6.2.15\ Shunt Catheter Calcification

6.2.15.1\ Discussion

Dystrophic calcifications can form around the silicone tubing of shunt catheters within the subcutaneous tissues, particularly those impregnated with barium (Fig. 6.52). This phenomenon is likely attributable to a fibrotic reaction to the tube. Calcifications are most commonly encountered in the region of the clavicles. The presence of calcification surrounding shunt catheters may be associated with malfunction, pain, and fever. Removal of the affecting tubing can relieve symptoms although the catheter can be difficult to remove due to associated fibrosis. The condition is readily depicted on radiographs or CT in which the calcifications are usually coarse, irregular, and scattered along the length of the shunt tubing.

6.2.16\ Pulmonary Embolism

from Ventriculoatrial

Shunting

6.2.16.1\ Discussion

In rare cases, the presence of a catheter in the deep venous system and right atrium can ­predispose to thrombus formation along the intracardiac portion of the catheter and lead to pulmonary embolism. Patients may present with chest pain and shortness of breath. Pulmonary embolism protocol CT is the modality of choice for evaluating pulmonary artery filling defects (Fig. 6.53).

6.2.17\ Chiari Decompression

Surgery and Associated

Complications

6.2.17.1\ Discussion

The goal of neurosurgical intervention in patients with Chiari type 1 malformation is to reduce symptomatic cerebrospinal fluid pressure gradients across the craniocervical junction. Decompression typically involves suboccipital craniectomy and C1 laminectomy, with or without duraplasty. Regardless of the particular technique implemented, decompression should result in a widened neo-foramen magnum, with improved cerebrospinal fluid flow, which can be assessed qualitatively or quantitatively via phase-­ contrast imaging, as well as diminished syringomyelia (Fig. 6.54).

There are several adjunct procedures that can be implemented in conjunction with Chiari decompression, particularly as a second resort, including craniocervical decompression without or with duraplasty, fourth ventricular stenting, endoscopic third ventriculostomy, tonsillar reduction, and syringohydromyelia decompression. In particular, fourth ventricular stenting can be performed when there is obstruction of the fourth ventricular outflow in patients with refractory syringohydromyelia. Silastic tubes that are typically used for this purpose are visible on conventional MRI sequences as low-signal-intensity structures on T1and T2-weighted sequences (Fig. 6.55).

Tonsillar cauterization or reduction leads to a characteristic finding on early postoperative imaging, which is essentially related to ischemia at the margins of the resected tissues, along with microhemorrhages (Fig. 6.56). Enhancement along the margins of the cauterized tissue can also be observed in the perioperative period. Over time, the ischemia evolves to encephalomalacia with further shrinkage of the inferior cerebellum and greater flow across the neo-foramen magnum.

Complications of Chiari decompression include hemorrhage, infection, stroke, cerebrospinal fluid leak with pseudomeningocele formation,

hydrocephalus, craniocervical instability, arachnoid adhesion formation, inflammatory or granulomatous reaction to implanted materials, and cerebellar ptosis or cerebellar slump syndrome. Some of these complications may warrant revision surgery, and some are discussed in more detail in the following pages.

Infarction is a rare complication of Chiari I malformation decompression, but is more likely to occur during complex revision surgeries. The posterior inferior cerebellar artery territory is most often involved, and the extent is typically beyond the areas affected by ischemia induced by cauterization performed for tonsillar reduction. DWI and FLAIR MRI sequences are useful for evaluating perioperative infarcts (Fig. 6.57).

Pseudomeningoceles consist of cerebrospinal fluid collections that extend into the upper neck and scalp soft tissues from the site of ­decompression. This phenomenon occurs even if duraplasty is performed, since a completely watertight ­closure is not always possible to achieve. The pseudomeningoceles can occasionally produce enough mass effect to aggravate the syringohydromyelia. Furthermore, the pseudomeningoceles can also fluctuate in size over time, particularly with changes related to intracranial shunting (Fig. 6.58).

Arachnoid adhesions can tether the cerebellum to overlying dura and impede cerebrospinal fluid flow. The adhesions are best depicted on high-resolution cisternogram type sequences, such as FIESTA, CISS, or DRIVE, and appear as low-signal-intensity bands that distort the parenchyma. These are often located posterior to the cerebellum or at the craniocervical junction and attach to the overlying dura or dural graft (Fig. 6.59).

Cerebellar slump syndrome can manifest with aggravated symptoms after decompression surgery for Chiari I malformation due to further inferior descent of the cerebellum, which can compress the upper spinal cord and distort the brainstem, as demonstrated on MRI (Fig. 6.60). This complication can be predisposed by a neo-­foramen magnum that is too large.

Fig. 6.54  Expected findings following Chiari decompression surgery. Preoperative sagittal T2-weighted MRI (a) and phase-contrast flow image (b) show low-lying cerebellar tonsils with impeded cerebrospinal fluid flow across the foramen magnum and extensive syringohydromyelia.

Postoperative, preoperative sagittal T2-weighted MRI (c) and phase-contrast flow image (d) show a widened­ neoforamen magnum with improved cerebrospinal fluid flow and decrease in the degree of syringohydromyelia

Fig. 6.57  Perioperative stroke. The patient is status post re-exploration of Chiari decompression, direct midline myelotomy for syrinx drainage, exploration/reestablishment of fourth ventricular outflow by stenting from fourth ventricle to the cervical subarachnoid space. Axial CT

image (a) shows edema in the bilateral medial cerebellar hemispheres. Axial FLAIR (b), DWI (c), and ADC map (d) show corresponding acute infarction in the bilateral cerebellar hemispheres