Complications in Surgery of the Parapharyngeal Space
The most important factors in avoiding or managing complications from surgery of the parapharyngeal space are appropriate patient selection and informed consent. Thorough preoperative assessment of patients with parapharyngeal space pathology is critical. Parapharyngeal space surgery can result in significant morbidity, typically related to lower cranial nerve deficits. In experienced hands and with proper patient selection and counseling, morbidity can be significantly reduced. A multidisciplinary tumor board and team are critical to management of these patients. Depending upon the extent and nature of the lesion, team members include the head and neck surgeon, neurootologist, laryngologist, vascular surgeon, neurosurgeon, neuro-ophthalmologist, speech pathologist, audiologist, physical therapist, and a variety of other ancillary staff.
Preoperative lower cranial neuropathies (e.g., glossopharyngeal, vagus, accessory, and hypoglossal cranial nerves) are common in patients with tumors that originate at or invade the parapharyngeal space.1–3 These patients present a wide spectrum of swallowing or speech problems including hypernasal or slurred speech, nasal regurgitation, dysphagia, aspiration, and dysphonia (because of deficits in CNs of glossopharyngeal, vagus, and hypoglossal cranial nerves). These and other preexistent neurologic and functional deficits need to be considered during the preoperative planning, because they significantly impact postoperative recovery and the functional rehabilitation of the patient. For example, pulmonary aspiration, caused by lower cranial neuropathies, has a significant morbidity and mortality. If the patient has long-standing deficits, then compensation may have occurred. However, even if a patient has adjusted well to deficits preoperatively, the effects of additional cranial nerve deficits should be considered and discussed with the patient.
Elderly and unhealthy patients require special consideration preoperatively. A majority of complications involving parapharyngeal space surgery involve lower cranial deficits (glossopharyngeal, vagus, accessory, and hypoglossal cranial nerves). If no deficits exist preoperatively, then proper counseling and discussion of alternative therapies should occur depending upon the pathology. If the cranial nerves are already affected by the tumor, patients have generally already compensated for the deficits and do better postoperatively. If little or no cranial nerve dysfunction is present preoperatively, acute denervation by the surgery can have a higher probability of causing significant morbidity in individuals, particularly the elderly population.4 In nonaggressive pathologies, radiotherapy or observation should be strongly considered in elderly or infirm patients.
A thorough physical examination will reveal specific cranial nerve dysfunction, such as decreased elevation of the ipsilateral palate causing deviation of the uvula to the unaffected side (glossopharyngeal and vagus cranial nerves) ( Fig. 26.1 ), decreased mobility/strength of the tongue with deviation to the involved side upon protrusion (hypoglossal cranial nerve) ( Fig. 26.2 ), decreased supraglottic sensation, pooling of secretions in the hypopharynx with spillage into the laryngeal airway, ipsilateral vocal cord paralysis (vagus cranial nerve), and atrophy and paralysis of the sternocleidomastoid and trapezius muscles (accessory cranial nerve). These findings suggest the possible need for a tracheotomy for tracheopulmonary toilet and a gastrostomy tube for nutrition, hydration, and administration of medications.
Patients with a high vagal paralysis may benefit from a medialization laryngoplasty and an arytenoid adduction procedure.5–8 These may be performed in a single stage with the tumor removal or during the early postoperative period. The authors prefer to delay the medialization and perform it in standard fashion under local anesthesia with sedation.4,8 Laryngeal framework surgery improves the glottic competency; therefore, decreasing the risk for aspiration and improving the effectiveness of the coughing mechanism. This may avoid the need for a tracheotomy for the sole purpose of tracheopulmonary toilet.
It should be noted, however, that laryngeal framework surgery improves the compensatory mechanisms related to motor dysfunction but does not improve the dysfunction related to afferent denervation; hence, patients remain at risk for aspiration and nutritional deficiencies.5–8 An experienced speech and language pathologist can assist with the monitoring of the patient, recommend modifications in diet, and provide intensive swallowing therapy; therefore complementing the improvements produced by the laryngeal framework surgery.
Patients with severe deficits who do not respond to conservative treatment or those with severe cognitive problems that do not allow them to comply with the rehabilitation benefit from a tracheotomy for tracheopulmonary toilet and from a gastrostomy tube to facilitate postoperative nutrition and decrease the risk of prandial aspiration.
Velopharyngeal insufficiency may be treated with a palatal lift prosthesis although this may not be tolerated in some.9 Patients who do not tolerate the prosthesis may undergo a pharyngeal flap or a palatopexy (palatal adhesion surgery).4,9
Eustachian tube dysfunction due to mechanical or functional obstruction caused by tumors of the infratemporal fossa, may lead to conductive hearing loss. Such tumors may destroy the temporal bone or posterior cranial fossa leading to sensorineural hearing loss. Persistent presbyacusis may also compound the hearing loss. A myringotomy or amplification facilitates communication with the patient.
Trigeminal sensory dysfunction is commonly overlooked. Preoperatively evaluation of the corneal sensation and reflex will reveal any significant deficit. This is especially relevant if the patient also presents incomplete closure or a dry eye. Limitations of the extraocular movements usually present with diplopia and may occur as a result of direct tumor invasion of the orbit or extraocular muscles or through invasion or compression of the oculomotor, trochlear, and abducens cranial nerves. We recommend a neuro-ophthalmologic evaluation to elucidate these problems and to provide objective measures of the deficit. Similarly, patients with optic nerve problems or with tumor adjacent to the optic nerve, chiasm, or optic tract, are also referred for neuro-ophthalmologic evaluation.
Tumors that invade the facial nerve may cause facial paresis or paralysis, facial spasms, and epiphora ( Figs. 26.3 and 26.4 ). A gold weight (implanted in the upper eyelid) or surgical tightening (lateral tarsal strip procedure) of the lower lid may be necessary to protect the cornea. Corneal anesthesia associated with lagophthalmos due to facial nerve palsy or other causes requires aggressive measures (e.g., tarsorrhaphy) to prevent corneal injury.
Lateral deviation of the mandible upon mouth opening may indicate paralysis or tumor invasion of the pterygoid muscles or dysfunction of the temporomandibular joint. Similarly, trismus may be due to mechanical effects of the bulk of the tumor, tethering of the mastication muscles due to scarring or tumor invasion, ankylosis of the temporomandibular joint, or pain. Severity and etiology of the trismus must be considered to ascertain management of the airway during the induction of anesthesia and during the postoperative period. Trismus due to pain resolves with the induction of general anesthesia. If the extirpative surgery is expected to resolve the trismus, the patient may be managed with an awake nasotracheal intubation. Conversely, if the trismus is expected to persist even after tumor removal, the patient may require a tracheotomy performed under local anesthesia.
Owing to the relative inaccessibility of the infratemporal space to physical examination, radiologic imaging is a critical part of the evaluation. Computed tomography (CT) and magnetic resonance imaging scans provide valuable information. The CT scan is superior to demonstrate enlargement of neural foramina or erosion of bone. Magnetic resonance imaging provides better resolution of soft tissue planes and tumor invasion along neural and vascular structures ( Figs. 26.5 and 26.6 ). CT and magnetic resonance imaging are often complementary for the evaluation of cranial base tumors.
A critical consideration is the relationship of the neoplasm to the internal carotid artery (ICA). Magnetic resonance angiography or CT angiography provides a noninvasive assessment of the ITF and intracranial vasculature. If preoperative embolization of the tumor is warranted, as is the case for some juvenile angiofibromas, paragangliomas, or other highly vascularized tumors, angiography is preferable to magnetic resonance angiography, because the tumor can be embolized during the initial angiogram. In addition to providing information about tumor vascularity and involvement of the ICA, the angiogram provides important information regarding intracranial circulation and collateral blood supply. Neither study is adequate, however, to reliably assess the adequacy of collateral intracranial circulation in the event that manipulation or sacrifice of the ICA is necessary. Whenever manipulation of the ICA is likely, evaluation of collateral cerebral blood flow with angiography balloon occlusion xenon CT (ABOX-CT) is recommended.10
During an ABOX-CT a nondetachable balloon is introduced into the ICA and it is inflated for 15 minutes, as the awake patient is monitored for sensory, motor, or higher cortical function deficits. The balloon is deflated, and the patient is transferred to a standard CT suite. The balloon is reinflated, and a mixture of 32% xenon and 68% oxygen is then administered to the patient via facial mask for 4 minutes. The CT scan will demonstrate the distribution of xenon within the cerebral tissue, which reflects the blood flow. This provides a quantitative assessment of millimeters of blood flow per minute per 100 g of brain tissue (mL/min/100 g tissue). This test accurately predicts those patients at risk for a cerebrovascular accident when blood flow through the ICA is compromised. This test, however, is fallible. Patients can still suffer ischemic brain injury despite negative ABOX-CT testing owing to embolic phenomena or the loss of collateral vessels, which are not assessed by balloon occlusion testing. For these reasons, every attempt is made to preserve or reconstruct the ICA when feasible. Other techniques that provide similar information regarding collateral cerebral blood flow include single photon emission CT (SPECT) with balloon occlusion and transcranial Doppler monitoring.
Need for blood replacement should also be considered; if deemed necessary, type and cross the patient for 2 to 6 units of packed red blood cells according to the extent and nature of the tumor and surgery. We advocate autologous blood banking when feasible, although it is frequently impractical. A cell-saver or autotransfusion device may be used during the resection of benign vascular tumors. Angiography and embolization in highly vascular tumors, such as glomus and angiofibromas, may curtail the need for blood replacement. Embolization of paragangliomas, however, is controversial. Vagal paragangliomas rarely have a single blood supply and their resection usually is not associated with excessive blood loss. Carotid body tumors do not have an obvious dominant vessel supply, but depend upon the adventitia of the carotid artery. Embolization of these lesions may result in an inflammatory response that obscures the subadventitial plane of the tumor; hence, adding to the difficulty of the dissection. We prefer not to embolize most carotid body tumors. In the rare cases when we choose embolization, it must be performed within 24 hours of the planned resection because of collateralization and the inflammatory response of embolization.