Are you having problems with epistaxis? Try this unique solution!
A healthy graduate student presents to the ER in the middle of the night with facial swelling and voice hoarseness. She states that she has been feeling generally unwell with aches and a sore throat for the past two days. Tonight, she took a throat lozenge shortly before going to bed, but awoke a while later with worsening hoarseness, throat tightness, and facial swelling. She states that the swelling is over her jawline and appears symmetric. She provides her license photo, which shows a dramatic difference in the contour of her mandible.
She is allergic to cats, but denies any recent exposure. She has no other known allergies and multiple prior exposures to this brand of throat lozenge. She denies wheezing, abdominal discomfort, and rash. She is only on birth control. She denies any inhalational drug use. She denies any dental pain or recent dental manipulation.
Her vital signs are within normal limits and she is afebrile. She has no stridor, drooling, or dysphonia, but exam demonstrates marked bilateral parotid/submandibular swelling. The region is not tender nor is it erythematous or warm. Her uvula is midline and without swelling. No lesions are noted in the posterior oropharynx. The tongue is unremarkable. She endorses ongoing throat tightness.
Lab work is obtained. She has a mild leukocytosis to 12.8. EBV and Strep are both negative. Given the extent of swelling and her subjective complaint of throat tightness, you obtain CT imaging (Figure 1).
The radiologist calls you to discuss the case. He says that she has enlargement of bilateral parotid glands and submandibular glands. He notes extensive subcutaneous edema in the retromandibular tissues and upper neck. Fortunately he says her airway looks patent. He inquires, “What do you think is going on?”
You start to worry that she may have mumps. You’ve never seen mumps, but you know it exists. Time for a quick review…
Mumps is a viral illness that is generally preventable by vaccine.
Peak incidence is late winter and early spring.
Mumps still occurs in outbreaks in closed environments such as college dormitories, military barracks, and schools, but is rare <1 yo due maternal antibodies.
An outbreak is defined as ≥3 cases linked by place and time.
Mumps is much more likely to occur in unvaccinated individuals than in vaccinated individuals, but there are rare reports of vaccinated patients developing mumps.
Transmission occurs by direct contact, respiratory droplets and fomites. Viral shedding precedes onset of symptoms.
Prolonged incubation period of 12-25 days.
There is often a non-specific prodrome of myalgias, headache, fever, and malaise.
Salivary gland swelling usually occurs within the first 2-3 days of symptom onset.
The hallmark of mumps is parotid swelling. It can be painful and tender, but not always, and can last up to 10 days.
The swelling can be unilateral (25% of cases) or bilateral. The swelling can start on one side and then progress to involve both sides.
Other salivary glands such as the sublingual glands and submandibular glands can swell, but this only occurs in 10% of cases.
Orchitis (typically develops 5-10 days following parotitis with high fevers and severe testicular pain).
Meningitis (more common in males. May develop before, during or after parotitis. In some cases, meningitis occurs in the absence of parotitis. Associated with CSF pleocytosis).
Other rare complications: encephalitis, pancreatitis, and arthritis.
Many other viral infections can cause parotid swelling (EBV, HSV, HIV, CMV, coxsackie, etc.).
Bacterial parotitis presents as typically firm, tender swelling associated with high fevers and toxic appearance. S.aureus is most often implicated.
Salivary gland stone, salivary tumor, sarcoidosis, Sjögren's syndrome.
Patient should be placed on droplet precautions.
At the time of presentation, two laboratory specimens should be drawn. A serum mumps IgM level and a buccal or oral swab should be sent for RT-PCR. At our institution, these are send-out labs.
The IgM level should be sent in a red-top tube.
The IgM level is not always accurate if the sample is obtained within the first 5-days of symptom onset. Therefore, if the IgM level returns as normal and the RT-PCR has not resulted (or was never sent), the CDC recommends a second serum sample be sent 5-10 days after symptom onset.
It is recommended that the parotid gland be “milked” and the swab be taken from the site of Stensen’s duct (buccal mucosa).
The swab used for strep testing can be used for the buccal swab.
Buccal swabs should be obtained as soon as possible after symptom onset. It provides the best means for laboratory confirmation, particularly in patients who have been vaccinated.
A CBC typically demonstrates leukopenia and a relative lymphocytosis.
Often serum amylase will be elevated.
No specific treatment.
20-30% of cases are asymptomatic.
Supportive care with NSAIDs/Tylenol.
If a patient is admitted, they should be placed on droplet precautions until parotid swelling resolves.
Individuals treated on an outpatient basis should remain at home and minimize contact with others for five days following symptom onset.
Patients who are incompletely immunized and at risk during a mumps outbreak (i.e. college students on a campus with mumps cases) should receive two doses or the MMR vaccine separated by at least 28-days.
As of January 2018, the Advisory Committee on Immunization Practices (AICP) made a change regarding the MMR vaccination. In the setting of a mumps outbreak, they now recommend those individuals at risk and who are >2 years out from their last MMR vaccination receive a third dose of the MMR vaccine. This recommendation comes following a large study involving university students. Approximately 5000 students who had previously received 2-MMR vaccinations received a third MMR vaccination during an outbreak. There was a significant reduction in the attack rate in those individuals receiving a third dose compared to those who had only received two doses (6.7 vs 14.5 cases per 1000). The effect was more pronounced in those students that had >2 years elapse since their last MMR vaccination.
Reporting varies state by state. Rhode Island DOH mandates reporting within four days of Mumps recognition.
Mumps is not mandatorily reported to the CDC, but often the CDC will be aware and involved in large outbreaks.
Patient reported that she had previously been completely vaccinated. At the time of her evaluation, two local universities had reported mumps cases. Her presentation occurred prior to the AICP recommendation. Serum IgM and buccal samples were collected. Patient was clinically stable and comfortable with discharge. She was advised to stay at home for 5-days. Her IgM levels were undetectable and the buccal PCR returned as negative. She most likely had a viral adenitis.
Faculty Reviewer: Dr. Kristina McAteer
A 26 year-old male presents after a motorcycle accident. He was the helmeted, single-occupant of a motorcycle that crashed into the back of a stopped car. There are no external signs of injury, but he believes his neck may have hit the handlebars as he was thrown from the bike. He denies loss of consciousness. His only complaint is that his voice sounds hoarse and he is having difficulty swallowing. He denies any intoxicants.
The patient has a normal primary traumatic survey. His secondary survey is notable for crepitus of the anterior neck. No chest wall crepitus is noted. No stridor or bruit is appreciated on anterior neck auscultation. There is no cervical hematoma or ecchymosis. There is no midline C-spine tenderness. There is no blood in the oropharynx. His voice is raspy, but he is able to phonate and adequately handle his secretions. He has no other traumatic complaints or physical exam abnormalities on secondary survey.
A chest x-ray is without any evidence of pneumothorax.
You wonder what imaging should be performed next. Does he need a CT brain based on his history? Does crepitus count as a distracting injury? Should he have a CTA in the absence of any hard vascular signs? After discussion with the trauma team, CT imaging including a CTA neck is performed (Figure 1).
CT imaging reveals a left hyoid bone fracture, as well as a comminuted fracture of the right thyroid cartilage. His CTA is normal. He has no intracranial injuries, face or C-spine fractures. There is considerable soft tissue emphysema.
Background on blunt laryngeal trauma
Blunt laryngeal trauma is rare. The reported incidence of laryngeal fractures is 1:30,000 patients presenting to the ER. The low incidence is secondary to the relative protection by adjacent bony structures (the mandible, manubrium, and vertebral bodies). Furthermore, humans are equipped with a protective reflex to flex their heads downward when startled, further shielding this vulnerable region from trauma.
Laryngotracheal injury occurs when patients lose their ability to protect this area, and are most commonly associated with motor vehicle accidents, when a hyperextended neck strikes a fixed object (steering wheel, dash board). Recreational vehicles are also increasingly implicated (motorcycles, four-wheelers striking branches). Other mechanisms of injury include strangulation, assault, or hanging.
The patterns of injury vary depending upon the age and gender of the patient. Women are at increased risk for subglottic and cervical tracheal injuries owing to their tendency towards longer necks. The thyroid and cricoid cartilage also ossify as part of the normal aging process (typically beginning around age 18-20), and for this reason, elderly patients are at increased risk for comminuted fractures of these structures. Conversely, children have flexible cartilage and are much less likely to sustain laryngeal fractures.
Brief review of anatomy
The larynx consists of a cartilaginous skeleton, the intrinsic and extrinsic muscles, and a mucosal lining. The cartilaginous skeleton houses the vocal cords. It consists of the thyroid cartilage, the cricoid cartilage, and the paired arytenoid cartilages. The thyroid cartilage is connected superiorly to the hyoid bone. The extrinsic muscles connect the cartilage of the larynx to other structures of the head and neck (i.e. sternothyroid muscle, etc.). The intrinsic muscles alter the shape, tension and position of the vocal cords (Figure 2).
Injuries range from mucosal hematomas and lacerations to fractured cartilage. The most severe laryngeal injury is complete laryngotracheal separation (Figure 3). Classification of these injuries will be covered in the Classification and Definitive Management section.
Signs and Symptoms
The mechanism of injury is important. The provider should take careful consideration of any history which lends itself to the possibility of “clothesline” type injury, namely forced hyperextension and forward propulsion or direct trauma to the anterior neck (strangulation, hanging).
Patients will report dysphonia, odynophagia, dysphagia, neck pain, dyspnea or hemoptysis. Studies suggest that hoarseness is the most common presenting symptom of laryngeal trauma. Juutilainen et al reviewed 33 cases of external laryngeal trauma, and 28 (85%) of those cases presented with hoarseness. Physical exam may reveal stridor, dyspnea, ecchymosis, subcutaneous emphysema, hemoptysis, loss of the thyroid prominence or drooling. However, it is important to note that no single symptom correlates with injury severity and the absence of these findings does not exclude the possibility of laryngeal injury.
Airway management is crucial. If a patient with a suspected laryngeal injury has no evidence of respiratory distress or airway compromise, proceed with a standard traumatic work-up.
If the airway is not patent (respiratory distress, airway obstruction, stridor, not handling secretions, hypoxic), establishing an airway becomes a priority. In these cases, tracheotomy is preferred to endotracheal intubation, as intubation can exacerbate laryngeal trauma and precipitate complete obstruction. It can also be extremely challenging to intubate because of distorted anatomy and poor visualization, with a risk for passing the ET tube through a false lumen created by the trauma. Furthermore, adequate positioning can be challenging if there is associated maxillofacial injuries and/or the need for C-spine precautions. That being said, there is no absolute contraindication for endotracheal intubation and if the patient is crashing, the most experienced airway provider should attempt it. Again, most of the otolaryngology literature favors tracheotomy, but if palpation of the larynx reveals continuity of the thyroid cartilage and cricoid cartilage, cricothyroidotomy can be performed if it is the only available, expedient airway.
Importantly, laryngeal trauma carries a high risk of concomitant injury. There is a 13-15% incidence of associated intracranial injuries; skull base and facial fractures are seen in approximately 21%; C-spine fractures are seen in 8%; and esophageal/pharyngeal injuries occur in approximately 3% of these cases. Thus, it is best to have a low threshold for additional imaging studies. CT is the imaging modality of choice, but should only be undertaken in those patients with a stable or secured airway. There is no definite literature on the utility of CTA in blunt laryngeal trauma, but if a patient has any hard signs of vascular injury (bruit/thrill, expanding hematoma, pulse deficit) or signs of an acute ischemic stroke, there should be significant concern for an associated vascular injury.
Classification and Definitive Management
The Schafer-Fuhrman Classification scheme has been created to characterize laryngeal injuries.
Grade I: Minor endolaryngeal hematomas or lacerations, no fracture
Grade II: Edema, hematoma, minor mucosal disruption without exposed cartilage, non-displaced fracture, varying degrees of airway compromise
Grade III: Massive edema, large mucosal lacerations, exposed cartilage, displaced fracture(s), vocal cord immobility
Grade IV: Group III with severe mucosal disruption, disruption of the anterior commissure, and unstable fracture, 2 or more fracture lines
Grade V: Complete laryngotracheal separation
This classification scheme relies on both CT imaging and direct visualization. As part of the work-up for laryngeal injury, flexible fiberoptic laryngoscopy should be performed, usually by otolaryngology. During laryngoscopy, care should be taken to observe for any deformities, edema, hematomas, lacerations, exposed cartilage and partial or complete vocal cord fixation (suggesting a recurrent laryngeal nerve injury).
There is no definite recommendation for the work-up of esophageal injury. In some instances, esophageal injury can be seen on CT imaging (paraesophageal stranding or gas, lumen communicating with gas/fluid). If, however, the suspicion for esophageal injury is high, additional studies can be pursued, beginning with a gastrograffin swallow study, followed by a dilute barium swallow for more complete evaluation.
The definitive management of laryngeal injuries depends on the injury pattern. Group I and some Group II injuries can be conservatively managed. This generally consists of humidified air, voice rest, head of bed elevation, steroids, anti-reflux medications, and antibiotics. Patients will often be admitted to the ICU for the first 24-48 hours given the potential airway compromise. They may undergo serial laryngoscopy for daily injury surveillance.
Group III-Group V injuries require operative intervention. These are the injury patterns that usually undergo tracheotomy. Group V patients always have tracheotomies and represent a significant surgical challenge. Notably, there are multiple operative approaches and interventions for laryngeal trauma that are beyond the scope of this post.
The patient was seen and scoped by otolaryngology in the ED. This showed a supraglottic hematoma, but no lacerations or exposed cartilage. His vocal folds were mobile. He was admitted to the trauma ICU, where he underwent a negative barium swallow, and ultimately, did not require operative intervention.
Faculty Reviewer: Dr. Kristina McAteer
Becker M, Leuchter I, Platon A, Becker CD, Dulguerov P, Varoquaux A. Imaging of laryngeal trauma. Europeal Journal of Radiology. Jan 2014: 83(1):142-154.
Eller RL, Dion G, Spadaro E. Management of Acute Laryngeal Trauma. http://www.cs.amedd.army.mil/FileDownloadpublic.aspx?docid=a1ab55ed-56b2-4a65-ade1-666e80a582cf. Accessed on 12.05.07.
Font JP, Quinn FB, Rayan MW. Laryngeal Trauma. http://www.utmb.edu/otoref/grnds/laryng-trauma-070328/laryng trauma-070328.pdf Accessed on 12.05.17.
Jalisi S, Zoccoli M. Management of laryngeal fractures—A 10-year experience. Journal of Voice. Jul 2011;25(4):473-479.
Jewett BS, Shockley WW, Rutledge R. External laryngeal trauma analysis of 392 patients. Archives of Otolaryngology–Head & Neck Surgery. Aug 1999;125(8):877-880.
Juutilainen M, Vintturi J, Robinson S, Bäck L, Lehtonen H, Mäkitie AA. Laryngeal fractures: clinical findings and considerations on suboptimal outcome. Acta Otolaryngol. Feb 2008: 128(2):213–218.
Murr AH and Amin MR. "Laryngeal Trauma"In CURRENT Diagnosis & Treatment in Otolaryngology - Head & Neck Surgery, 2nd Edition Ed. by Anil K. Lalwani.
Mendelsohn AH, Sidell DR, Berke GS, John MS. Optimal timing of surgical intervention following adult laryngeal trauma. Laryngoscope. Oct 2011;121(10):2122-2127.
Schaefer SD. The acute management of external laryngeal trauma. A 27-year experience. Arch Otolaryngol Head Neck Surg. Jun 1992 :118(6):598–604
Schaefer N, Griffin A, Gerhardy B, Gohchee P. Early Recognition and management of Laryngeal Fractures: A Case Report. Ochsner J. 2014: 14)10):264-265.