Oropharyngeal and Laryngeal Emergencies

• The oral cavity extends from the lips to the oropharynx. The roof consists of the hard and soft palates, and the cheeks form the lateral borders.
• The pharynx consists of the nasopharynx, oropharynx and hypopharynx. The nasopharynx is located just posterior to the nasal choanae. The oropharynx extends from the soft palate to the hyoid bone at the level of the third cervical vertebrae. The hypopharynx is the distal continuation of the oropharynx extending from the third to the sixth cervical vertebrae at which point the esophagus begins.
• The larynx, the uppermost part of the tracheobronchial system, also runs the length of the third through sixth cervical vertebrae just anterior to the hypopharynx. The prominent thyroid and cricoid cartilages are usually palpable and are excellent references for structures of the neck. The thyroid cartilage is present at the level of the fourth to fifth cervical vertebrae while the cricoid is at the sixth cervical vertebrae. The vocal cords are located at the level of the midpoint of the anterior thyroid cartilage.
• The pharynx, larynx, deep neck spaces, carotid artery, jugular vein, mediastinum and prevertebral soft tissue are in close contact with one another. Thus, disease in one area can have widespread consequences.
• Innervation of the face, oropharynx and larynx is complex and includes cranial nerves V, VII, IX, X, XI, XII. Referred pain is common and thorough examination of all surrounding structures is warranted.

Dysphagia

• Difficulty swallowing (not painful swallowing).
• Most common etiologies: neurologic and musculoskeletal disorders.
• Other causes: collagen vascular disorders, myopathies, motility disorders, obstructive lesions, and extrinsic compression secondary to thoracic/neck masses.

• Painful swallowing.
• Etiology: infectious and irritant lesions of the oropharynx and esophagus.

• Change in phonation. Secondary to laryngeal, vocal cord, or recurrent laryngeal nerve pathology.
• Most common etiology: viral inflammation ("laryngitis") and voice abuse.
• Other causes: vocal cord nodules, neoplasm, allergies, local irritants, granulomatous/ automimmune disease, endocrine disease, and trauma.

• This common condition is of concern because of the possible sequelae. Streptococcal disease may lead to rheumatic fever, glomerolunephritis, scarlet fever and toxic shock syndrome. Infectious mononucleosis (IM) has numerous potential complications including hemolytic anemia, hepatitis, splenic rupture, myocarditis, pericarditis and neurologic dysfunction. Other complications of pharyngitis include deep space infections, peritonsillar abscess, OM and rarely sepsis or meningitis. 14
• Differential diagnosis includes deep space infections, peritonsillar abscess and epiglottitis. Symptoms of pharyngitis are also seen in irritant and thermal injuries, gastroesophageal reflux, pemphigus, otic emergencies, hematologic malignancy and trauma.

• Overall, respiratory viruses are the most common etiology of pharyngitis.
• The most common bacterial agent, Group A ß-hemolytic streptococcus (GAS), occurs primarily in the 5-15 yr age group.
• Other bacterial etiologies include C. hemolyticum, H. influenzae, M. pneumoniae, S. pneumoniae, C. diphtheriae, Chlamydia, syphilis, anaerobes and gonococcus.
• Infectious mononucleosis (IM) caused by Epstein-Barr virus often presents as pharyngitis in young adults and college students. Other viral causes are CMV and HSV.

• The primary symptom is odynophagia. Cough, upper respiratory symptoms, myalgias and headache are classically associated with viral disease but are also seen in bacterial disease especially Chlamydia and Mycoplasma.
• Physical Examination Signs
  • Pharyngeal edema and erythema is present and may extend to the uvula and soft palate. Fever, purulent exudates and ulcerations occur in both viral and bacterial disease and do not pinpoint the source. When ulcerations are present, consider anaerobes, herpes (I and II), syphilis, and herpangina.
  • An oropharyngeal membrane is seen with diphtheria and anaerobes.
  • Tender cervical adenopathy occurs with both bacterial and viral pharyngitis. Posterior cervical adenopathy is classically associated with IM.
  • Patients with IM can have a generalized maculopapular rash especially if they have received amoxicillin or ampicillin. Also consider scarlet fever.
  • Extrapharyngeal findings are often found in IM including hepatomegaly and splenomegaly.
• Laboratory Evaluation
  • Throat culture is the gold standard for diagnosing GAS and is 90-95% sensitive. Results take about 48 h to finalize.
  • Rapid streptococcal antigen tests are readily available and provide results in as little as 30 min. Sensitivity of these tests is approximately 60-90%.
  • A positive monospot test, leukocytosis with atypical forms and abnormal liver function tests support the diagnosis of IM.
  • Serologies and special culture media exist (i.e., for HSV, gonococcus and diphtheria) although use is not frequently indicated and results are not readily available in the ED.

• Bacterial Pharyngitis
  • GAS: The recommended therapy remains penicillin VK (or a single dose of benzathine penicillin IM if noncompliance is likely). Alternatives include macrolides and second and third generation cephalosporins. Azithromycin is the only agent approved for a five-day course. Ten days of therapy is recommended with all other agents in order to prevent rheumatic fever. Patients with chronic or recurrent disease should receive clindamycin or amoxicillin/clavulanate.
  • Mycoplasma and Chlamydia: erythromycin or tetracycline.
  • Diphtheria: antitoxin plus erythromycin or penicillin.
  • Gonococcus: IM ceftriaxone and other approved regimens such as oral fluoroquinolones.
• Viral Pharyngitis
  • IM does not require specific therapy although a tapered course of steroids can provide symptomatic relief. Immunocompromised people with HSV are treated with acyclovir. Otherwise, viral disease is treated symptomatically.
• Ancillary treatment includes analgesics, oral hygiene and intravenous fluids for both viral and bacterial disease.

• Most patients with pharyngitis are safely discharged. Patients with recurrent and chronic symptoms should be referred to ENT for possible tonsillectomy.
• Patients with IM need discharge information detailing the possibility of multi-organ involvement. All potential contact sports should be avoided to reduce risk of splenic rupture.
• Admission is warranted for dehydrated patients or if any question exists regarding airway patency or ability to handle secretions.

Risk Factors/Etiology

• This occurs most commonly in young adults. It is unusual in children.
• Patients with previous episodes are at increased risk for recurrent abscess development.
• The process is usually seen in the setting of tonsillitis and can occur even if appropriate treatment has been initiated.
• Infection originates from either the tonsillar crypts or the surrounding minor salivary gland emergencies. As a result, peritonsillar abscess is possible even if the patient has had a tonsillectomy.
• Infections are typically polymicrobial involving both aerobes and anaerobes.

• Patients complain of unilateral odynophagia, dysphagia, malaise and muffling of the voice. There is often a history of peritonsillar abscess or recent pharyngitis.
• Examination reveals localized erythema and unilateral swelling at the peritonsillar area.
• If present, trismus makes exam difficult. The uvula is often displaced medially. If the abscess has spontaneously ruptured, gross purulent material will be visible. Patients usually have temperature elevation and clinical evidence of dehydration. Respiratory difficulty is less common but occurs when there is inferior extension of purulent material.
• Diagnosis of peritonsillar abscess is made clinically.
• Complications: dehydration; airway obstruction; aspiration of purulent drainage; cavernous sinus thrombosis; spread to contiguous areas including the deep spaces of the neck and intracranial structures; and spontaneous carotid artery erosion or trauma during treatment.
• Peritonsillar abscess is commonly confused with peritonsillar cellulitis. Cellulitis tends to be bilateral whereas abscess is unilateral in over 90% of cases. Differentiation is made via needle aspiration.
• The differential diagnoses also include neoplasm, carotid artery aneurysm, infectious mononucleosis, parapharyngeal space infection and pharyngitis.

• Drainage is required and, in most cases, is accomplished by aspiration using an 18 gauge spinal needle after application of topical anesthesia. Treating physicians must be aware of the inferior and lateral location of the carotid artery. Children and patients with significant trismus often require treatment under general anesthesia.
• In certain cases incision is required for adequate decompression. These include patients with recurrent or continued abscess after aspiration.
• Ideally, decompression is done by an ENT specialist unless the EP has the necessary expertise. If ENT is not available and the patient has impending airway obstruction, the EP should perform needle aspiration.

• Patients with uncomplicated abscess drainage are sent home with antibiotics and pain medications provided that they have appropriate follow-up.
• Admission is necessary for toxemia, presence of severe underlying disease, significant dehydration, airway compromise or if the patient is unable to tolerate PO fluids.

• Ludwig’s angina is infection of the submandibular space which includes both the sublingual space and the deeper submaxillary space located beneath the mylohyoid muscle.
• Infection begins in the submaxillary space and spreads upward and posteriorly.
• Typically, this is rapidly progressive bilateral cellulitis rather than a purulent fluid collection.
• Spread is via direct invasion rather than lymphatics or hematogenous route.
• Airway obstruction from tongue displacement is the main concern and can occur acutely.

• The primary risk factor is dental infection. The second and third mandibular molars are most commonly involved; the roots of these teeth are located beneath the mylohyoid muscle in the submaxillary space.
• Other risk factors are penetrating trauma to the floor of the mouth and mandible fractures.

• Infections are usually polymicrobial with both aerobes and anaerobes.

• There is often a history of dental trauma or recent dental work. Symptoms include odynophagia and pain to the floor of the mouth and anterior neck. Difficulty swallowing and speaking occur because of tongue displacement.
• Examination reveals an indurated edema of the floor of the mouth and anterior neck.
• Serosanguinous discharge is present but there is usually no frank pus or fluctuance. When significant edema is present, the tongue will be elevated and posteriorly displaced. Drooling, muffled voice, trismus, high fever and toxicity are common. Ludwig’s angina may progress to involve adjacent structures of the head and neck as well as the mediastinum and thorax. Look for corresponding signs and symptoms.
• Diagnosis is made clinically.
  • Both CT scan and MRI delineate the extent of infection and should be obtained if abscess is suspected. Only stable patients with mild disease or those with a secure airway should leave the ED for special radiographic studies.
  • Soft tissue films of the neck help define the extent of tissue edema and reveal localized gas collections.
  • CXR is indicated in patients with suspected thoracic or mediastinal spread.
  • Blood cultures and blood count should be ordered but are not helpful acutely.
• The primary differential diagnoses are deep space and submandibular abscess.

• Airway control: airway compromise can occur rapidly and is the primary cause of mortality in Ludwig’s angina.
  • Keep the patient in an upright position in order to minimize respiratory distress.
  • Orotracheal intubation is likely to be difficult or impossible. The best methods of securing the airway are fiberoptic nasotracheal intubation or primary tracheostomy; emergent ENT consultation is imperative. If ENT is not immediately available, the EP must be prepared for cricothyrotomy.
• Intravenous antibiotics: agents of choice are high-dose penicillin plus metronidazole or cefoxitin. An alternative for the penicillin-allergic patient is clindamycin. Other effective single-drug therapies are piperacillin/tazobactam, ampicillin/sulbactam and ticarcillin/clavulanate.
• Surgical treatment of this condition is indicated in cases where antibiotic therapy has failed or if there is evidence of an obvious purulent fluid collection.

All patients with Ludwig’s angina should be admitted to a monitored bed setting in anticipation of sudden airway deterioration.

Adult Epiglottitis

• Epiglottitis, also referred to as supraglottitis, is usually considered a disease of young children but occurs in adults as well. It often involves other supraglottic structures including the tongue base, arytenoid cartilages and aryepiglottic folds. Adult disease tends to have a more insidious onset and benign course although this is not always the case. Even the larger adult airway can rapidly lose patency.

• Common bacterial pathogens include H. influenza, Streptococcus sp. and S. aureus.
• Also consider viral pathogens, namely herpes simplex. Epiglottitis has also been reported secondary to thermal injury after smoking crack cocaine. In the majority of cases, however, the etiology is unknown.

• Symptoms include severe odynophagia, dysphagia, anterior neck pain and dyspnea.
• Examination:
  • Tongue blade examination in the stable adult is acceptable and will be notable for a relative absence of obvious pathology. This lack of oropharyngeal disease should lead the EP to suspect epiglottitis.
  • Patients often have fever, muffled voice, difficulty in handling secretions, tender cervical adenopathy and tenderness to palpation of the anterior neck. When present, stridor and respiratory distress indicate impending airway obstruction.
• Epiglottitis is a clinical diagnosis made via history and indirect laryngoscopy. Stable adult patients can undergo bedside radiographs of the lateral soft tissue of the neck. An edematous epiglottis and narrowed pharyngeal airway support the diagnosis. As with pediatric patients, take care to avoid any agitation in adult patients with respiratory distress.
• The most common mistake is to diagnose the patient with pharyngitis. Other conditions to consider are deep space infection, allergic reaction, foreign bodies, inhalation and trauma.

• Airway control is the priority. Patients with respiratory distress should undergo immediate airway control. Adult patients with an intact airway do not require prophylactic intubation. However, the EP should have airway equipment present at the bedside in anticipation of worsening symptoms.
  • The ideal mode of airway control is either orotracheal or nasotracheal intubation under direct visualization by ENT and Anesthesiology in the operating room setting. Blind nasotracheal intubation is contraindicated.
  • If the patient requires an immediate airway by the EP, orotracheal intubation can be attempted but the physician must be prepared to perform cricothyrotomy.
• Additional treatment includes humidified oxygen and antibiotics. Recommended antibiotic regimens include cefotaxime, ceftriaxone and ampicillin/sulbactam. Steroids are commonly administered although their effectiveness has not been proven.

• All patients with epiglottitis, irregardless of stability, should be admitted to an ICU in case of precipitous airway obstruction. ENT and Anesthesiology should be involved early in the event that airway control becomes necessary.

Risk Factors

• RP abscess in childhood usually develops secondary to regional adenopathy with suppuration. After approximately 5 yr of age, these nodes atrophy. In adults, this condition occurs in association with trauma to the posterior pharynx as seen with ingested foreign bodies, endoscopic procedures and intubation. RP abscess also occurs secondary to direct extension from other contiguous areas of the head and neck including the vertebrae.
• Parapharyngeal abscess is usually secondary to dental or pharyngeal infections. Cervical vertebral osteomyelitis and other head and neck infections also predispose to this condition.

• Infections are typically polymicrobial. The predominant organism depends upon the source. Abscesses secondary to local spread from cervical vertebral osteomyelitis are more likely to be caused by S. aureus while those with a dental source are usually mixed aerobic and anaerobic.

• Symptoms include dysphagia, voice changes, odynophagia and neck/jaw pain which is increased by movement. Patients may also give a history of IV drug use or recent head, neck or dental infection.
• Physical Examination Signs
  • Common findings with both RP and parapharyngeal abscess: meningismus, respiratory difficulty/stridor, trismus, cervical lymphadenopathy, dysphonia, drooling, and fever. Infants and small children may have nonspecific signs such as irritability.
  • Parapharyngeal abscess: submandibular induration and edema as well as swelling of the lateral pharyngeal wall on examination of the oral cavity.
  • RP abscess: pediatric patients will often prefer to lay supine and hold their neck in extension as this minimizes respiratory difficulty.
• Ancillary Evaluation
  • Lateral soft tissue neck radiographs: retropharyngeal disease will manifest as prevertebral air-fluid levels or abnormal widening of the prevertebral soft tissue.
  • In children, this would be anything >5-7 mm at the level of the second cervical vertebrae and 14 mm at the sixth cervical vertebrae (22 mm in adults). Ideally, neck films should be performed with the neck extended and the patient at end-inspiration since respiratory expiration and neck flexion cause prevertebral soft tissue prominence and mimic disease. Also look for loss of normal cervical lordosis. Swelling of the pharyngeal soft tissue is an indicator of possible parapharyngeal infection.
  • Chest radiographs are recommended in order to rule out mediastinal spread. CT scan of the neck defines the extent of infection and delineates areas of abscess and cellulitis but is rarely necessary to make the diagnosis.
  • Radiographs should only be done in patients who are completely stable or after the airway has been secured. A physician should be in attendance.

• The first goal of therapy is to ensure a patent airway. Significant abscess formation compresses the airway and makes intubation difficult. In addition, intubation attempts may cause abscess rupture and subsequent aspiration. ENT should be consulted for emergent tracheostomy if the patient has respiratory distress. The EP should be prepared to establish an airway via cricothyrotomy if necessary. Avoid blind nasotracheal intubation.
• Once the diagnosis is suspected, intravenous antibiotics should be initiated. Appropriate agents include those listed under "Ludwig’s Angina".
• All patients with deep space abscess require admission to a monitored bed.

• Elderly patients are most often affected secondary to underlying altered mental status, dysphagia and use of dental appliances. Children are also frequently involved because of their propensity to put objects in their mouth, their immature teeth and inadequate chewing.
• Differential diagnosis includes peritonsillar abscess, deep space abscess, epiglottitis, croup, local trauma, allergic reaction and functional disorders.

• Hypopharyngeal/upper esophageal FBs:
  • Older children and adults present with dysphagia, odynophagia and a foreign body sensation at their throat or neck. The patient is often able to pinpoint the area of involvement. If complete or near-complete obstruction is present, patients will be unable to swallow their own secretions.
  • Hypopharyngeal and esophageal FBs, if they are very large, can cause airway compromise in pediatric patients or in older patients.
• Laryngeal and tracheal FBs
  • Partially obstructing upper airway FBs cause stridor, hoarseness, coughing and varying degrees of respiratory difficulty with a prolonged inspiratory phase.
  • Complete obstruction results in cyanosis, inability to phonate/cough and abrupt respiratory failure.
• Symptoms that are initially mild sometimes become more severe in the case of organic FBs secondary to progressive moisture absorption and swelling.
• Sharp objects can cause rapid perforation. Blunt objects also cause perforation via pressure necrosis.
• Diagnosis in older children and adults is straightforward based upon history and presentation. In younger children, suspect FBs in anyone who presents with the above mentioned signs and symptoms especially if there is sudden onset and no history of airway disease. Various methods exist for localizing the object:
  • Direct visualization of the oral cavity and pharynx with a tongue blade.
  • Direct and indirect laryngoscopy: both require a cooperative patient and, thus, may be difficult to perform in children. Appropriate topical anesthesia prevents gagging. Fiberoptic laryngoscopy.
  • Radiographs of the neck and chest sometimes contribute to diagnosis if the offending FB is radiopaque. Many fish bones and aluminum pull-tabs are often not visible.
  • Take care during examination not to further impact the FB and worsen obstruction.

• Upper Airway
  • The priority is to maintain airway patency.
  • Complete obstruction: immediate Heimlich maneuver should be done in the prehospital care setting or if airway equipment is not available (back blows for infants). In the ED, removal of the obstructing FB should be attempted by direct laryngoscopy. If this is unsuccessful, it will be necessary to either advance the FB (usually to the right side) using the endotracheal tube or to place a surgical airway.
  • Patients with partial airway obstruction who are able to maintain oxygenation can sometimes clear the object on their own with coughing. If not, FB removal in the controlled setting of an operating room by ENT is suggested. In cooperative patients, laryngeal FBs can also be removed by the EP via direct laryngoscopy.
• Pharynx
  • Oropharyngeal FBs are easily removed using Magill forceps under direct visualization.
  • It is often possible for the EP to remove hypopharyngeal FBs using either indirect or direct laryngoscopy. If visualization is inadequate or if the patient cannot tolerate attempts at removal, direct laryngoscopy by ENT under general anesthesia is indicated. An alternative is to consider procedural sedation in centers that have appropriately trained staff.
  • Upper esophageal lesions warrant ENT evaluation for rigid esophagoscopy.
  • Patients with mild FB sensation upon swallowing who are able to tolerate PO intake without difficulty may have symptoms secondary to minor mucosal trauma. These patients are safely discharged home with prompt ENT follow-up.

• Bleeding after tonsillectomy typically occurs in the immediate postoperative period (< 24 h) or 7-10 days after surgery. Significant hemorrhage places the patient at risk for aspiration, airway compromise and hemodynamic instability. If necessary, immediate care should be directed toward providing an airway and treating life-threatening hemorrhage.
• Adequate visualization of the area is imperative for control of bleeding. Remove all clots via suction or forceps prior to definitive care. Once the bleeding site has been identified, hemostasis is attempted through various means:
  • Generalized oozing or bleeding is treated with hemostatic material or direct pressure to the area using ring forceps and gauze that has been soaked with lidocaine and 1:1000 epinephrine.
  • More circumscribed bleeding is often controlled with silver nitrate cautery or local injection of lidocaine with epinephrine.
  • Patients with brisk bleeding unresponsive to above measures should have emergent ENT evaluation. In these cases, hemostasis is best achieved in the operating room via electric cautery or suture ligation. Pediatric patients should also be treated by ENT in a controlled setting if possible unless the bleeding is very minor and the child is able to cooperate.