Complications of Pituitary Surgery

Abstract

Complications of pituitary surgery are rare, particularly in the hands of experienced surgeons. Endoscopic transsphenoidal surgery has not significantly reduced their frequency. Cushing disease and reintervention are risk factors. Diabetes insipidus, anterior lobe dysfunction, vascular and nerve injuries, and CSF leakage can occur. Diabetes insipidus is the most frequent postoperative complication, mostly being transient. Permanent diabetes insipidus appears after manipulation or injury of the posterior lobe, pituitary stalk, or hypothalamus. Whether the preoperative presence of an ectopic posterior lobe has a protective effect against the occurrence of diabetes insipidus is a topic of debate. ADH insufficiency is correlated with loss of posterior lobe or pituitary stalk bright spot. Decreased T1 hyperintensity of the posterior lobe is best appreciated on axial T1WI and can be progressive a few days after surgery. Surgical bed hemorrhage or sellar packing can mask ADH storage and chemical shift artifact from a fatty dorsum sellae. In the latter case, axial T1W fat-saturated sequence is recommended. Late reappearance—after months—of a weak bright spot either intrasellarly or at the stalk level may announce the spontaneous cure of diabetes insipidus (Fig. 28.1). CSF fistula is usually recognized during surgery and sealed immediately, frequently with a fat graft. If unrecognized, CSF fistula can lead to rhinorrhea, intracranial hypotension, pneumocephalus (Fig. 28.2), or meningitis. Direct visualization of CSF fistula is rarely observed (Fig. 28.3). Intracranial hypotension secondary to CSF leakage gives rise to venous congestion with bulging of the pituitary gland and enlargement of the venous compartment of the cavernous sinus, inferior coronary sinus, and retroclival venous plexus (Fig. 28.4). Visual complications are secondary to surgical bed hemorrhage or overpacking. Optic chiasm and/or intracavernous oculomotor nerve compression can occur. Slow flow of laterosellar veins attests to impaired pituitary drainage (Fig. 28.5). Inadvertent introduction of surgical tools within the cavernous sinus may be responsible for oculomotor nerve (Fig. 28.6) or internal carotid artery injuries. Intracavernous internal carotid and, more rarely, basilar artery injuries are the most serious complications of transsphenoidal surgery. Internal carotid artery injury can manifest itself immediately during surgery or later with epistaxis. Medial position of internal carotid arteries (Fig. 28.7a–f) and extreme thinness of the carotid sulcus of the sphenoid bone are risk factors, as is acromegaly. Hard packing of cavernous sinus can lead to internal carotid artery thrombosis, which can be asymptomatic in cases of complete circle of Willis and is revealed only on serial MRI (Fig. 28.7g–i). False aneurysm of the carotid siphon is sometimes detected postoperatively; in this case, the optimal strategy remains under debate. Endovascular treatment of the false aneurysm or occlusion of the parent artery are discussed in cases of late epistaxis after surgery. Basilar artery injury, which fortunately is exceptional, can arise with aggressive pituitary adenomas or malignant tumors involving the clivus (Fig. 28.7j–l). Aggravation of pre-existing pituitary deficiency may occur if the normal residual pituitary gland is not preserved, as in large or aggressive pituitary macroadenomas. The sella appears completely empty in these cases. Symptomatic sphenoid mucoceles are rare; risk factors include nonexcision of sphenoid sinus mucosa and obstruction of sphenoid sinus ostium (see Chap. 39).