Week 16: HEENT

The patient presents with brisk hemorrhage from the nose with a failed anterior pack suggestive of a posterior nasal bleeding source. The initial management of any patient presenting with epistaxis should focus on the airway and assessment of hemodynamic status. This should be followed by application of direct pressure and localization of the bleeding cause. Anterior epistaxis results from bleeding from Kiesselbach’s area, which can be directly visualized during evaluation. Posterior bleeding usually originates from the nasopalatine branch of the sphenopalatine artery, which cannot be visualized directly. In a patient where a properly placed anterior pack does not control bleeding, placement of a posterior pack should be performed. In the Emergency Department, this is typically performed by placing a Foley catheter into the nares and advancing it into the posterior pharynx followed by inflation of the balloon and application of anterior traction to tamponade bleeding while waiting for ENT to arrive. After placement of a posterior pack, patients should be given prophylactic antibiotics to avoid the development of sinusitis and toxic shock (via colonization of packing material). Patients with posterior packs must be admitted to the hospital and likely require intensive care management. Posterior packing has been shown to decrease partial pressures of oxygen and increase the partial pressure of carbon dioxide. Dysrhythmias, bradycardia and aspiration have been described after posterior packing.

After a properly placed anterior pack fails to control bleeding, placement of a contralateral pack (B) is unlikely to contribute to hemostasis. Similarly, replacing the anterior pack (D) is unnecessary and will delay definitive management. Although the patient will require admission (A) this does not obviate the need to control bleeding emergently in the Emergency Department.

This patient is exhibiting signs and symptoms consistent with cavernous sinus thrombosis. These signs and symptoms are the result of structures affected by cavernous sinus thrombosis. The internal carotid artery passes through the cavernous sinus. The third, fourth, sixth, and portions of the fifth cranial nerves also course through the sinus. This close proximity of veins, arteries, nerves, and paranasal sinuses accounts for the classic presentation of cavernous sinus thrombosis. The clinical presentation is usually due to the venous obstruction as well as impairment of the cranial nerves that are near the cavernous sinus. Headache is the most common presenting symptom and is usually followed by fevers, periorbital edema, and cranial nerve signs. Lateral gaze palsy secondary to an abducens nerve (CN VI) palsy is most common as it lies freely within the sinus while the others course within the lateral walls of the sinus. CST is usually a late complication of an infection of the paranasal sinuses. Cavernous sinus thrombosis is a clinical diagnosis although imaging is often used in cases of diagnostic uncertainty or to confirm the diagnosis. MRI with MR venography (MRV) is the preferred imaging choice as the MRV will show the absence of venous flow in the affected cavernous sinus. Staphylococcus aureus accounts for approximately 70% of all infections.

While the oculomotor nerve (B) and trochlear nerve (D) course through the cavernous sinus and may also be affected in cavernous sinus thrombosis, the abducens nerve lies freely in the cavity and is most commonly affected. The optic nerve (C) is rarely affected due to its location outside of the cavernous sinus.

The patient is complaining of symptoms consistent with iatrogenic tympanic membrane perforation that occurred during disimpaction. Tympanic membrane perforations (TMPs) can result from a complication of infection (acute otitis media, myringitis); blast injury (explosion, slap, lightening); barometric pressure changes (flying in airplane, scuba diving); and improper attempts at wax removal or ear cleaning. The pars tensa is the most common area of the TM to perforate because it is the most anterior and thinnest portion. Patients typically experience decreased or complete hearing loss, pain, and bleeding. In the setting of tympanic membrane perforation, the goal is to keep the ear dry, provide analgesics, and arrange for follow-up with an ENT. Most heal within a few months.

The patient does not require admission (A) to the hospital. ENT care can be arranged for as an outpatient. Traumatic tympanic membrane perforations do not require otic antibiotics (B) unless the ear was contaminated such as from diving in seawater or the rupture is secondary to infection. The patient should receive more than a cotton ball (D) in her ear. Her management should include analgesia and ENT follow-up because complications of tympanic membrane rupture include facial nerve palsy, vertigo, and hearing loss.

This patient has Ménière’s disease. This disorder is associated with increased endolymph within the cochlea and labyrinth. The common triad is tinnitus, vertigo, and unilateral hearing loss (sensorineural). A key finding in Ménière’s disease is fluctuating hearing loss. Episodes are abrupt in onset and associated with nausea and vomiting. There are often long, symptom-free intervals between attacks.

Benign paroxysmal positional vertigo (A) is sudden in onset, short-lived, and positional in nature. It is not associated with tinnitus or hearing loss. Salicylate (aspirin) toxicity (C) is associated with tinnitus and reversible hearing loss. The patient has a history of osteoarthritis and may be using aspirin for her pain; however, salicylate toxicity is usually associated with bilateral hearing loss. Symptoms of vertigo are also uncommon in such patients. Vestibular neuronitis (D) manifests with severe vertigo positional in nature but not associated with hearing loss. It is usually preceded by a viral upper respiratory infection.

Cholesteatoma is a mass of keratinized squamous epithelium that occurs in the middle ear or mastoid process occurring most frequently in teenagers. This ear-related metaplasia is not associated with cholesterol or gallbladder problems, as the name suggests. There are two types of cholesteatoma. The congenital type is less common and occurs medial to the tympanic membrane. The acquired type is more common and grows from the tympanic membrane. Conductive hearing impairment prevails, with imbalance and facial weakness being the most common associated symptoms. Examination may reveal inflammation, retrotympanic waxy appearing polyps or white-pasty discharge from the tympanic membrane. As such, this can easily be confused with chronic, suppurative otitis media. Microscopic excision surgery is required to prevent complications and to maintain or improve hearing.

Acoustic neuromas (A) present with sensorineural, not conductive, hearing impairment. Furthermore, these masses occur in the inner ear and temporal bone on the vestibular nerve and would not likely be viewable during an otoscopic examination. Otitis media (C) presents with otalgia, hearing loss, fever and tympanic membrane abnormalities like erythema, bulging, or cloudiness. Although retrotympanic masses can result from chronic suppurative middle ear infections, current infection is unlikely in the above patient. Squamous cell carcinoma (D) is an epithelial cell malignancy that typically occurs on the external, not middle, ear due to prolonged sun exposure. It has an ulcerated, erythematous appearance with or without bleeding.

This patient is exhibiting signs and symptoms of posterior epistaxis. Posterior epistaxis is less common than anterior epistaxis and is most commonly due to bleeding from the sphenopalatine artery, located at the posterior aspect of the middle nasal turbinate. Patients with posterior epistaxis typically complain of bleeding from both nostrils. Inspection of the posterior pharynx may reveal profuse bleeding. In treating epistaxis, start by having the patient gently blow his nose or suction out the blood. If the bleeding is profuse, apply cotton balls soaked in a topical anesthetic and vasoconstrictor for at least five minutes. A good option is 1% tetracaine plus 0.05% oxymetazoline solution. In posterior epistaxis, this may not achieve hemostasis or allow visualization of the location of bleeding. Management of posterior epistaxis should be with either a Foley catheter or dual balloon pack. A 10 to 14 French Foley catheter with a 30 cc inflatable balloon may be inserted past the site of the bleeding and inflated with 5 to 7 cc of air or saline. It should then be pulled back onto the site of the posterior bleed and inflated until it is snug. An anterior nasal pack should then be placed in both nares. A dual balloon pack is placed by anesthetizing the nare and advancing the pack past the site of the bleeding. The posterior balloon is inflated with 5 to 7 cc of saline or air and pulled back onto the site of bleeding. It is the further inflated until it is snug. The anterior balloon is then inflated. The opposite nare should be packed as well. Complications of posterior epistaxis packing include aspiration, hypoxia, hypercarbia, and symptomatic bradycardia. Antibiotics should be administered after all packing; however, there is significant controversy regarding whether prescribing antibiotics actually prevents toxic shock syndrome as there is no evidence to support this. All patients with posterior packing should be admitted to a telemetry bed for further monitoring while the packing is in place.

The facial artery (A) may be injured during oncologic surgery of the parotid gland or in severe facial trauma. Kiesselbach plexus (B) is the most common source of anterior bleeding. Given that this patient has profuse bleeding that appears bilateral, the source is most likely to be posterior. The labial artery (C) is most commonly injured in children who suffer electrical burns of the commissure of the lip while chewing on electrical cords.

This patient is showing signs and symptoms consistent with necrotizing or malignant otitis externa. Necrotizing otitis externa is defined as the progression of otitis externa through the periauricular tissue and into the temporal bone. It most commonly occurs in immunocompromised or diabetic patients. The causative agent is typically Pseudomonas aeruginosa. Signs and symptoms of necrotizing otitis externa include persistent, excruciating pain that interferes with sleep and continues despite topical treatment. Additional signs and symptoms include fever, erythema of the periauricular tissues, and facial or vagal nerve palsy. Diagnosis of necrotizing otitis externa is by CT of the temporal bone. The key to management is with systemic antibiotics. Antipseudomonal double-coverage is preferred with a penicillin-based antipseudomonal and an aminoglycoside. Ciprofloxacin is a reasonable alternative in patients who cannot take one of these antibiotics. Surgical debridement may be necessary. Mortality is as high as 50% if untreated. Patients should be evaluated by ENT for further management.

Moraxella catarrhalis (A) and Streptococcus pneumoniae (D) are two of the most common causes of otitis media; however, this patient has signs and symptoms of malignant otitis externa given his exam findings with severe persistent pain. Staphylococcus aureus (C) is a common cause of cellulitis; however, cellulitis of the external ear is rare and the edema of the external ear and severe pain are more consistent with necrotizing otitis externa.

In this case, the patient has symptoms concerning for mastoiditis. Mastoiditis is most common in children between 1 and 3 years old. It is a complication of acute otitis media with extension of the infection into the mastoid bone. Patients typically present with ear proptosis, fever, an injected tympanic membrane on the infected side, and postauricular erythema. Organisms involved in this infection are similar to those in otitis media, including Streptococcus pyogenes, Staphylococcus aureus, and Pseudomonas aeruginosa. Diagnosis is confirmed by CT, and consultation with ENT is indicated. If the patient has not taken antibiotics before, the initial treatment is with oral antibiotics if the disease is mild and close follow-up can be ensured. If a patient develops mastoiditis after an appropriate course of oral antibiotics, then admission, ENT consultation, and intravenous antibiotic therapy are warranted. Antibiotics with good gram-positive coverage like ampicillin-sulbactam or third-generation cephalosporins are the first-line choice.

B. This patient has already completed one course of antibiotic therapy, so starting her on a different oral antibiotic is not appropriate. Admission is warranted for more aggressive management.

C. Discharging the patient with instructions for supportive care is not the right course of action, again, because initial antimicrobial treatment failed. Admission and additional antibiotics are needed to treat the acute infection process.

D. At this point in the patient’s care, intravenous antibiotic therapy is the next step. Mastoidectomy should be considered only if intravenous antibiotic therapy fails and the infection spreads beyond the mastoid.

Acute mastoiditis is usually a complication of untreated or inadequately treated acute otitis media. It has also been described as a complication of leukemia, mononucleosis, sarcoma of the temporal bone, and Kawasaki disease. Acute mastoiditis is a natural extension of otitis media because the mastoid air cells are generally inflamed during acute otitis media. The aditus ad antrum is a narrow connection between the middle ear and mastoid air cells. When this is obstructed, there is increased risk for abscess development and bone destruction. Progression results in destruction of the mastoid bone trabeculae resulting in acute mastoid osteitis. Clinically, patients present with otalgia, fever, headache, and erythema. Pain is universally present. Physical exam findings mimic acute otitis media in addition to postauricular or supra-auricular tenderness and edema. Most cases resolve after administration of antibiotics. For persistent cases, surgical intervention is required for drainage.

Orbital cellulitis (A) is a complication of ethmoid sinusitis, not mastoiditis. Otorrhea (C) can occur in mastoiditis (secondary to marked otitis media with ruptured tympanic membrane). However, it is uncommon. Otorrhea is more commonly observed with otitis externa. Trismus (D) is a complication of suppurative parotitis.

The patient has symptoms consistent with acute otitis media. He is a candidate for a “wait-and-see” prescription for an antibiotic if his symptoms do not improve in 48 to 72 hours. He meets the criteria for “wait and see” including age ≥ to 2 years old, unilateral infection, symptoms for fewer than 48 hours, and temperature is less than 39⁰C. Assuming there are no contraindications, amoxicillin (90 mg/kg/day PO for 5-10 days) is the first-line treatment. Amoxicillin-clavulanate is appropriate if the patient has failed a course of amoxicillin. Cephalosporins like cefdinir or cefuroxime or clindamycin are appropriate in penicillin-allergic patients. Streptococcus pneumoniae is the most common bacterial organism, although most cases are viral.

A. Given the tympanic membrane visualized, antipyretics alone are not sufficient if there is no improvement within 48 to 72 hours. Complications from untreated bacterial otitis media include mastoiditis and hearing complications.

B. If the wait-and-see approach fails, the patient should complete a course of antibiotics. Referral to an ENT for possible tympanostomy should only occur after repeated episodes of otitis media.

C. Immediate use of antibiotics has been shown not to improve outcomes when using these criteria. In addition, there is an increased risk of diarrhea and antibiotic resistance for those who take antibiotics.