N e u r o r a d i o l o g y / H e a d a n d N e c k I m a g i n g • R ev i ew Wallace et al. Imaging Evaluation of CSF Shunts

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Neuroradiology/Head and Neck Imaging Review

Adam N. Wallace1 Jonathan McConathy Christine O. Menias Sanjeev Bhalla Franz J. Wippold II Wallace AN, McConathy J, Menias CO, Bhalla S, Wippold FJ II

Imaging Evaluation of CSF Shunts OBJECTIVE. The objective of this article is to describe an approach to imaging CSF shunts. Topics reviewed include the components and imaging appearances of the most common types of shunts and the utility of different imaging modalities for the evaluation of shunt failure. Complications discussed include mechanical failure, infection, ventricular loculation, overdrainage, and unique complications related to each shunt type. CONCLUSION. This article reviews the imaging features of common CSF shunts and related complications with which radiologists should be familiar.

M

ore than 40,000 CSF shunts are placed annually in the United States, the majority of which are for the treatment of hydrocephalus [1]. Shunt failure occurs in 40–50% of patients during the first 2 years after shunt surgery [2]. The diagnosis is initially suspected on the basis of history and physical examination findings of increased intracranial pressure; however, imaging often confirms the diagnosis and reveals the underlying cause. Therefore, radiologists should be familiar with the radiologic manifestations of shunt malfunction and complications.

Keywords: CSF shunt complications, hydrocephalus, pseudocyst, ventriculoatrial shunts, ventriculoperitoneal shunts, ventriculopleural shunts DOI:10.2214/AJR.12.10270 Received November 6, 2012; accepted after revision February 4, 2013. 1

All authors: Mallinckrodt Institute of Radiology, 510 S Kingshighway Blvd, St. Louis, MO 63110. Address correspondence to A. N. Wallace ([email protected]).

This article is available for credit. AJR 2014; 202:38–53 0361–803X/14/2021–38 © American Roentgen Ray Society

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Shunt Types The basic components of a CSF shunt include a proximal catheter, reservoir, valve, and distal catheter. The proximal catheter tip is ideally positioned in the frontal horn of either lateral ventricle, anterior to the foramen of Monro away from the choroid plexus [3] (Fig. 1). The proximal catheter exits through a burr hole to connect to a reservoir in the subcutaneous tissues, through which CSF may be sampled and intraventricular pressure measurements obtained. Flow into the distal catheter is regulated by a one-way valve [4], which often contains magnets that enable transcutaneous valve pressure adjustment [5]. The distal catheter can be tunneled subcutaneously to drain into, theoretically, any body cavity capable of fluid resorption. Modern shunts are most commonly placed in the peritoneum, right atrium, or pleural space. Ventriculoperitoneal shunts are pre-

ferred by most neurosurgeons because of fewer complications and the relative ease of peritoneal access [6]. Intraabdominal pathology, such as peritoneal adhesions or recurrent peritonitis, necessitates placement or relocation to an alternative drainage site [5]. Ventriculoatrial shunts are generally preferred when ventriculoperitoneal shunting is contraindicated. The right atrium is typically accessed percutaneously via the facial, subclavian, or internal jugular vein [7], and proper placement may be ensured with the use of real-time transesophageal echocardiography [8]. The primary disadvantage of ventriculoatrial shunts is the risk of serious intravascular complications [9–11]. Ventriculopleural shunts are rarely used for long-term shunting because of the high incidence of hydrothorax [12]. The most common uses are temporary CSF drainage during management of ventriculoperitoneal or ventriculoatrial shunt infection and decompression of acute hydrocephalus before removal of an obstructing tumor [13]. Evaluation of Shunt Malfunction The incidence of ventriculoperitoneal shunt failure ranges from 25% to 40% at 1 year and 63% to 70% at 10 years [14]. Failure rates with ventriculoatrial and ventriculopleural shunts are slightly higher [15]. Patient presentation varies depending on patient age as well as the cause and acuity of failure [6]. Symptoms with the highest positive predictive value include nausea and vomiting and decreased level of consciousness [16]. Seizures,

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Imaging Evaluation of CSF Shunts diplopia, and weakness are less frequent presentations [17]. Neurologic examination may show papilledema, focal deficits, hyperactive reflexes, and ataxia [6]. In children, a bulging fontanelle or splaying of the cranial sutures may be observed [6]. The initial study for evaluating the size of the ventricles, shunt location, and integrity of the visualized components varies by institution. Unenhanced CT is a common choice but exposes the patient to ionizing radiation. Low-dose shunt protocols, which reduce tube current, result in suboptimal image quality compared with standard-dose CT but are diagnostically acceptable in the evaluation of shunt failure [18]. Ventricular enlargement may be subtle and comparison with prior examinations is mandatory; however, the shunt may fail without definite ventriculomegaly. Secondary signs of acute shunt failure that may be helpful in equivocal cases include transependymal flow of CSF, edema adjacent to the catheter, and subgaleal fluid collections [19] (Fig. 1). MRI shows similar findings and is being increasingly used to minimize radiation exposure [20]. In some institutions, single-shot T2-weighted MRI is the initial imaging modality of choice in suspected shunt failure. Significant MRI-induced heating has not been shown to be an issue with modern shunt valves. However, programmable shunt valves are adjusted with an external magnet. Changes in the valve-pressure setting have occurred after exposure of programmable valves to an MRI magnetic field [21]. Before performing MRI on a patient with a programmable shunt, the radiologist must confirm that the shunt is resistant to reprogramming at the magnetic field strength of the scanner. Newer valves such as the Polaris (Sophysa) and ProGAV (Aesculap) are resistant to reprogramming even at a 3-T magnetic field. If an unfamiliar valve is encountered, the radiologist should contact the manufacturer for specific MRI safety guidelines. After scanning, the neurosurgeon will frequently check whether the valve pressure setting has changed using a compass provided by the manufacturer [4]. Conventional radiography is primarily performed to evaluate for breaks, disconnections, or distal catheter migration. A typical series includes frontal and lateral radiography of the head and neck and frontal radiography of the chest and abdomen (Figs. 2 and 3). The goal is simply to include the entire course of the shunt. Evaluation of the intraperitoneal catheter may be difficult in obese patients in whom

image contrast is degraded both by photon scatter and the increased peak kilovoltage required to penetrate the soft tissues. Image quality may be further degraded by longer exposure times, which increase the likelihood of motion artifact. A potential solution is to obtain separate radiographs of each abdominal quadrant. The reduced FOV decreases image noise, which improves diagnostic quality; however, a keen eye is needed to follow the course of the catheter across multiple radiographs. Intraperitoneal catheters can also be evaluated with ultrasound or CT, the former being preferred in children because of the absence of radiation. Radionuclide CSF shunt studies can evaluate shunt patency, differentiate proximal versus distal limb obstruction, and in some cases show the site of obstruction where activity fails to progress through the system (Fig. 4). In fact, the combination of CT and radionuclide imaging is more sensitive than CT alone in diagnosing shunt malfunction [22]. A small amount of 99mTc-pentetate or pertechnetate (0.25–1.5 mCi) is typically injected into the shunt reservoir with the patient supine. Care must be taken to ensure that the radiopharmaceutical is suitable for intrathecal injection because the sensitivity to endotoxin effects is higher for intrathecal injections compared with IV injections. To maintain physiologic conditions, small volumes (≤ 0.4 mL) should be injected, the syringe should not be flushed, and local pressure at the injection site should be avoided. In addition, CSF should not be aspirated before injection because this may cause CSF pressure to drop below the valve opening pressure and produce a false-positive obstruction. Immediately after the injection, dynamic imaging is performed for up to 30 minutes, typically using 30 seconds per frame. Activity should progressively accumulate along the length of the catheter and disperse quickly at the distal drainage site. Depending on the type of valve, radionuclide may also reflux into the ventricular system. If flow is absent or sluggish when the patient is supine, the patient should be placed in the upright position to determine whether flow is enhanced by an increase in the hydrostatic pressure gradient. If flow is not seen with the patient in the upright position, mechanical means (i.e., pumping the reservoir) can be used to further assess patency. Activity that remains localized at the injection site indicates either obstruction or dose extravasation (Fig. 4). The latter is excluded by imaging the chest and abdomen for evidence of systemic absorption.

Mechanical Complications Obstruction Within the first 2 years after shunt placement, obstruction of the proximal catheter accounts for 50% of all failures, and distal blockages account for 14% [23]. The risk of obstruction is highest during the early postoperative period because of debris and blood products; however, obstruction can occur at any time after shunt placement, approaching a rate of 0.5% per month [19]. Obstruction can be caused anywhere along the course of the catheter by kinking of the tubing [6] (Fig. 5). The most common cause of proximal obstruction is occlusion of the ventricular catheter tip by ingrowth of choroid plexus and particulate debris or blood products in the shunt valve [24]. Radionuclide imaging will show failure of activity progression beyond the site of obstruction (Fig. 4). The proximal catheter can also migrate within the ventricle into a position where CSF does not drain properly. This is most commonly caused by tethering of the distal catheter by scar tissue along the chest wall or the peritoneal entry site [6]. Diagnosis is made by comparing postoperative catheter placement on CT and conventional radiographs with images obtained when the patient is symptomatic. Pseudocyst formation is a common cause of distal catheter obstruction. Pseudocysts are loculated collections of CSF that form around the terminal end of the catheter. In patients with ventriculoperitoneal shunts, pseudocysts are caused by peritoneal adhesions or migration of the greater omentum over the shunt tip [25]. Pseudocysts can also develop around ventriculopleural shunts due to adhesions caused by chronic pleural irritation. Conventional radiography may show coiling of the distal catheter within an intraabdominal soft-tissue mass or loculated pleural effusion. Definitive diagnosis can be made by CT or ultrasound showing a loculated fluid collection surrounding the catheter tip. Alternatively, radionuclide imaging will show localized activity around the catheter tip (Figs. 6 and 7). Treatment entails externalization of the catheter and drainage of the pseudocyst. If the fluid is sterile, the existing shunt is reimplanted or converted to a different site [26]. Infected pseudocysts require shunt removal, external ventricular drain placement, and antibiotics [2]. Other causes of distal obstruction include catheter migration or erosion into soft tissues. Children with ventriculoperitoneal shunts are at greater risk for distal catheter migration because of redundancy of the intraperitoneal catheter to allow for future growth of the child [19]

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Wallace et al. (Figs. 3 and 8). Erosion into a hollow viscous can present acutely with signs and symptoms of peritonitis or indolently with migration of the catheter to any location in the genitourinary or gastrointestinal tract [27]. Shunted CSF increases intraperitoneal pressure that can dilate inguinal hernias and patent vaginal processes allowing catheter migration into the scrotum [28] (Fig. 9). The catheter may also erode into solid organs, such as the liver, or into the abdominal wall [25] (Figs. 10 and 11). Rarely, the catheter may encircle the bowel, causing mechanical obstruction [25] (Fig. 12). Intrathoracic migration of the distal ventriculoperitoneal catheter into the pleural space, heart, and pulmonary arteries is rare but well documented [29, 30]. The course of the catheter into the pleural space may be supradiaphragmatic because of incorrect subcutaneous tunneling or transdiaphragmatic via a congenital diaphragmatic defect, foramen of Bochdalek, foramen of Morgagni, esophageal hiatus, or diaphragmatic perforation [31, 32]. Complications of intrathoracic migration include CSF hydrothorax or pneumothorax with tension physiology, bronchial perforation, or pneumonia [33, 34]. Proposed mechanisms of intracardiac migration include unintentional transvenous placement of the shunt [29, 30] and suction of the catheter into the heart by negative inspiratory pressures [35]. Unlike ventriculoperitoneal shunts, the length of the distal ventriculoatrial catheter cannot be initially redundant to allow for growth of the child because the excess tubing would impinge on the atrial wall [25]. Consequently, as the patient grows, the catheter tip often rises into the superior vena cava, which is suboptimal for CSF drainage [36]. If shunt malfunction occurs, surgical lengthening of the distal catheter is necessary. In some cases, surgical lengthening is performed prophylactically [37]. Failure of ventriculoatrial shunts may be caused by migration within the right atrium or through a patent foramen ovale to a position where drainage is impaired [11]. Erosion of the distal catheter tip through the free wall of the right ventricle into the pericardial space has been reported, resulting in massive CSF pericardial effusion and lifethreatening cardiac tamponade [38]. Erosion through the interatrial septum creates a conduit for paradoxical emboli [39]. There are few reports of distal ventriculopleural catheter migration, possibly because of the relative infrequency of use. Erosion of a ventriculopleural shunt into the chest wall resulting in subcutaneous edema and shunt malfunction has been reported [40]. 40

Disconnection and Fracture Disconnection most commonly occurs shortly after shunt placement [3]. Material defects or surgical error are generally responsible [6]. CSF accumulation under the skin at the site of disconnection may be visible on CT. Shunt radiographs readily show a gap between the proximal catheter and the reservoir or the valve and the distal catheter. It is important to note that some valves and connectors are radiolucent and can be mistaken for disconnection. The tubing proximal and distal to a radiolucent connector is linearly aligned, whereas the tubing proximal and distal to a disconnection may be angulated. Comparison with previous radiographs is also helpful in making the distinction [19] (Fig. 8). Years of biomechanical stress coupled with calcification and biodegradation may cause the catheter to fracture [19]. Breaks most commonly occur in the neck region where the catheter is most mobile. This complication is more common in older children due to tethering of the catheter by scar tissue with distraction as the child grows [41–43]. Patients often do not develop symptoms immediately because scar tissue encasing the catheter temporarily acts as a conduit between the catheter fragments [6]. As with disconnection, a palpable subcutaneous collection of CSF may form at the fracture site. Shunt radiography is most sensitive for showing discontinuity of the catheter and migration of the distal fragment (Fig. 8). The distal fragment of ventriculoperitoneal shunts may coil completely in the peritoneum [6]. Migration of the distal fragment of ventriculoatrial shunts is obviously more dangerous because the catheter can lodge in the right atrium causing arrhythmia or embolize to the pulmonary vasculature [44] (Fig. 13). Infection Shunt infection most commonly occurs within 6 months of placement due to intraoperative contamination with skin flora, such as Staphylococcus aureus and Staphylococcus epidermidis [6]. The intracranial catheter may also be seeded in the setting of bacterial meningitis [45]. The incidence of infection of ventriculoperitoneal shunts was approximately 8–10% in large trials [46]. Infection may be evidenced by wound infection, fever, shunt malfunction, or peritonitis [47]. Ventriculoatrial shunts are associated with a similar incidence of infection; however, endocarditis and septic emboli result in higher morbidity and mortality [48] (Fig. 14). Similarly, infection of ventriculopleural shunts may result in empyema [49].

Positive blood cultures are common with infected ventriculoatrial shunts but are often negative with other shunt types [50]. Cultures of CSF aspirated from the shunt reservoir have the highest yield [51]. CT and MRI show irregular leptomeningeal and ventricular ependymal enhancement consistent with meningitis and ventriculitis, respectively (Fig. 15). However, pachymeningeal enhancement can normally persist postoperatively for months and should not be confused with a sign of infection [52]. Debris within the ventricles, especially on diffusion-weighted imaging, is the best sign of ventriculitis. Patients with ventriculoatrial shunts are also at risk for a unique infectious complication termed “shunt nephritis.” Chronic infection of the ventriculoatrial shunt catheter activates the complement system resulting in glomerular deposition of immune complexes [53]. The most common causal organisms are S. aureus and S. epidermidis, which account for 70% and 20% of cases, respectively [54]. Only 51% of patients recover full kidney function [6]. Although shunt nephritis is most common within the first few years of shunt placement, one documented case occurred 17 years after surgery [55]. Ultrasound will show nonspecific findings of interstitial nephritis, including increased renal size and echogenicity. Ventricular Loculations Ventricular loculations create noncommunicating pockets of CSF. Therefore, a single shunt does not drain the entire ventricular system. Over time, loculations that do not communicate with the shunted ventricular segment enlarge and produce symptoms of hydrocephalus [56]. Such loculations may be congenital or acquired after prior intraventricular hemorrhage or ventriculitis. MRI best delineates the anatomy of the loculations and may show transependymal flow adjacent to isolated locules. Definitive diagnosis can be made by injecting a contrast agent, such as iohexol dye, into the ventricular system through an extraventricular device. After 30–60 minutes, the dye will fail to diffuse into isolated loculations or become sequestered in a specific locule [2, 6]. This is managed by fenestrating the locules or placement of a complex-system ventriculoperitoneal shunt with multiple ventriculostomy catheters (Fig. 16). A trapped fourth ventricle occurs when loculations isolate the fourth ventricle from the shunted lateral ventricle. The two causes are scarring of the cerebral aqueduct, the foramina of Magendie, and the foramen of AJR:202, January 2014

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Imaging Evaluation of CSF Shunts Luschka and secondary closure of the Sylvian aqueduct induced by the shunt itself [57]. The expanding fourth ventricle produces symptoms of increased intracranial pressure and brainstem compression. Imaging shows normal or small lateral ventricles and an enlarged fourth ventricle exerting mass effect on the brainstem (Fig. 17). Sagittal MRI is particularly useful at showing occlusion of the cerebral aqueduct [19]. Placement of a second ventriculostomy catheter in the fourth ventricle is necessary to relieve the pressure. Overdrainage and Slit Ventricle Syndrome Ventricular size returns to normal within 24 hours of shunt placement, with more gradual reduction depending on the cause and chronicity of hydrocephalus [19]. However, if the lateral ventricles collapse too rapidly, the brain may not be elastic enough to fill the space. The resulting disparity between the sizes of the brain and calvarium leads to formation of a subdural hygroma or hematoma [19] (Fig. 18). Most cases are asymptomatic and resolve without intervention; however, large collections can cause increased intracranial pressure [3]. Furthermore, patients who develop subdural effusions after shunting are at increased risk for acute subdural hematoma after minor head trauma [58, 59]. The acute drop in supratentorial pressure can also cause transtentorial herniation of the cerebellum through the incisura. Chronic overdrainage is common, with small slitlike ventricles seen in up to 50% of children with shunts [60] (Fig. 19). Slitlike ventricles are more common with ventriculoperitoneal than ventriculoatrial shunts [61]. Chronic overdrainage is partially due to a siphoning effect at the catheter terminus [62]. When patients are upright, the catheter tip is below the level of the ventricles. As a result, gravity siphons CSF from the ventricular system, even at low intracranial pressures. Slitlike ventricles are less common in patients with ventriculoatrial shunts because of the greater siphoning effect of ventriculoperitoneal shunts [61]. Although slitlike ventricles are usually clinically insignificant, the finding should be reported because of a phenomenon called “slitventricle syndrome.” There are many competing definitions in the literature; however, slitventricle syndrome most commonly refers to symptoms of intermittent intracranial hypertension without ventricular dilatation [62]. Overdrainage collapses the lateral ventricle, causing functional catheter obstruction. Nor-

mally, the increased intraventricular pressure would dilate the ventricles and relieve the obstruction. However, chronic overdrainage causes noncompliant ventricles due to a combination of venous congestion [61], subependymal gliosis [63, 64], and microcephaly with craniosynostosis [65]. As a result, the ventricles remain collapsed around the catheter despite intraventricular pressure rises to dangerous levels [60]. Diagnosis is made purely clinically by showing elevated intracranial pressure that correlates with patient symptoms in the absence of ventriculomegaly. There are no imaging criteria for the diagnosis. First-line treatment is diuretics or antimigraine medications [66]. CSF Accumulation Hydrothorax Ventriculopleural shunts commonly cause small asymptomatic effusions that do not necessitate shunt revision [67]. However, symptomatic hydrothorax may develop at any time and may progress to tension physiology [68]. Irritation from the shunt catheter or shunt infection results in accumulation of bacteria, leukocytes, and inflammatory mediators that mix with the protein-rich CSF. The resulting increase in oncotic pressure in the pleural space increases accumulation of pleural fluid, which adds to the shunted CSF volume. Atelectasis of the underlying lung further reduces visceral pleural surface area, impairing absorption [68]. Children, particularly infants, are more prone to hydrothorax because of the relatively smaller pleural surface available for absorption and enhanced immune response from frequent viral infections and routine immunizations [69]. Antisiphon devices and newer valves that prevent overdrainage have decreased the incidence of hydrothorax [12]. CSF hydrothorax can occur as a result of intrathoracic migration of a distal ventriculoperitoneal catheter. The course of the catheter into the pleural space may be supradiaphragmatic due to incorrect subcutaneous tunneling or transdiaphragmatic via a congenital diaphragmatic defect, foramina of Bochdalek or Morgagni, esophageal hiatus, or diaphragmatic perforation [31, 32]. However, both symptomatic and tension hydrothorax secondary to ventriculoperitoneal shunting have also been described in the absence of transthoracic catheter migration [28, 70, 71]. This likely occurs because of a combination of asymptomatic CSF ascites, microcommunications in the diaphragm, and inflammation that impairs pleural absorption

[28]. Although more common in children due to the higher prevalence of suboptimal peritoneal absorption, adult cases have also been reported [72]. Diagnosis is made radiographically by injecting contrast material or radionuclide into the shunt reservoir and visualizing accumulation in the pleural space [73] (Fig. 20). Thoracentesis and chemical analysis can also confirm the presence of CSF in the pleural fluid [70]. Ascites Ascites in the presence of a ventriculoperitoneal shunt is caused by decreased peritoneal absorption with or without increased oncotic pressure of intraperitoneal fluid [26]. The absorptive capacity of the peritoneum is reduced by scarring from previous peritonitis or surgical procedures [74]. Oncotic pressure of intraperitoneal fluid is increased by inflammation from infection, foreign body reaction to the catheter, or shunt-disseminated metastasis [26, 75–77]. Increased protein content of CSF caused by tumors, particularly optochiasmatic gliomas, also increases the intraperitoneal oncotic pressure [78, 79]. Ascites accumulation with abdominal distention and respiratory compromise may occur within weeks, months, or even years after shunt placement [80]. Ascites is easily visualized with ultrasound or CT. In 15% of children with ventriculoperitoneal shunts, the increase in intraperitoneal pressure due to CSF ascites causes an inguinal hernia or hydrocele to develop [28]. The vaginal processes, which are patent in 80% of newborns, are dilated, leading to these complications [81]. The incidence is higher in children shunted before 2 years of age when peritoneal absorption is least efficient [28, 82]. Additional Complications Tricuspid Valve Pathology Chronic mechanical irritation of the tricuspid valve by the distal catheter may cause fibrosis, calcification, and stenosis of the tricuspid valve [9]. The catheter may also damage the valve, directly leading to tricuspid regurgitation. Other causes of catheter-related valvular damage include endocarditis and bland thrombus [83]. Thromboembolic Disease and Pulmonary Arterial Hypertension The intravascular catheter promotes clot formation in the internal jugular vein, which may then propagate into the superior vena cava, or at the tip of the catheter in the right atrium [25]. These thrombi may calcify [84].

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Wallace et al. Inappropriate position of the catheter tip in the superior vena cava increases the risk of venous thrombosis [85, 86]. Real-time 2D echocardiography is used to determine the size, site, and area of attachment for surgical planning [87]. Catheter or CT angiography will show occlusion of the superior vena cava with concomitant collateral vessels [84]. Coronary sinus thrombosis with acute myocardial infarction has been reported [88]. Although rare in children, the prevalence of pulmonary arterial hypertension after ventriculoatrial shunting in adults may be as high as 8% on the basis of echocardiography and lung function testing [89]. Pulmonary hypertension may be secondary to chronic thromboembolic disease because pulmonary embolism with infarction occurs in up to 50% of patients with ventriculoatrial shunts [90] (Fig. 21). Another proposed mechanism is a thrombogenic response of pulmonary arterial endothelium to brain thromboplastin [89]. Because of the serious complications of pulmonary hypertension, surveillance echocardiography and pulmonary function testing are recommended every 12 months for patients with ventriculoatrial shunts [91]. Fibrothorax Fibrothorax with lung entrapment is a rare complication of ventriculopleural shunts [92]. Fibrosis of the pleural cavity is believed to be caused by an inflammatory reaction to CSF proteins or chronic low-grade infection [92]. The duration of ventriculopleural shunting required to develop fibrosis is highly variable [92]. Pneumocephalus Pneumocephalus is a rare complication that can occur months to years after intraventricular shunt placement [93]. Air enters the subdural space during surgery and becomes trapped. Siphoning at the catheter tip produces negative intracranial pressure that draws the air into the brain [94]. The resulting pneumocephalus may produce acute tension physiology, especially in patients with cerebral atrophy [94] (Fig. 22). Pneumothorax and Subcutaneous Emphysema Postoperative pneumothorax with or without periincisional subcutaneous emphysema complicates 10–20% of ventriculopleural shunt surgeries but can occur with any shunt type [95]. Air may enter the subcutaneous tissues via the surgical excision. Other sources of air after ventriculopleural shunting include bronchopleural fistulas and the pleural space in

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the setting of positive-pressure ventilation [96]. Subcutaneous emphysema is usually clinically insignificant but can rarely cause upper airway obstruction or tension pneumomediastinum [96] (Fig. 23). References 1. Martin JE, Keating RF, Cogen PH, Midgley FM. Long-term follow-up of direct heart shunts in the management of hydrocephalus. Pediatr Neurosurg 2003; 38:94–97 2. Browd SR, Gottfried ON, Ragel BT, Kestle JR. Failure of cerebrospinal fluid shunts. Part II. Overdrainage, loculation, and abdominal complications. Pediatr Neurol 2006; 34:171–176 3. Goeser CD, McLeary MS, Young LW. Diagnostic imaging of ventriculoperitoneal shunt malfunctions and complications. RadioGraphics 1998; 18:635–651 4. Lollis SS, Mamourian AC, Vaccaro TJ, Duhaime AC. Programmable CSF shunt valves: radiographic identification and interpretation. AJNR 2010; 31:1343–1346 5. Garton HJ. Cerebrospinal fluid diversion procedures. J Neuroophthalmol 2004; 24:146–155 6. Browd SR, Ragel BT, Gottfried ON, Kestle JR. Failure of cerebrospinal fluid shunts. Part I. Obstruction and mechanical failure. Pediatr Neurol 2006; 34:83–92 7. Ellegaard L, Mogensen S, Juhler M. Ultrasoundguided percutaneous placement of ventriculoatrial shunts. Childs Nerv Syst 2007; 23:857–862 8. Machinis TG, Fountas KN, Hudson J, Robinson JS, Troup EC. Accurate placement of the distal end of a ventriculoatrial shunt with the aid of realtime transesophageal echocardiography: technical note. J Neurosurg 2006; 105:153–156 9. Akram Q, Saravanan D, Levy R. Valvuloplasty for tricuspid stenosis caused by a ventriculoatrial shunt. Catheter Cardiovasc Interv 2011; 77:722– 725 10. Amigo-Castaneda MC, Soto-Lopez ME, Espinola-Zavaleta N, Romero-Cardenas A, Vargas-Barron J. Valvulopathy in primary antiphospholipid syndrome: prospective echocardiography study [in Spanish]. Gac Med Mex 2000; 136:3–8; discussion, 9 11. Vargas-Barron J, Buenfil-Medina C, SanchezUgarte T, et al. Ventriculoatrial shunts for hydrocephalus and cardiac valvulopathy: an echocardiographic evaluation. Am Heart J 1991; 121:1498–1501 12. Grunberg J, Rebori A, Verocay MC, Ramela V, Alberti R, Cordoba A. Hydrothorax due to ventriculopleural shunting in a child with spina bifida on chronic dialysis: third ventriculostomy as an alternative of cerebrospinal diversion. Int Urol Nephrol 2005; 37:571–574 13. Kanev PM, Park TS. The treatment of hydroceph-

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Imaging Evaluation of CSF Shunts displacement of a peritoneal catheter. Childs Nerv Syst 2002; 18:179–182 29. Hermann EJ, Zimmermann M, Marquardt G. Ventriculoperitoneal shunt migration into the pulmonary artery. Acta Neurochir (Wien) 2009; 151:647–652 30. Fewel ME, Garton HJ. Migration of distal ventriculoperitoneal shunt catheter into the heart: case report and review of the literature. J Neurosurg 2004; 100(2 suppl Pediatrics):206–211 31. Martin LM, Donaldson-Hugh ME, Cameron MM. Cerebrospinal fluid hydrothorax caused by transdiaphragmatic migration of a ventriculoperitoneal catheter through the foramen of Bochdalek. Childs Nerv Syst 1997; 13:282–284 32. Di Roio C, Mottolese C, Cayrel V, Artru F. Respiratory distress caused by migration of ventriculoperitoneal shunt catheter into the chest cavity. (letter) Intensive Care Med 2000; 26:818 33. Dickman CA, Gilbertson D, Pittman HW, Rekate HL, Daily WJ. Tension hydrothorax from intrapleural migration of a ventriculoperitoneal shunt. Pediatr Neurosci 1989; 15:313–316 34. Doh JW, Bae HG, Lee KS, Yun IG, Byun BJ. Hydrothorax from intrathoracic migration of a ventriculoperitoneal shunt catheter. Surg Neurol 1995; 43:340–343 35. Morell RC, Bell WO, Hertz GE, D’Souza V. Migration of a ventriculoperitoneal shunt into the pulmonary artery. J Neurosurg Anesthesiol 1994; 6:132–134 36. Kurlander GJ, Chua GT. Roentgenology of ventriculo-atrial shunts for the treatment of hydrocephalus. Am J Roentgenol Radium Ther Nucl Med 1967; 101:157–167 37. Cowan MA, Allen MB Jr. Retrograde migration of the venous catheter as a complication of ventriculoatrial shunts in adults: case report. J Neurosurg 1971; 35:348–350 38. El-Eshmawi A, Onakpoya U, Khadragui I. Cardiac tamponade as a sequela to ventriculoatrial shunting for congenital hydrocephalus. Tex Heart Inst J 2009; 36:58–60 39. Gelfand ET, Callaghan JC. Mycotic pulmonary artery aneurysm: an unusual complication of ventriculo-atrial shunt. Cardiovasc Dis 1981; 8:271–275 40. Pearson B, Bui CJ, Tubbs RS, Wellons JC 3rd. An unusual complication of a ventriculopleural shunt: case illustration. J Neurosurg 2007; 106(5 suppl):410 41. Sainte-Rose C, Piatt JH, Renier D, et al. Mechanical complications in shunts. Pediatr Neurosurg 1991; 17:2–9 42. Cuka GM, Hellbusch LC. Fractures of the peritoneal catheter of cerebrospinal fluid shunts. Pediatr Neurosurg 1995; 22:101–103 43. Morishita A, Nagashima T, Kurata H, Eguchi T, Tamaki N. Clinical analysis of pediatric shunt catheter fracture [in Japanese]. No Shinkei Geka 2002; 30:839–845

44. Irie W, Furukawa M, Murakami C, et al. A case of V-A shunt catheters migration into the pulmonary artery. Leg Med (Tokyo) 2009; 11:25–29 45. Tunkel AR, Scheld WM. Therapy of bacterial meningitis: principles and practice. Infect Control Hosp Epidemiol 1989; 10:565–569 46. Kestle J, Drake J, Milner R, et al. Long-term follow-up data from the Shunt Design Trial. Pediatr Neurosurg 2000; 33:230–236 47. Patrick D, Marcotte P, Garber GE. Acute abdomen in the patient with a ventriculoperitoneal shunt. Can J Surg 1990; 33:37–40 48. Borgbjerg BM, Gjerris F, Albeck MJ, Hauerberg J, Borgesen SV. A comparison between ventriculoperitoneal and ventriculo-atrial cerebrospinal fluid shunts in relation to rate of revision and durability. Acta Neurochir (Wien) 1998; 140:459–464; discussion, 465 49. Rekate HL. Treatment of hydrocephalus in adults. Neurosurg Focus 2007. 22:editorial 50. Schoenbaum SC, Gardner P, Shillito J. Infections of cerebrospinal fluid shunts: epidemiology, clinical manifestations, and therapy. J Infect Dis 1975; 131:543–552 51. Gardner P, Leipzig T, Phillips P. Infections of central nervous system shunts. Med Clin North Am 1985; 69:297–314 52. Burke JW, Podrasky AE, Bradley WG Jr. Meninges: benign postoperative enhancement on MR images. Radiology 1990; 174:99–102 53. Iwata Y, Ohta S, Kawai K, et al. Shunt nephritis with positive titers for ANCA specific for proteinase 3. Am J Kidney Dis 2004; 43:e11–e16 54. Arze RS, Rashid H, Morley R, Ward MK, Kerr DN. Shunt nephritis: report of two cases and review of the literature. Clin Nephrol 1983; 19:48–53 55. Kubota M, Sakata Y, Saeki N, Yamaura A, Ogawa M. A case of shunt nephritis diagnosed 17 years after ventriculoatrial shunt implantation. Clin Neurol Neurosurg 2001; 103:245–246 56. James HE. Spectrum of the syndrome of the isolated fourth ventricle in posthemorrhagic hydrocephalus of the premature infant. Pediatr Neurosurg 1990; 16:305–308 57. Zimmerman RA, Bilaniuk LT, Gallo E. Computed tomography of the trapped fourth ventricle. AJR 1978; 130:503–506 58. Aoki N, Mizutani H. Acute subdural hematoma due to minor head trauma in patients with a lumboperitoneal shunt. Surg Neurol 1988; 29:22–26 59. Kamiryo T, Hamada J, Fuwa I, Ushio Y. Acute subdural hematoma after lumboperitoneal shunt placement in patients with normal pressure hydrocephalus. Neurol Med Chir (Tokyo) 2003; 43:197–200 60. Buxton N, Punt J. Subtemporal decompression: the treatment of noncompliant ventricle syndrome. Neurosurgery 1999; 44:513–518; discussion, 518–519

61. Foltz EL. Hydrocephalus: slit ventricles, shunt obstructions, and third ventricle shunts: a clinical study. Surg Neurol 1993; 40:119–124 62. Olson S. The problematic slit ventricle syndrome: a review of the literature and proposed algorithm for treatment. Pediatr Neurosurg 2004; 40:264–269 63. Epstein F, Lapras C, Wisoff JH. “Slit-ventricle syndrome”: etiology and treatment. Pediatr Neurosci 1988; 14:5–10 64. Engel M, Carmel PW, Chutorian AM. Increased intraventricular pressure without ventriculomegaly in children with shunts: “normal volume” hydrocephalus. Neurosurgery 1979; 5:549–552 65. Albright AL, Tyler-Kabara E. Slit-ventricle syndrome secondary to shunt-induced suture ossification. Neurosurgery 2001; 48:764–769; discussion, 769–770 66. Abbott R, Epstein FJ, Wisoff JH. Chronic headache associated with a functioning shunt: usefulness of pressure monitoring. Neurosurgery 1991; 28:72–76; discussion, 76–77 67. Jones RF, Currie BG, Kwok BC. Ventriculopleural shunts for hydrocephalus: a useful alternative. Neurosurgery 1988; 23:753–755 68. Beach C, Manthey DE. Tension hydrothorax due to ventriculopleural shunting. J Emerg Med 1998; 16:33–36 69. Bryant MS, Bremer AM, Tepas JJ 3rd, Mollitt DL, Nquyen TQ, Talbert JL. Abdominal complications of ventriculoperitoneal shunts: case reports and review of the literature. Am Surg 1988; 54:50–55 70. Born M, Reichling S, Schirrmeister J. Pleural effusion: beta-trace protein in diagnosing ventriculoperitoneal shunt complications. J Child Neurol 2008; 23:810–812 71. Adeolu AA, Komolafe EO, Abiodun AA, Adetiloye VA. Symptomatic pleural effusion without intrathoracic migration of ventriculoperitoneal shunt catheter. Childs Nerv Syst 2006; 22:186–188 72. Matushita H, Cardeal D, Pinto FC, Plese JP, de Miranda JS. The ventriculoomental bursa shunt. Childs Nerv Syst 2008; 24:949–953 73. Chang CP, Liu RS, Liu CS, et al. Pleural effusion resulting from ventriculopleural shunt demonstrated on radionuclide shuntogram. Clin Nucl Med 2007; 32:47–48 74. Diluna ML, Johnson MH, Bi WL, Chiang VL, Duncan CC. Sterile ascites from a ventriculoperitoneal shunt: a case report and review of the literature. Childs Nerv Syst 2006; 22:1187–1193 75. Donovan DJ, Prauner RD. Shunt-related abdominal metastases in a child with choroid plexus carcinoma: case report. Neurosurgery 2005; 56:E412; discussion, E412 76. Schupper A, Kornreich L, Yaniv I, Cohen IJ, Shuper A. Optic-pathway glioma: natural history demonstrated by a new empirical score. Pediatr Neurol 2009; 40:432–436

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Wallace et al. 77. Kornreich L, Blaser S, Schwarz M, et al. Optic pathway glioma: correlation of imaging findings with the presence of neurofibromatosis. AJNR 2001; 22:1963–1969 78. Olavarria G, Reitman AJ, Goldman S, Tomita T. Post-shunt ascites in infants with optic chiasmal hypothalamic astrocytoma: role of ventricular gallbladder shunt. Childs Nerv Syst 2005; 21:382–384 79. Mobley LW 3rd, Doran SE, Hellbusch LC. Abdominal pseudocyst: predisposing factors and treatment algorithm. Pediatr Neurosurg 2005; 41:77–83 80. Binitie OP, Abdul-Azeim SA, Annobil SH. Hydrocephalus, ventriculo-peritoneal shunt and cerebrospinal fluid ascites. West Afr J Med 2002; 21:260–261 81. Kimura T, Tsutsumi K, Morita A. Scrotal migration of lumboperitoneal shunt catheter in an adult: case report. Neurol Med Chir (Tokyo) 2011; 51:861–862 82. Davidson RI. Peritoneal bypass in the treatment of hydrocephalus: historical review and abdominal complications. J Neurol Neurosurg Psychiatry 1976; 39:640–646 83. Dervanian P, Mace L, Bucari S, Folliguet TA, Grinda JM, Neveux JY. Valved conduit bypass for

extensively calcified tricuspid valve stenosis. Ann Thorac Surg 1995; 60:450–452 84. Gabriele OF, Clark D. Calcified thrombus of the superior vena cava: complication of ventriculoatrial shunt. Am J Dis Child 1969; 117:325–327 85. Overton MC 3rd, Derrick J, Snodgrass SR. Surgical management of superior vena cava obstruction complicating ventriculoatrial shunts. J Neurosurg 1966; 25:164–171 86. Overton MC 3rd, Kirksey TD, Snodgrass SR, Nelson WJ, Derrick JR. Direct atrial and vena caval shunting procedures for hydrocephalus. Surg Gynecol Obstet 1967; 124:819–825 87. Iqbal SM, Pezzella AT, Effler DB. Infection and right atrial pseudotumor complicating a ventriculoatrial shunt for hydrocephalus. Am J Cardiol 1984; 54:668–670 88. Wells CA, Senior AJ. Coronary sinus thrombosis and myocardial infarction secondary to ventriculoatrial shunt insertion. J Pediatr Surg 1990; 25:1214–1215 89. Pascual JM, Prakash UB. Development of pulmonary hypertension after placement of a ventriculoatrial shunt. Mayo Clin Proc 1993; 68:1177–1182 90. Milton CA, Sanders P, Steele PM. Late cardiopul-

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Fig. 1—62-year-old man with metastatic melanoma. A, Transaxial CT image shows ventriculostomy catheter tip in left frontal horn anterior to foramen of Monro. B, Patient presented 3 months later with altered mental status. Transaxial CT image shows catheter position is unchanged; however, there is now hydrocephalus and transependymal flow of CSF, concerning for shunt malfunction. Right occipital metastasis is also present.

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Fig. 2—32-year-old man with history of meningitis. A–C, Conventional radiographs of head, neck, and chest depict ventriculostomy catheter placed via left frontal approach and normal course of distal ventriculoatrial shunt catheter terminating in right atrium. Note radiolucency of reservoir (arrow, B).

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Fig. 3—4-year-old boy with aqueductal stenosis. A–C, Conventional radiographs of head, neck, and chest depict ventriculostomy catheter placed via right frontal approach (white arrow, A and B) and normal course of distal ventriculoperitoneal shunt catheter terminating in lower abdomen (arrowheads). Note redundancy of intraperitoneal catheter to allow for vertical growth of child (black arrow, C).

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Wallace et al.

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Fig. 4—82-year-old woman with normal pressure hydrocephalus. A, Radionuclide CSF shunt image shows activity that remains localized at injection site with no renal activity to suggest extravasation with systemic absorption and excretion. These findings are consistent with obstruction of distal catheter. B, Repeat radionuclide image obtained after shunt revision initially shows normal activity throughout distal catheter. After radionuclide empties into right atrium it is distributed throughout systemic circulation. Fig. 5—3-year-old girl with cerebral palsy. Anteroposterior radiograph shows kink (arrow) within distal ventriculoperitoneal shunt catheter in region of neck.

Fig. 6—58-year-old woman with ventriculoperitoneal shunt who presented with altered mental status. A, Radionuclide CSF shunt image shows loculated fluid collection surrounding catheter tip that does not disperse within peritoneal cavity. B, Transaxial CT image shows CSF pseudocyst within anterior abdominal wall.

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Fig. 7—29-year-old man who presented with fluid leaking from ventriculopleural incision site. A and B, Chest radiograph (A) and transaxial CT image (B) show tip of ventriculopleural shunt coiled within left pleural pseudocyst (arrows). C, Radionuclide CSF shunt image shows no spontaneous flow of tracer into pleural space.

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Fig. 8—35-year-old man with aqueductal stenosis. A, Anteroposterior radiograph of head and neck shows discontinuity of heavily calcified, long-standing ventriculoperitoneal catheter (arrow). Note radiolucent connector more proximally (arrowhead), which should not be mistaken for discontinuity. B, Anteroposterior radiograph of abdomen shows catheter tip coiled in right upper quadrant. Intraperitoneal catheter was redundant when patient was child but shortened to depicted length as he grew.

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Fig. 9—84-year-old man with ventriculoperitoneal shunt who presented with abdominal pain, nausea, and vomiting. A, Abdominal radiograph shows distal ventriculoperitoneal catheter extending into perineum (arrow). B, Oblique coronal CT image shows catheter extending into right inguinal hernia containing obstructed small bowel (arrow).

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Fig. 10—27-year-old man with Chiari II malformation. A, Abdominal radiograph shows distal ventriculoperitoneal catheter coiled in left upper quadrant of abdomen (arrow). B, Transaxial CT image shows catheter coiled anterior to omentum with loculated CSF surrounding tip (arrow). Multiple adhesions were identified at surgery.

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Imaging Evaluation of CSF Shunts

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Fig. 11—34-year-old man with ventriculoperitoneal shunt who presented with abdominal pain. A and B, Transaxial (A) and coronal (B) CT images show erosion of ventriculoperitoneal catheter tip into subcapsular space with resulting CSF pseudocyst formation, which then ruptured into liver. Fig. 12—35-year-old man with ventriculoperitoneal shunt who presented with abdominal pain, nausea, and vomiting. Oblique transaxial CT image shows ventriculoperitoneal catheter encircling loop of obstructed jejunum.

Fig. 13—59-year-old man with history of traumatic subarachnoid hemorrhage who underwent ventriculoatrial shunt placement and later presented with 2 weeks of lethargy and confusion. A and B, Conventional radiographs show discontinuity of shunt catheter in neck region (arrow, A) with embolization of distal segment into pulmonary vasculature (arrow, B).

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Fig. 14—31-year-old man with ventriculoatrial shunt who presented with fever and lethargy. Transaxial CT image shows catheter tip in right atrium and bilateral pulmonary nodules, some of which are cavitated, consistent with septic emboli.

Fig. 15—37-week-old boy with Chiari I malformation and septooptic dysplasia who was admitted with Escherichia coli bacteremia. A and B, Transaxial contrast-enhanced T1-weighted MR images show diffuse ventriculomegaly and ependymal enhancement, consistent with shunt failure with ventriculitis. Shunt reservoir is visible in right parietal scalp (arrow).

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Fig. 16—10-year-old girl with cerebral palsy. A–C, T2-weighted MR images show decompressed lateral ventricles with posterior ventriculostomy catheter in place (A) and marked dilatation of trapped fourth ventricle (B). After placement of second ventriculostomy catheter, fourth ventricle is partially decompressed (C).

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Imaging Evaluation of CSF Shunts

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Fig. 17—3-week-old boy with macrocephaly. A, Transaxial CT image of head shows markedly dysmorphic and dilated ventricular system after injection of iohexol, which layers dependently in isolated locule. B, T2-weighted MR image with different patient orientation better delineates anatomy of loculations. C, Lateral radiograph after endoscope-assisted fenestration of loculations shows placement of complexsystem ventriculoperitoneal shunt. D, Transaxial CT image shows two catheter tips.

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Fig. 18—54-year-old man with history of aneurysmal subarachnoid hemorrhage complicated by hydrocephalus who underwent ventriculoperitoneal shunt. A, Coronal T1-weighted MR image shows loculated subdural fluid collection with heterogeneous T1 signal intensity adjacent to right ventriculostomy catheter. B and C, Collection shows high T2 signal intensity (B) with signal drop-off on T2*-weighted image (C), consistent with hematoma. There is mass effect on right lateral ventricle and midline shift to left.

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Fig. 19—19-year-old woman with glioneuronal tumor, World Health Organization grade 1. A and B, Transaxial CT images show slitlike ventricles (arrows). This patient was asymptomatic.

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Fig. 20—3-month-old girl with repaired myelomeningocele who underwent ventriculoperitoneal shunt placement. Patient presented with persistent right pleural effusion. A and B, Initial images from 99mTc CSF shunt study show rapid filling of distal shunt limb (A). There is normal free spill of activity in peritoneal cavity consistent with patent shunt system (B). C, Delayed images obtained approximately 30 minutes after tracer injection show activity in right hemithorax, consistent with free communication of fluid in peritoneum with right pleural space. Thin, membranous region in right hemidiaphragm was noted and repaired at surgery.

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Imaging Evaluation of CSF Shunts

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Fig. 21—33-year-old man with history of intraventricular hemorrhage who underwent ventriculoatrial shunting and presented with dyspnea. A and B, Transaxial CT images show left upper lobe infarctions (arrow, A) as well as bilateral pulmonary emboli (arrows, B). Web in left pulmonary artery (white arrowhead, B) indicates chronic component. Superior vena cava is thrombosed with mediastinal collateral formation (black arrowheads, B). C, Right pulmonary arteriogram shows changes of chronic pulmonary emboli, including truncation (white arrows) and concentric stenosis (black arrow) of multiple segmental arteries. Mean pressures in right and left pulmonary arteries were 47 and 49 mm Hg, respectively, consistent with pulmonary hypertension.

C Fig. 22—49-year-old woman with pseudotumor cerebri. Transaxial CT image shows subdural air overlying left frontal convexity with midline shift concerning for tension pneumocephalus (arrowhead). Right frontal ventriculostomy catheter tip is seen anterior to foramen of Monro (arrow). 

Fig. 23—56-year-old man with recent ventriculoperitoneal shunt placement. Chest radiograph shows extensive pneumomediastinum and subcutaneous emphysema. Shunt catheter courses over right hemithorax (arrowheads). There are overlying ECG leads. 

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