7.4\ Transsphenoidal Resection

Complications

7.4.1\ Discussion

Sellar hematomas are not uncommon after transsphenoidal resection. When large, these can cause mass effect upon surrounding structures and produce symptoms. Subacute hematomas in the sella can display high signal on T1and T2-weighted MRI sequences and should not be mistaken for fat graft or residual tumor (Fig. 7.26). Gradient echo (GRE) or susceptibility-weighted imaging (SWI) techniques can sometimes be useful for identifying blood products on MRI, although susceptibility effects from air in the adjacent sphenoid sinus can limit assessment.

Arterial injury during transsphenoidal resection is uncommon, but can manifest as pseudoaneurysm and/or subarachnoid hemorrhage, which can lead to vasospasm. Most arterial complications related to transsphenoidal surgery involve the internal carotid artery, but the ophthalmic, posterior communicating, and anterior cerebral arteries may also be affected. Arterial injury may occur during dural opening, tumor resection, or reconstruction of the sinuses and may be predisposed by anatomic variants of the sinuses and internal carotid arteries and large tumors that involve the cavernous sinus. Therefore, meticulous preoperative planning with imaging is important for minimizing arterial injury.

Once arterial injury is suspected during transsphenoidal resection, angiography is essential for identifying the presence of pseudoaneurysms. The speculum and packing material may be kept within the sphenoid sinus in order to prevent exsanguination, and excess packing may result in arterial stenosis or occlusion. Endovascular control of bleeding may be achieved by either balloon occlusion or coil embolization of the affected internal carotid artery, coil embolization of the pseudoaneurysm, or stenting alone of the affected segment of the internal carotid artery (Fig. 7.27). Peritumoral hemorrhage can lead to delayed cerebral vasospasm and associated progressive worsening neurological deficits.

Malposition or migration of packing ­material for transsphenoidal resection is uncommon. The displaced packing material can exert mass effect upon the optic chiasm, resulting in visual symptoms that may differ from the preoperative deficits (Fig. 7.28). Alternatively, the packing material can extend posteriorly and compress the brainstem (Fig. 7.29). Such complications can be readily demonstrated on multiplanar CT or MRI. However, in some cases, displacement of packing material can potentially mimic tumor invasion.

Mucosal inflammation is fairly common after transsphenoidal resection and most commonly involves the sphenoid sinuses (Fig. 7.30). On the other hand, mucocele formation after transsphenoidal resection is a rare or perhaps under-­reported complication. Scar tissue can obstruct the egress of mucous secretions, resulting in their accumulation. On MRI, mucoceles are often homogeneously isoto hyperintense on T1and T2-weighted sequences and display peripheral enhancement. These may sometimes be ­multilocular. The main differential consideration is a postoperative hematoma, although these can be distinguished by their time course. Hematomas tend to resorb over time, while mucoceles persist or even expand. Susceptibilityweighted imaging can also be helpful, whereby hematomas are hypointense, while mucoceles do not. Postoperative mucoceles can cause symptoms, such as headache and diplopia, but they can be successfully treated via incision and drainage.

Although prophylactic antibiotics are routinely given before transsphenoidal surgery, the incidence of postoperative meningitis is in the range of 0.4–9%. This complication can manifest as leptomeningeal enhancement in the basilar cistern region on MRI (Fig. 7.31). The presence of postoperative cerebrospinal fluid leakage is an important risk factor for meningitis after transsphenoidal surgery.

Cerebrospinal fluid leak is a known complication of transsphenoidal resections. This is a serious complication that can predispose to meningitis and intracranial hypotension. The beta-2-transferrin assay is an accurate test for confirming the presence of cerebrospinal fluid leaks. Imaging also

plays an important role in the workup of cerebrospinal fluid leak: it is used to confirm the diagnosis, localize the site of cerebrospinal fluid leak, identify a potential cause, and help plan surgical repair. Several imaging modalities are available to evaluate cerebrospinal fluid leak, including high-resolu- tion CT, CT cisternography, MRI, and radionuclide cisternography (Fig. 7.32). However, high-resolu- tion CT is the first-line imaging modality and can correctly predict the site of cerebrospinal fluid leak in over 90% of cases. When beta-2 transferrin is positive and high-resolution CT demonstrates a single bony defect without any sign of encephalocele, no other imaging is necessary. CT cisternography is reserved for patients with a negative high-­resolution CT or multiple bony defects and active cerebrospinal fluid leakage. The sensitivity of CT cisternography is only about 50% in patients with intermittent cerebrospinal fluid leak. MR cisternography should be performed if high-resolu- tion CT shows a bony defect with an associated soft tissue opacity in order to exclude the possibility of meningocele or encephalocele. Contrast-­ enhanced sequences are useful for detecting dural enhancement at the site of the leak. Nuclear cisternography using In-111 is sometimes ­performed for complex cases and to help determine whether there is indeed a cerebrospinal fluid leak.

A variety of endocrinological disturbances can occur after transsphenoidal resection. In the acute postoperative setting, a minority of patients experience diabetes insipidus. This is associated with absence of the posterior pituitary bright spot on imaging. On the other hand, hyponatremia related to transsphenoidal surgery tends to have a delayed onset. Panhypopituitarism can result from transection of the hypophysis. This can best be evaluated using high-resolution MRI sequences, such as CISS and thin-section

T1-weighted images (Fig. 7.33). In addition, an ectopic posterior pituitary bright spot can be observed in this condition.

Ptosis of the optic chiasm is not an uncommon finding following pituitary tumor resection. This phenomenon tends to occur when a large portion of the pituitary sella contents have been evacuated resulting in a nearly or completely empty sella (Fig. 7.34). Ptosis is recognized by a convex-­ down configuration of the optic chiasm on a coronal or sagittal plane. When severe, this condition has the potential to cause visual deficits. The problematic empty sella with optic chiasm ptosis can be treated via chiasmopexy. This procedure consists of supporting the optic chiasm in near-­ anatomic position via transsphenoidal Silastic struts and coils, among other materials (Fig. 7.35). Acute visual loss related to transsphenoidal surgery can result from infarction of the optic apparatus if the blood supply is disrupted during tumor resection. This can be assessed on coronal T2-weighted MRI, which may show new signal abnormality in the optic apparatus (Fig. 7.36).

Fibrosis following transsphenoidal pituitary surgery is not an uncommon finding on postoperative MRI. Fibrosis can manifest as linear or amorphous areas within the sella. The imaging appearance is often indistinguishable from implant materials or residual tumor. Occasionally, adhesion bands form that extend across the sella or diaphragm to the brain or residual tumor. Adhesions appear as linear structures with low to intermediate signal intensity on T1-weighted and T2-weighted MRI sequences and enhance less and/or slower than the pituitary stalk (Fig. 7.37). These adhesions can hamper subsequent surgical resection of residual tumor. Fibrosis may also prevent normal pituitary gland re-expansion and cause stalk deviation.

Fig. 7.27  Carotid artery injury. Preoperative coronal postcontrast T1-weighted MRI (a) shows a large pituitary adenoma that extends into the cavernous sinuses. Postoperative scout (b) and axial CT image (c) show transsphenoidal­

speculum. Digital subtraction carotid angiograms show a right cavernous carotid pseudoaneurysm (arrow) adjacent to the speculum (d). The pseudoaneurysm was ­successfully treated via endovascular coiling (e)

Fig. 7.30  Sinus inflammation. The patient presented with symptoms of congestion following transsphenoidal pituitary adenoma resection. Preoperative sagittal contrast-­enhanced T1-weighted MRI (a) shows a pituitary

macroadenoma (*) but a clear sphenoid sinus. Postoperative sagittal post-contrast coronal T1-weighted MRI (b) demonstrates complete extensive mucosal thickening of the sphenoid sinus (arrow)

Fig. 7.32  Cerebrospinal fluid leak. The patient underwent transsphenoidal resection of a pituitary adenoma. Approximately 1 week after surgery, the patient presented with a cerebrospinal fluid leak. Oblique coronal CT (a) cisternogram image with the patient scanned in a prone position shows pooling of contrast around the fat graft that has partially herniated inferiorly into the sphenoid sinus through a bony defect in the floor of the sella with a

meningocele and spillage of contrast into the sphenoid sinus (arrow). The patient was scanned in a prone position in order to direct a maximum amount of contrast to the site of suspected cerebrospinal fluid leakage. Nuclear medicine cisternogram (b) also shows radiotracer activity localizing to the paranasal sinuses (arrow). Cerebrospinal fluid was also seen percolating around the fat graft during the subsequent surgery

b

Fig. 7.34  Optic chiasm ptosis. Preoperative coronal T2-weighted MRI (a) shows a large macrocystic pituitary adenoma that uplifts the optic chiasm (arrow). Postoperative coronal T2-weighted MRI (b) demonstrates ptosis of the optic chiasm (arrow) into an otherwise empty sella

Fig. 7.36  Optic nerve ischemia. The patient presented with new visual deficits after transsphenoidal surgery. Coronal T2-weighted MRI shows hyperintensity and swelling of the right optic chiasm (arrow)