Emergency Medicine

Managing Common Otolaryngologic Emergencies

Continuing their discussion from last month's issue, the authors cover sinusitis and its complications, anterior and posterior epistaxis, nasal and mandibular fractures, midface fractures, and a variety of emergent conditions involving the ear.

By Giovana R. Thomas, MD, Sandeep Dave, MD, Alexis Furze, David Lehman, MD, Jose Ruiz, MD, Mark Checcone, MD, and Thomas Balkany, MD

As noted in last month's article, about 30% to 80% of presentations seen by emergency department physicians in the United States are otolaryngologic emergencies. It is important tbat these emergencies be recognized and managed promptly because many of them can lead to respiratory failure and subsequent cardiopulmonary arrest. Last month, we discussed management of common otolaryngologic emergencies involving the neck and upper airway and pediatric stridor. This month, we will review emergencies of the nose, face, and ear.

SINUSITIS AND ITS COMPLICATIONS

Acute sinusitis is defined as an infection and inflammation of the mucosal lining of the paranasal sinuses of less than four weeks' duration. The most common bacterial organisms involved in this infection include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Typically, adult patients will report recent or concomitant symptoms of upper respiratory tract infection, such as nasal obstruction, fever, malaise, lethargy, and purulent nasal discharge. They may also complain of facial pain, headaches, or dental pain.

Acute uncomplicated sinusitis is managed medically, typically with antibiotics and a systemic decongestant. Rarely, the patient with acute sinusitis may exhibit potentially serious orbital or intracranial complications. Patients with these complications will have the symptoms of acute uncomplicated sinusitis noted above, along with additional signs and symptoms of the specific complication.

Chandler and colleagues described four progressive stages of orbital involvement from acute sinusitis: preseptal cellulitis, orbital cellulitis, subperiosteal abscess, and orbital abscess.

Preseptal cellulitis. This condition is characterized by swollen, nontender eyelids. Extraocular muscles and visual acuity are not affected, but slight exophthalmos may result from edema of the orbital contents.

Orbital cellulitis. This condition is defined as diffuse edema of the orbital contents without the presence of a discrete abscess. Exophthalmos is noted on physical examination. These patients may also experience decreased visual acuity.

Subperiosteal abscess. This is a purulent collection between the periorbita and the bony wall of the orbit. The orbital contents and the globe can be displaced inferolaterally. As the abscess progresses, eye movement may be compromised. This abscess also has the propensity to rupture the orbital septum and can present as a collection in the eyelid.

Orbital abscess. This is a discrete, purulent collection that forms in the orbital tissues (see photo and CT scan). It can be a result of orbital cellulitis. On physical examination, exophthalmos and chemosis can be observed. Complete ophthalmoplegia and severe visual impairment are also present.

Orbital abscess. Top: This young patient's exophthalmos is the result of an orbital abscess, which causes complete ophthalmoplegia and severe visual impairment. Above: An orbital abscess as seen on coronal computed tomography scan.

Intracranial complications of acute sinusitis include cavernous sinus thrombosis and meningitis and intracranial abscess.

Cavernous sinus thrombosis. This condition is the result of the posterior extension of phlebitis into the cavernous sinus. The patient presents with progressive symptoms similar to those of an orbital abscess—exophthalmos, chemosis, progressive ophthalmoplegia, and visual impairment. However, cavernous sinus thrombosis causes orbital symptoms bilaterally, as opposed to the unilateral symptoms caused by an orbital abscess. In addition to the orbital symptoms, this condition can present with meningismus or with edema over the emissary vein of the mastoid. Early diagnosis and surgical drainage of the underlying source of infection, along with long-term intravenous (IV) antibiotic therapy, are critical for an optimal clinical outcome.

Meningitis and intracranial abscess. Intracranial extension of acute sinusitis can result in meningitis or intracranial abscess. This diagnosis should be considered in any patient with neurologic findings such as focal deficits and symptoms of sinusitis.

In addition to a detailed history and physical exam, imaging modalities such as computed tomography (CT) or magnetic resonance imaging (MRI) can be useful in the diagnosis of many of the complications of acute sinusitis. Computed tomography remains the standard modality for diagnosing sinusitis, but MRI is frequently necessary, especially for patients with intracranial complications. Management is best conducted with a multidisciplinary approach, including an otolaryngologist, an ophthalmologist for orbital complications, and a neurosurgeon for any intracranial complications.

EVALUATING EPISTAXIS

Epistaxis is the most common bleeding disorder of the upper aerodigestive tract, with an estimated lifetime incidence of up to 60% of the population. Studies suggest that approximately 10% of epistaxis sufferers seek medical attention, the vast majority at emergency departments. Several factors may predispose patients to epistaxis, including local trauma or manipulation, cold temperature, topical drug administration (such as nasal decongestants, steroid sprays, or illicit drugs), and systemic bleeding disorders.

Hypertension's association with epistaxis is controversial. Several studies found no etiologic implications; others have associated hypertension with posterior epistaxis.

A focused history and physical exam are essential in guiding the evaluation and treatment of the patient with epistaxis. An initial rapid evaluation of the patient's bleeding severity and hemodynamic status must first be performed. In the event of an exsanguinating hemorrhage, the airway must be protected and secured, either by intubation or a surgical airway if there is severe head and neck trauma. Large-bore IV access must be established and fluid resuscitation begun.

Laboratory evaluation should include a complete blood cell count, prothrombin time, and partial thromboplastin time, and type and crossmatch for extensive bleeding. In severe cases, immediate tamponade of the bleeding should be attempted through placement of transnasal balloon catheters with anterior and posterior balloons. In their absence, urinary catheters may be used.

Examination of the nasal cavity is best performed with a headlight or head mirror, nasal speculum, and nasal suction. If these are not available, an otoscope with a large speculum may be used. The examination proceeds from anterior to posterior until a bleeding source is found. Using this technique, only anterior sources may be directly visualized. For proper evaluation and diagnosis, blood and clots should be debrided with a straight, rigid nasal suction or flexible suction catheter or bayonet forceps. The oral cavity and oropharynx should also be examined to determine the extent of hemorrhage flowing posteriorly.

ANTERIOR BLEEDING MORE COMMON

Anterior nasal cavity epistaxis is far more common than posterior epistaxis, occurring in approximately 90% to 95% of cases. The most common site is Kiesselbach's plexus on the anterior septum, which has a rich anastomotic vasculature from branches of the sphenopalatine and greater palatine arteries. Bleeding at this site may easily be treated with local measures. Initial treatment with a topical decongestant and bilateral manual pressure should be attempted; this will often achieve hemostasis in milder cases.

If bleeding continues despite these measures, local cauterization may be performed. A topical anesthetic should first be applied to the bleeding site, using a cottonball or a swab. Silver nitrate may then be directly applied until the bleeding has stopped. To prevent necrosis of the underlying cartilage and septal perforation, it is important to avoid cauterizing with silver nitrate on directly apposing areas of the bilateral septal mucoperichondrium. Once hemostasis is achieved, a topical antibiotic ointment may be applied and continued twice daily for prevention of local Staphylococcus aureus infection.

If local cauterization fails or an anterior bleeding site is not clearly identified, anterior nasal packs may be used. Several types of packing materials exist, differing mainly in application style and surface material. They range from simple nasal tampons placed with a bayonet forceps to balloons lined with hemostatic mesh that come with an applicator plunger.

An anterior petroleum jelly gauze pack may be placed if hemostasis is not achieved with a pre-formed pack. With the use of any anterior pack, applying contralateral pressure by packing the side of the nose that is not bleeding may help achieve hemostasis if unilateral packing fails.

Once hemostasis has been achieved with an anterior pack, patients may be discharged home if they are hemodynamically stable and have no significant comorbidities. Patients with known obstructive sleep apnea and bilateral nasal packing should be admitted overnight for airway monitoring. On discharge, all patients with anterior packing must be given antistaphylococcal antibiotics for the duration of the packing period, usually 48 to 72 hours. Patients should also be instructed to keep the packs moist with sterile saline or oxymetazoline spray twice daily. All patients requiring packing should be referred to an otolaryngologist for pack removal and a complete endoscopic exam.

MEASURES FOR POSTERIOR BLEEDING

Posterior epistaxis usually will not respond to the packing measures recommended for anterior bleeding. It can be recognized by persistent bleeding in the oropharynx or bleeding through the anterior packing material. In these cases, the anterior packing material is removed and posterior packing must be performed. This can be most easily accomplished with nasal balloon packs that have both anterior and posterior balloons.

Regardless of the type of posterior pack used, all patients requiring this treatment must be admitted for the duration of the packing period (48 hours) for cardiac monitoring, since packing of the nasopharynx may result in cardiac arrhythmias. Antibiotics must be administered, as with anterior-packing patients.

In a small number of patients with epistaxis, bleeding will persist despite packing. These patients must be referred to an otolaryngologist immediately for evaluation for possible embolization of the external carotid artery branches or surgical intervention, which may include endoscopic cauterization, anterior and posterior ethmoid artery cauterization, external ethmoid artery ligation, transantral internal maxillary artery ligation, or, in extreme cases, external carotid artery ligation. More recently, endonasal endoscopic ligature of the sphenopalatine artery has become a preferred approach.

NASAL FRACTURES

The nasal bones are the most frequently fractured bones of the facial skeleton. Studies evaluating maxillofacial trauma in both adult and pediatric patients report nasal bone fractures in 14% to 50% of all facial fractures. The most common etiologies include assault, sporting activities, and traffic accidents. Isolated fractures of the nasal bones are usually accompanied by epistaxis, local edema, anosmia, or hyposmia. A thorough history should investigate the mechanism of injury, pre-existing nasal deformities, a history of nasal airway obstruction, previous sense of smell, and a complete medical history including any prior nasal allergies, sinusitis, or nasal septal surgery.

The physical examination should involve both internal and external evaluation of the nose, regardless of the mechanism of injury. Although isolated nasal fractures rarely require radiographic studies, it is appropriate to order a CT scan after a thorough history and physical exam when other facial fractures are suspected.

Management of nasal trauma should begin with control of the bleeding. Topical vasoconstrictors and direct pressure with ice should be attempted before moving on to tamponade with gauze packing, catheters, or stents. For uncontrolled epistaxis that fails to resolve with these measures, ligation or embolization may be necessary. Prophylactic antibiotics to cover against gram-positive bacteria are recommended, particularly with mucosal lacerations. Patients should be given nasal decongestants and saline irrigations to maintain humidification and cleanse the intranasal mucosa.

Reduction by a qualified specialist is typically performed early (within five days of the injury) to maximize function and cosmesis. In cases of exposed cartilage or avulsion injury, immediate referral is necessary to maximize preservation of cartilage, which can become devitalized within eight hours. Early referral is always recommended. Within 5 to 10 days after injury, the bones can become fixed, making reduction difficult.

Minor ongoing bleeding can be controlled with a topical vasoconstrictor, such as phenylephrine 0.25% or oxymetazoline hydrochloride, administered as a spray or soaked cotton pledgets. The septum should be assessed for hematoma, dislocation, mucosal lacerations, or exposed cartilage. Palpation of the anterior nasal spine via the sublabial sulcus is important because of the increased incidence of septal hematoma with fractures in this region.

Complications most commonly encountered with nasal fractures include septal hematoma, nasal obstruction, and significant deformity. Undiagnosed hematomas of the nasal septum can result in cartilage destruction and so-called saddle-nose deformity.

MANDIBULAR FRACTURES

The mandible, the largest of the facial bones, is the second most frequently fractured bone of the face. Blunt trauma is the most common etiology in mandible fractures, usually as a result of motor vehicle accidents, assaults, athletic activities, and falls. The mandible is often fractured at more than one location because of the ring structure formed by its articulation at the temporomandibular joint. In addition to the traditional fracture classifications—open, closed, simple, complex, or comminuted—mandibular fractures are also described as favorable or unfavorable, depending on whether the muscles of mastication tend to reduce or distract the fracture, respectively. Dentoalveolar fractures involve only the alveolar ridge and associated teeth and are, by definition, open fractures.

The most common presenting symptoms of patients with mandibular fractures are pain and malocclusion. Additional signs and symptoms include intraoral bleeding, lower lip and chin hypoesthesia or anesthesia, trismus, deviation with jaw movement, swelling or hematoma of the floor of the mouth, and ecchymosis of the gingiva. Securing a stable airway should be the primary concern in a patient with a maxillofacial injury. A posteriorly displaced tongue, blood, vomitus, denture fragments, or foreign material may obstruct the airway and cause asphyxia.

A thorough clinical examination will usually reveal mandibular fractures before x-rays are taken. Inspection of the oral cavity may reveal ecchymosis of the alveolus, sublingual hematoma, and gingival bleeding-all signs of a possible mandibular fracture. Palpation of the bone and a bimanual mandibular stress test can reveal a step-off or displacement with pain, indicating a likely fracture.

Radiography is helpful to delineate fracture patterns and locations. The best study to evaluate most of the mandible is a Panorex. A mandibular series, which includes a lateral oblique, posteroanterior (PA), and Towne's views, is also helpful, but alone it is less sensitive than Panorex. The Towne's view is best to visualize condylar regions; a PA view is helpful in seeing the mandibular symphysis. Computed tomography scans are not necessary for isolated mandibular fractures documented by x-rays; however, complex facial fractures involving the mandible may necessitate a CT scan and eliminate the need for plain radiographs. In cases where missing teeth are unaccounted for, a chest x-ray should be performed to evaluate for aspiration.

The principles of management include re-establishing pre-injury dental occlusion, reducing and stabilizing fractures, and closing any soft-tissue defects. Other head and neck injuries must be ruled out, especially cervical spine injuries; pain medication and prophylactic antibiotics against oral bacteria, particularly for open fractures, should be administered. Nondisplaced fractures can be managed with observation and a soft diet if the patient has normal occlusion. For displaced fractures, early referral (less than seven days) is required for closed reduction or open reduction with internal fixation. Potential complications include infection, malocclusion or nonunion, temporomandibular joint ankylosis, and inferior alveolar nerve disturbances.

MIDFACE FRACTURES

Fractures to the midface include zygoma, malar, orbital floor, and maxillary bone (LeFort) fractures. Initial evaluation of these fractures requires a thorough evaluation of adjacent structures. Compared to nasal fractures, the forces necessary to induce midface fractures are more severe and should raise suspicion for other injuries of the cranium, brain, orbits, and cervical spine.

Zygoma fractures commonly present with periorbital ecchymosis, lateral subconjunctival hemorrhage, infraorbital hypoesthesia, bony step-off of the orbital rim, and depression of the malar eminence. Displacement of the bone medially may impinge on the coronoid process of the mandible, resulting in trismus.

Orbital floor fractures typically result from a blunt force directed at the globe, causing increased pressure within the orbital cavity that blows out the thin bony floor. Patients usually present with edema, ecchymosis, and entrapment of the extraocular muscles, causing diplopia and restricted upward gaze.

LeFort fractures are much less common due to the strong forces required to fracture the maxilla. Initial workup should focus on injuries to the cervical spine, orbits, and central nervous system to rule out more serious injuries. A classic feature of a displaced fracture of the maxilla is malocclusion, with a depressed or flattened midface. By grasping the palate or upper incisors, the examiner can detect mobility of the maxillary bone relative to the rest of the skull. In severe cases, posterior displacement of the distal maxilla can impinge on the airway. Hemorrhage and edema can further obstruct the airway; thus, early airway management is always advised. Nasal instrumentation should be avoided because of the risk of anterior skull base penetration.

Diagnosis of all midface fractures has been enhanced by high-resolution CT scanning. Axial and coronal CT scans with thin cuts of the facial bones are recommended for all of these fractures.

With suspected orbital injury, early ophthalmology consultation must be arranged to assess for ocular injury. Neurosurgical consultation is indicated for suspected intracranial injury, cerebrospinal fluid leak, or cervical spine injury. Orthopedic consultation should be considered when other musculoskeletal injuries are suspected. Early fracture reduction and fixation have replaced conservative "wait and see" management for midface fractures. Thus, many functional and cosmetic complications can be avoided, such as malocclusion, enophthalmos, malunion, and malar flattening.

OTOLOGIC EMERGENCIES

Ear emergencies include auricular hematomas, complications of otitis media, temporal bone fracture, necrotizing otitis externa, and acute facial paralysis.

Auricular hematomas. Serious attention should be paid to diagnosing auricular hematomas since they can result in necrosis of the perichondrium, which can lead to significant cosmetic deformity such as "cauliflower ear." They present as nontender, dark, fluctuant collections of blood in the auricle. These hematomas can develop after trauma as blood accumulates between cartilage and the overlying skin. Blunt trauma, as in wrestling and boxing, can produce shearing forces between the perichondrium and cartilage, resulting in the formation of auricular hematomas.

Treatment includes aspiration with an 18-gauge needle or incision and drainage, followed by application of a compressive dressing for a week to allow the cartilage to readhere to the perichondrium. Coverage with an antistaphylococcal antibiotic is recommended.

Complications of otitis media. Due to the common use of antibiotics to treat ear infections, complications of middle ear infection have become less frequent. Early recognition, diagnosis, and imaging are critical to adequate management and prevention of severe complications. These complications, which usually follow an acute infection, even in patients with chronic disease, can be categorized as intracranial and extracranial.

Intracranial complications include (in order of frequency) meningitis, intracranial abscess (temporal lobe, cerebellar, or extradural), sinus thrombosis (lateral/transverse, sigmoid, or cavernous sinus), cerebritis, and otitic hydrocephalus. Patients with meningitis often present with neck stiffness and headache; they will have positive bacterial cerebrospinal fluid (CSF) cultures. Intracranial abscesses can be diagnosed on the basis of clinical exam findings and CT scan results. Extradural abscess presents with local tenderness and headache.

Fever, otalgia, and otorrhea despite antibiotic treatment are seen in patients with lateral/transverse sinus thrombosis. Blood cultures help identify the causative organism or organisms, which are often polymicrobial and predominantly anaerobic. Prognosis is good if treatment is initiated early with IV antibiotics and mastoidectomy. Clot removal during surgery and anticoagulation are controversial. Otitic hydrocephalus is an increase in CSF pressure after lateral/transverse sinus thrombosis from otitis media.

Extracranial complications of otitis media include mastoiditis (specifically, mastoid abscess), mastoid subperiosteal abscess, Bezold's abscess, facial nerve paralysis, labyrinthitis, and petrositis. Often, mastoid abscess develops despite seemingly appropriate antibiotic therapy for otitis media. These extracranial complications can be seen in patients with a cholesteatoma, which is a middle ear mass of keratinizing epithelium and cholesterol that leads to infections and bony erosion. Cholesteatoma should be suspected when an older child presents with acute mastoiditis.

Mastoiditis causes postauricular swelling and erythema, auricle protrusion, and coexisting otitis media. The tympanic membrane is usually inflamed and thickened, and it may also be perforated with mucopurulent otorrhea. Staphylococcus pneumoniae, S. aureus, S. pyogenes, and H. influenzae are the most frequently isolated pathogens.

Subperiosteal abscess, the most common form of mastoid abscess, is usually observed in children with poorly pneumatized mastoid bones. Postauricular swelling is the most consistent finding, but it may be absent in up to 15% of patients. Erythema, tenderness, and protrusion of the auricle are also inconsistent findings. A CT scan is usually performed to evaluate for the presence and path of a mastoid abscess.

Treatment includes IV antibiotics, myringotomy, and mastoidectomy. Intraoperative findings often reveal cholesteatoma or granulation tissue. Bezold's abscess is a rare, deep-neck abscess arising from acute mastoiditis due to extension of the infection into the digastric groove. An otolaryngologist should be involved in the early management of patients with Bezold's abscess because surgical intervention may be required.

Temporal bone fracture. The temporal bone contains important sensory and neural structures that may be damaged in patients who experience craniofacial trauma. Patients with temporal bone fractures may present with otorrhea, hemotympanum, CSF rhinorrhea, ear canal laceration, and facial weakness on the affected side. The most serious complications of these fractures are hearing loss (35% to 85% of patients), CSF fistula (15%), facial nerve paralysis (7%), and meningitis (1.8%).

Facial nerve function following temporal bone fractures should be evaluated. The prognosis is good for recovery without surgical intervention in cases of delayed or incomplete facial paralysis. However, recovery of function is poor in 40% of patients with immediate onset of complete paralysis. Early surgical intervention with repair of the nerve is required for facial paralysis of immediate onset after temporal bone fractures. Within one week, about 78% of CSF fistulas close spontaneously. The risk of meningitis may increase significantly if a CSF fistula persists for more than seven days. For this reason, prophylactic antibiotics should be considered when a CSF fistula is present.

Temporal bone fractures may violate the otic capsule and result in immediate and profound sensorineural hearing loss. Early audiometric assessment is important to document the severity of hearing loss. Occasionally, patients with residual auditory function will present with a progressive or fluctuating hearing loss as a result of a perilymphatic fistula. Surgical exploration with closure of perilymphatic fistulas may help preserve hearing in these patients.

Necrotizing otitis externa. Necrotizing otitis externa (NOE), also referred to as skull-based osteomyelitis, is an advanced malignant infection of the external auditory canal. Diabetic patients account for 90% of cases, but immunocompromised patients are also susceptible. Pseudomonas is the causative organism in almost 98% of cases.

Necrotizing otitis externa should be suspected in any immunocompromised patient who presents with otalgia and otorrhea that are untreated or unresponsive to topical antibiotics. Water exposure and irrigation of the auditory canal (usually for cerumen disimpaction) have been implicated as causative factors. If NOE is untreated, facial nerve paralysis or other cranial neuropathies can develop from extension of the infection.

The diagnosis of NOE is based on the history, physical exam, laboratory tests such as blood glucose level and erythrocyte sedimentation rate, and CT or MRI evidence of otitis externa with possible bone erosion and infiltration into infratemporal soft tissues. Patients may, however, be afebrile with a normal white blood cell count. On otoscopy, the external ear canal will typically have granulation tissue at the bony-cartilaginous junction.

Although CT and MRI are superior tests, nuclear medicine studies may help in the diagnosis and evaluation of disease progression and resolution. Technetium bone scans are very sensitive because they identify osteoblastic activity. By targeting granulocytes and bacteria, gallium scans are more specific than bone scans and can be used to follow disease activity. Antibiotic treatment consists of prolonged antipseudomonal coverage (for six to eight weeks); an oral quinolone, for example, may be administered. Patients with resistant Pseudomonas aeruginosa generally require hospitalization for biopsy, debridement, and parenteral antibiotics.

Acute facial nerve paralysis. Acute facial nerve paralysis is challenging because most patients will present with idiopathic palsy, which resolves spontaneously. This diagnosis must be separated from other etiologies of facial paralysis, which include unusual or rare conditions, some of which have significant morbidity and mortality. A comprehensive history and detailed physical examination, including otoscopy and a complete neurologic exam, are essential.

Atypical signs and symptoms that may indicate additional pathology and require urgent specialist referral include otalgia, paresthesias, hearing loss, otitis media or externa, other cranial neuropathies, lymphadenopathy, skin vesicles, single facial nerve branch involvement, or mastoid swelling. Also of concern is a history of prior facial paralysis or a gradual progression of paralysis beyond three weeks. Radiologic imaging may be indicated to rule out a neoplasm if these atypical associated findings are present.

Etiologies of acute facial nerve paralysis may fall into the following categories: infection, inflammation, trauma, neoplasm, and hematologic or congenital causes. Facial paralysis due to infection may result from otitis media, mastoiditis, herpes zoster (Ramsay Hunt syndrome), varicella, mumps, temporal lobe abscess, meningitis, encephalitis, mycoplasma, cat scratch disease, Kawasaki disease, Guillain-Barré syndrome, HIV, or Lyme disease. Trauma-induced facial paralysis may result from burns, temporal bone fracture, penetrating nerve injury, or surgical injury. Examples of neoplasms that can cause facial paralysis include leukemia, cerebellar astrocytoma, and rhabdomyosarcoma. Hemophilia and histiocytosis are possible hematologic etiologies. Melkersson-Rosenthal syndrome, osteopetrosis, and intracerebral arteriovenous malformation are examples of congenital etiologies.

Prognosis for idiopathic facial palsy is good. The early use of steroids may reduce the duration of the paralysis and promote complete recovery in adults. Steroid therapy is most effective when started within one day of disease onset. Vitamin B₁₂, alone or in combination with steroids, may help patients recover faster than those treated with steroids alone. In one study, patients treated with 100% hyperbaric oxygen recovered faster than those treated with steroids and 7% oxygen at the same pressure. Surgical decompression of the facial nerve canal is no longer considered an effective or appropriate treatment for patients with idiopathic facial palsy.

About 95% of children with idiopathic facial palsy will recover full function, most within the first three weeks of the illness. The benefits of steroid therapy or any other treatment have yet to be proven for idiopathic facial palsy in children.

Facial paralysis can result in ocular complications due to incomplete closure of the eyelids, causing corneal exposure keratopathy. The cornea can be protected with artificial tears or ointments, overnight patching, or the use of moisture chambers. An ophthalmologic consult may be helpful.