventricular catheter using stereotactic-guided free hand passage. Technical note. J Neurosurg 1994; 80:750–4.
25. Nulsen FE, Becker DP. Control of hydrocephalus
by valve-regulated shunt. J Neurosurg 1967; 26:362.
26. Steinbok P, Cochrane DD. Removal of adherent ventricular catheter. Pediatr Neurosurg 1992; 18:167–8.
27. Whitfield PC, Guazzo EP, Pickard JD. Safe removal of retained ventricular catheters using intraluminal choroid plexus coagulation. Technical note. J Neurosurg 1995; 83:1101–2.
28. Martinez-Lage JF, Lopez F, Poza M. Hernandez M. Prevention of intraventricular hemorrhage during CSF shunt revisions by means of a flexible coagulating electrode. A preliminary report. Child Nerv Syst 1998; 14:203–6.
29. Handler MH. A complication in removing retained ventricular catheter using electrocautery. Pediatr Neurosurg 1996; 25:276.
30. Goldblum RM, Pelley RP, O'Donell AA, et al. Antibodies to silicone elastomers and reactions to ventriculoperitobeal shunts. Lancet 1992; 340:510–3.
31. Jimenez DF, Keating R, Goodrich JT. Silicone allergy in ventriculoperitoneal shunts. Child Nerv Syst 1994; 10:59–63.
32. Gowers DJ, Lewis JC, Kelly Jr. DL Sterile shunt malfunction
: a scanning electron microscopic perspective. J Neurosurg 1984; 61:1079–84.
33. Snow RB, Kossovsky N. Hypersensitivity reaction associated with sterile ventriculoperitoneal shunt malfunction
. Surg Neurol 1989; 31:209–14.
34. Sugar O, Bailey O. Subcutaneous reaction to silicone in ventriculoperitoneal shunts: long-term results. J Neurosurg 1974; 41:367–71.
35. Kalousdian S, Karlan MS, Williams MA. Silicone elastomer cerebrospinal fluid shunt systems. Neurosurgery 1998; 42:887–92.
36. Drake JM, Kestle JRW, Milner R, et al. Randomized trial of cerebrospinal fluid shunt valve design in pediatric hydrocephalus
. Neurosurgery 1998; 43:294–305.
37. Aschoff A, Kremer P, Benesch C, et al. Overdrainage and shunt technology. Child Nerv Syst 1995; 11:193–202.
38. Czosnyka M, Czosnyka Z, Whitehouse H, Pickard JD. Hydrodynamic properties of hydrocephalus
shunts: United Kingdom Shunt Evaluation Laboratory. J Neurol Neurosurg Psychiatr 1997; 62:43–50.
39. Drake JM, da Silva MC, Rutka JT. Functional obstruction of an antisiphon device by raised tissue capsule pressure. Neurosurgery 1993; 32:137–9.
40. Chapman PH. Optimum position of the antisiphon device. Neurosurgery 1990; 27:332–4.
41. Chiba Y, Tokoro K, Abe H. Importance of anti-siphon devices in shunt therapy of pediatric and adoloscent hydrocephalus
. In: Matsumoto S, Tamaki N, eds. Hydrocephalus
. Pathogenesis and Treatment. Berlin: Springer; 1991:375–82.
42. Fox JD, Portnoy HD, Schulte RR. Cerebrospinal fluid shunts: an experimental evaluation of flow rates and pressure values in the anti-siphon valve. Surg Neurol 1973; 1:299–302.
43. Portnoy HD. Optimum position of the anti-siphon device [letter]. Neurosurgery 1990; 27:332–3.
44. Pudenz RH. Optimum position of the anti-siphon device [letter]. Neurosurgery 1990; 27:333.
45. Tokoko K, Chiba Y. Optimum position for an anti-siphon device in cerebrospinal fluid shunt system. Neurosurgery 1991; 29:519–25.
46. Trost HA. Is there a reasonable differential indication for different hydrocephalus
shunt systems? Child Nerv Syst 1995; 11:189–92.
47. Chabbra DK, Agarwal GD, Mittal P. Z-flow hydrocephalus
shunts, a new approach to the problem of hydrocephalus
, the rationale behind its design and the initial results of pressure monitoring after Z-flow shunt implantation. Acta Neurochir 1993; 121:43–7.
48. Sekhar LN, Moosy J, Guthkelch AN. Malfunctioning ventriculoperitoneal shunts. Clinical and pathological features. J Neurosurg 1982; 56:411–6.
49. Cozzens JW, Chandler JP. Increased risk of distal ventriculoperitoneal shunt obstruction associated with slit valves or distal slits in the peritoneal catheter. J Neurosurg 1997; 87:682–6.
50. Couldwell WT, LeMay DR, McComb JG. Experience with use of extended length peritoneal catheters. J Neurosurg 1996; 85:425–7.
51. Borgbjerg BM, Gjerris F, Albeck MJ, et al. A comparison between ventriculoperitoneal and ventricoatrial cerebrospinal fluid shunts in relation to the rate of revision and durability. Acta Neurochir (Wien) 1998; 140:459–65.
52. Lam CH, Villemure JG. Comparison between ventriculoatrial and ventriculoperitoneal shunting in the adult population. Br J Neurosurg 1997; 11:43–8.
53. Jones RF, Currie BG, Kwok BC. Ventriculopleural shunts for hydrocephalus
: a useful alternative. Neurosurgery 1988; 23:753–5.
54. Philips MF, Schwartz SB, Soutter AD, Sutton LN. Ventriculofemoroatrial shunt. J Neurosurg 1997; 86:1063–6.
55. Willison CD, Kopitnik TA, Gustafson R, Kaufmann HH. Ventriculopleural shunting used as a temporary alternative. Acta Neurochir 1992; 115:67–8.
56. Ketoff JA, Klein RL, Maukkassa KF. Ventricular cholecystic shunts in children. J Pediatr Surg 1997; 32:181–3.
57. Novelli PM, Reigel DH. A closer look at the ventriculo-gallbladder shunts for the treatment of hydrocephalus
. Pediatr Neurosurg 1997; 26:197–9.
58. Bernstein RA, Hseuh W. Ventriculocholecystic shunt. A mortality report. Surg Neurol 1985; 23:31–7.
59. Barami K, Sood S, Ham SD, Canady AI. Chemical meningitis from bile reflux in a lumbar-gallbladder shunt. Pediatr Neurosurg 1999; 29:328–30.
60. Rengachary SS. Transdiaphragmatic ventriculoperitoneal shunting: technical case report. Neurosurgery 1997; 41:695–7.
61. Del Bigio MR. Biological reaction to cerebrospinal fluid shunt devices. Neurosurgery 1998; 42:319–26.
62. Echizenya K, Satoh M, Murai H, et al. Mineralization and biodegradation of CSF shunting systems. J Neurosurg 1987; 67:584–619.
63. Elisevich K, Mattar AG, Cheeseman F. Biodegradation of distal shunt catheters. Pediatr Neurosurg 1994; 21:71–6.
64. Irving I, Castilla P, Hall EG, Rickham PP. Tissue reaction to pure and impregnated Silastic. J Pediatr Surg 1971; 6:724–9.
65. Jamjoom AB, Jamjoom ZAB, Rahman N. Low rate of shunt revision in tumoral obstructive hydrocephalus
. Acta Neurochir 1998; 140:595–7.
66. Lazareff JA, Peacock W, Holly L, et al. Multiple shunt revisions: an analysis of relevant factors. Child Nerv Syst 1998; 14:271–5.
67. Decq P, Barat JL, Duplesis E, et al. Shunt failure in adult hydrocephalus
. Surg Neurol 1995; 43:333–9.
68. Hakim S. Observations on the physiopathology of CSF pulse and prevention of ventricular catheter obstruction in valve shunts. Dev Med Child Neurol Suppl 1969; 20:42–8.
69. Cinalli G, Sainte Rosa C, Chumas P, et al. Failure of third ventriculostomy
in the treatment of hydrocephalus
. J Neurosurg 1999; 90:448–54.
70. Hirsch JF, Hirsch E, Sainte Rosa C. Stenosis of aqueduct of Sylvius. Etiology and treatment. J Neurosurg Sci 1986; 30:29–39.
71. Tuli S, Alshail E, Drake J. Third ventriculostomy
versus cerebrospinal fluid shunt as a first procedure in pediatric hydrocephalus
. Pediatr Neurosurg 1999; 30:11–5.
72. Sainte Rosa C. Third ventriculostomy
. In: Manwaring KH, Crone KR, eds. Neuroendoscopy.
Vol. 1. New York: Mary Ann Liebert; 1992:47–62.
73. Fried A, Shapiro K. Subtle deterioration in shunted childhood hydrocephalus
. J Neurosurg 1986; 65:211–6.
74. Lawrence W, Hayward R, Andar U, Harkness W. The diagnosis of blocked cerebrospinal fluid shunts: a prospective study of referral to a pediatric neurosurgical unit. Child Nerv Syst 1994; 10:87–90.
75. Piatt Jr. JH Physical examination of patients with cerebrospinal fluid shunts: is there useful information in pumping the shunt? Pediatrics 1992; 89:470–3.
76. Martinez-Lage JF, Poza M, Izura V. Retrograde migration of the abdominal catheter as a complication of ventriculoperitoneal shunt: the fishhook sign. Child Nerv Syst 1993; 9:425–7.
77. Sood S, Kim S, Ham SD, et al. Useful components of shunt tap test for evaluation of shunt malfunction
. Child Nerv Syst 1993; 9:157–62.
78. Sweeney LE, Thomas PS. Contrast examination of cerebrospinal fluid shunt malfunction
in infancy and childhood. Pediatr Radiol 1987; 17:177–83.
79. Savoiardo M, Solero CL, Passerini A, Migliavacca F. Determination of cerebrospinal fluid shunt function with water-soluble contrast media. J Neurosurg 1978; 49:398–407.
80. Hayden PW, Rudd TG, Shurtleff DB. Combined pressure/radionuclide evaluation of suspected cerebrospinal fluid shunt malfunction
: a seven-year clinical experience. Pediatrics 1980; 66:679–83.
81. Graham P, Howman Giles P, Johnston I, Besser M. Evaluation of CSF shunt patency by means of technetium-99m DTPA. J Neurosurg 1982; 57:262–6.
82. French BN, Swanson M. Radionuclide imaging shuntography for evaluation of shunt patency. Surg Neurol 1981; 16:173–82.
83. Vernet O, Farmer JP, Lambert R, Montes JL. Radionuclide shuntogram: adjunct to manage hydrocephalic patients. J Nucl Med 1996; 37:406–10.
84. Kadowaski C, Hara M, Numato M, et al. CSF shunt physics: factors influencing in-shunt CSF flow. Child Nerv Syst 1995; 11:203–6.
85. Woodford J, Saunders RL, Sachs Jr. E Shunt system patency testing by lumbar infusion. J Neurosurg 1976; 45:60–5.
86. Czosnyka M, Whitehouse H, Smielewski P, et al. Testing of cerebrospinal compensatory reserve in shunted and non-shunted patients: a guide to interpretation based on an observational study. J Neurol Neurosurg Psychiatr 1996; 60:549–58.
87. Morgan MK, Johnston IH, Spittler PJ. A ventricular infusion technique for evaluation of treated and untreated hydrocephalus
. Neurosurgery 1991; 29:832–7.
88. Fouyas IP, Casey TH, Thompson D, et al. Use of intracranial pressure monitoring in the management of childhood hydrocephalus
and shunt related problems. Neurosurgery 1996; 38:726–32.
89. Cosman ER, Zervas NT, Chapman PH, et al. A telemetric pressor sensor for ventricular shunt
systems. Surg Neurol 1979; 11:287–94.
90. Miyake H, Ohta T, Kajimoto Y, Matsukawa M. A new ventriculoperitoneal shunt with a telemetric intracranial pressure sensor: clinical experience in 94 patients with hydrocephalus
. Neurosurgery 1997; 40:931–5.