What’s Behind Stridor? Case Studies in Diagnosis and Care

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Few clinical signs command the attention of an EMT or paramedic more than stridor. Whether it’s present in a neonate, pediatric, adult or geriatric, it means the same thing: impending airway compromise.

Stridor is a harsh, loud sound of constant pitch, produced in the larynx, glottis or trachea. It is the result of turbulent airflow through a narrowed upper airway. Narrowing of the airway at or above the vocal cords (trachea or larynx) produces inspiratory stridor. Narrowing of the airway below the vocal cords (intrathoracic) produces expiratory or biphasic stridor.¹ Stridor is a sign that indicates critical narrowing of the airway and represents a medical emergency with potential for complete airway obstruction and subsequent asphyxiation. The timing and acuity of onset of stridor are important in determining the seriousness of the airway problem. Rapid onset suggests a high potential for immediate airway deterioration and total occlusion, while a more gradual onset suggests less of a risk.

This month’s article uses a case-based approach to explore some of the more common and life-threatening causes of stridor. For each case we work through a differential diagnosis to show how to evaluate the evidence supporting and opposing various etiologies and arrive at a best guess for a diagnosis. Lists of possible diagnoses are not inclusive; rather, they simply serve as a starting point for discussion.

Case #1

• Stridor and fever in a 6-year-old male.

• Differential to consider: foreign body airway obstruction, epiglottitis, croup.

A 6-year-old male presents conscious, alert and oriented, sitting up in bed in a “sniffing” position and complaining of a sore throat. He has a strong and rapid radial pulse, and his respiratory rate and tidal volume are normal, but you note inspiratory stridor with each breath. His skin is warm and dry. His mother says he went to bed last night without any complaint but woke up this morning with a sore throat and fever, so she kept him home from school as a precaution. Since he awoke 5 hours ago, the patient’s fever has risen to 102.3ºF (39.0ºC), and the stridor developed. The mother reports the patient has no significant medical history and takes no medications. He has not received all of his vaccinations to date, as the parents are concerned about vaccine side-effects. She is not aware of any recent trauma or potential for foreign body ingestion.

The child is slightly anxious but willing to answer your questions and allow you to perform a physical examination. He says his “throat hurts” and “it hurts to swallow.” You note his voice is slightly muffled, and his mother confirms this is not normal for him. The patient’s lung sounds are clear, and he does not complain of any respiratory distress. There is no accessory muscle use, nasal flaring, abdominal breathing or retractions. His vital signs are heart rate 112/min. and regular; respiratory rate 20/min. with good tidal volume; blood pressure 105/70 mmHg; pulse oximetry 97% on room air; and tympanic temperature 102.0ºF (38.8ºC). His blood glucose is 91 mg/dL.

Discussion

This patient’s stridor is the result of epiglottitis, a bacterial disease that causes inflammation and edema of the epiglottis and surrounding tissues. As the epiglottis and surrounding structures become inflamed, they can occlude the glottic opening, resulting in an airway obstruction that can vary from partial to complete. Epiglottitis is considered a potential life-threatening emergency because of the risk of complete airway obstruction.

The incidence of epiglottitis in children has significantly decreased in the United States since the H. influenzae type b (Hib) vaccine became widely available in the late 1980s, and has declined by more than 99% since the prevaccine era. The CDC reports that since the advent of widespread vaccination, the majority of children (68%) 6 months and older who contract Hib infections are either incompletely vaccinated or have unknown vaccination statuses. The remaining 32% received three or more doses of the vaccine.² The fact that this patient has not received his normal vaccinations increases his risk for Hib infection and epiglottitis. It is worth noting, however, that epiglottitis can still occur in children who have been properly vaccinated and even in those who have received a booster dose of the vaccine. In addition to H. influenzae, infection with other bacteria such as group A beta-hemolytic Streptococcus, S. aureus and Streptococcus pneumoniae can result in epiglottitis.

The classic presentation of epiglottitis is a patient with acute onset of high fever, sore throat and drooling. The acute onset of high fever tends to be characteristic for bacterial infection, in contrast to the slowly progressing lower fever associated with viral infection. Early in the development of epiglottitis, the patient will experience sore throat, pain with swallowing (odynophagia), inability to swallow (dysphagia) and a change in voice (for example, muffled voice) or cry as the supraglottic structures become inflamed. As the airway diameter decreases due to inflammation, stridor may develop as obstruction worsens. In a worst-case scenario, total airway obstruction can occur.

An older patient (child or adult) is less likely to exhibit signs of developing airway obstruction, as the diameter of their airway is relatively larger than a young child’s, and significant inflammation and swelling are necessary to produce symptoms.³ Drooling is a cardinal sign and results from a reluctance to swallow due to a severely inflamed and sore throat. As the infection becomes more severe and obstruction worsens, the patient may appear toxic or anxious and assume a tripod or sniffing position to maintain their airway. In addition, signs of severe airway obstruction such as tachypnea, retractions and cyanosis may be present.

This patient presented with many signs and symptoms consistent with epiglottitis, including the acute onset of fever, sore throat, odynophagia and inspiratory stridor. The acuity of the illness and the fever suggest an infectious etiology. He also has not been vaccinated, putting him at high risk for Hib infection. This patient appears rather stable at this time, as he does not appear toxic, is not tachypneic or hypoxic, and is managing his secretions well. He is, however, placing himself in the sniffing position. This, with the presence of stridor, indicates he is experiencing some degree of airway obstruction. While his condition appears stable now, it could deteriorate rapidly.

Prehospital management of epiglottitis, and of this patient, centers on maintaining adequate ventilation and oxygenation. In cases of minimal airway compromise, transport the patient in the most comfortable and relaxed position and manner possible. Typically this means allowing the patient to sit upright and assume a sniffing or tripod position. However tempting it may be for these patients, never allow a parent or caregiver to hold the child during transport. Do not agitate the patient unnecessarily, and do not insert any objects into the mouth to aid in visualization of the throat. In addition, avoid palpation or any other manipulation of the throat if the patient is experiencing pain. If hypoxia is present, administer humidified oxygen via an appropriate delivery device. Oxygen typically carried on ambulances has no humidity, and without adding humidity, it can cause further irritation.

No clear recommendations exist for cases of severe airway obstruction secondary to epiglottitis. That being said, there are some basic guidelines that are consistent in emergency medicine. If the obstruction is severe and signs of respiratory failure are present, perform ventilations with a BVM and provide rapid transport to an emergency department. If complete airway obstruction is imminent, attempt endotracheal intubation (ETI). ETI attempts will be complicated by swollen, distorted anatomy, and any trauma to the airway during ETI could result in additional swelling and bleeding, further complicating the procedure.

Typically, in cases of complete airway obstruction where ETI is unsuccessful, surgical cricothyrotomy is indicated. However, this procedure is contraindicated in infants and children due to the size of the cricothyroid membrane. Because of this, needle cricothyrotomy with transtracheal jet ventilation (TTJV) is the preferred approach. Negatives of TTJV such as decreased tidal volume and CO₂ retention are substantially reduced in the pediatric patient with smaller lungs.⁴ There is no need to intubate this patient right now, but pay close attention to the airway and transport expeditiously to an emergency department.

Croup (laryngotracheobronchitis) is another cause of stridor in the pediatric patient, and is usually the result of a viral infection that results in swelling of the laryngeal-tracheal tissues. It is most often the result of parainfluenza virus and occurs most often in children 6 months to 6 years.³ The typical progression of croup begins with 1–2 days of nasal congestion, rhinorrhea and low-grade fever prior to the onset of a harsh, seal-like barking cough, hoarse voice and stridor. Symptoms will typically last 3–7 days, with the most severe manifesting on days 3–4.⁵ Severe croup is characterized by worsening stridor, respiratory distress and retractions.

The treatment of croup is usually supportive and consists of placing the patient in a position of comfort and administering humidified oxygen. Patients with severe croup may benefit from administration of nebulized racemic epinephrine, which acts on alpha-adrenergic receptors in the subglottic tissue. The resultant vasoconstriction reverses the swelling of the subglottic tissue and airway obstruction.

This patient’s history of present illness and clinical presentation make a diagnosis of croup less likely. First, the onset was fairly rapid, and the fever was high-grade; with croup we’d expect a gradual onset of low-grade fever over days. In addition, the patient’s symptoms, sore throat and odynophagia, are not consistent with croup.

A partial foreign body airway obstruction (FBAO) should be high on the differential in any child presenting with stridor. We emphasize partial FBAO here, as a complete FBAO would result in no airway sounds, as no air is passing through the airway. FBAO is more common in younger children, especially those 1–3 years, as they become more mobile and explore the world around them. This patient is 6, and not only has less risk for FBAO, but would probably remember the event. In addition the acute onset of fever is not typical for FBAO, though it can occur if objects are aspirated into the main stem bronchi or lower in the respiratory tract. Patients who present with partial FBAOs should not be agitated and should be encouraged to try to cough in an effort to dislodge their object themselves. Attempts at forceful maneuvers, such as abdominal thrusts or hitting the patient on the back, should be avoided, as they may turn a partial airway obstruction into a full one.

Additional etiologies of stridor to consider include trauma, toxic or caustic inhalation, and tracheomalacia or laryngomalacia. There are no history or physical exam findings in this patient that suggest a traumatic etiology of his stridor. This and the history highly supportive of an infectious process etiology help rule out trauma. The same logic could be used to rule out, or at least make less likely, toxic or caustic inhalation. Tracheomalacia and laryngomalacia, which result in narrowing of the trachea and larynx, respectively, are etiologies of generally benign stridor in neonates and infants, and are generally identified long before 6 years of age.

Case #2

• Stridor, sore throat and drooling in a 37-year-old male.

• Differential to consider: epiglottitis, Ludwig’s angina, retropharyngeal abscess.

A 37-year-old male presents sitting up in a chair, tripoding, leaning forward and drooling, in obvious distress with inspiratory stridor. A quick primary exam reveals a normal respiratory rate and tidal volume, a rapid and strong radial pulse, and warm, dry skin. He is alert and oriented and complains of a sore throat and pain with swallowing. You note that talking also causes him pain, and he indicates that any movement of his neck or jaw is painful, so you both agree on yes or no answers to questions. You also note his voice is muffled.

The patient’s wife says he’s been taking antibiotics for the past 5 days for a sore throat he developed after having a molar extracted from his right mandible one week ago. His sore throat rapidly worsened over the past 24 hours, and he developed severe neck pain with movement and swallowing. Over the past 6 hours he has been placing himself in the tripod position, drooling, and his breathing has become noticeably worse. His wife called EMS when he started exhibiting stridor. The patient has no other significant medical history, takes no other medications and has no allergies.

Your clinical exam reveals pain with even slight palpation to his neck, and you note there is noticeable swelling and cellulitis to the submandibular tissues, especially on the right side. When asked, he cannot stick out his tongue, and it appears elevated in his mouth. There is inspiratory stridor, and his lung sounds are clear and equal bilaterally with good air movement to all fields. His vital signs are heart rate 122/min. and regular; respiratory rate 16/min. with good tidal volume; blood pressure 142/90 mmHg; pulse oximetry 95% on room air; and tympanic temperature 102.2ºF (39.0ºC). His blood glucose is 111 mg/dL.

Discussion

Ludwig’s angina is a rapidly progressing infection of the submandibular, sublingual and submental tissues of the neck. Inflammation and edema of the soft tissues of the neck can lead to tissue displacement and subsequent airway occlusion and asphyxiation within hours. Most cases of Ludwig’s angina have dental origins, and an infected or recently extracted lower molar is present in most cases, and in this one.⁶ Dental infections can easily migrate through the mandible into the submandibular space, then spread relatively easily through the deep tissues of the neck. Other etiologies of Ludwig’s angina include fractured mandible, tongue piercing, foreign body or trauma to the floor of the mouth, secondary infection of an oral malignancy, and peritonsillar abscess.

This patient exhibited many of the common signs and symptoms characteristic of Ludwig’s angina, including dysphagia, odynophagia, neck swelling and neck pain. Other symptoms and signs include dysphonia, muffled speech (sometimes referred to as a “hot potato voice”), drooling, tongue swelling, pain in the floor of the mouth, restricted neck movement and sore throat.⁷ This patient’s inability to handle secretions and the presence of stridor both indicate there is some degree of impending airway compromise.

Treatment for this patient would include transport in a position of comfort that allows him to manage his secretions—most likely sitting upright, if not in the tripod position in which he presented. Give humidified oxygen to increase his saturation, and consider avoiding use of a nonrebreather mask, as the patient is drooling. If the patient experiences respiratory failure, as evidenced by inadequate rate and/or tidal volume, initiate BVM ventilations. If a BLS airway adjunct is required, a nasopharyngeal airway (NPA) may be desirable over an oropharyngeal airway (OPA). An OPA may be obstructed by a swollen or displaced tongue, or cause damage to swollen oral tissues, resulting in blood or pus entering the airway.

The question of advanced airway techniques such as ETI, needle cricothyrotomy or a surgical airway is not an easy one to answer. If you suspect airway obstruction is imminent, it is appropriate to consider an attempt at endotracheal intubation. ETI is likely to be quite difficult because of distortion of the oral anatomy rendering landmarks unrecognizable, inability to displace the tongue with the laryngoscope, inability to open the mouth (trismus), and the tendency for development of laryngospasm in cases of Ludwig’s angina.⁸

Also high on the differential diagnosis for this patient is epiglottitis, discussed in the previous case. Previously a disease of childhood, epiglottitis has been on the increase in adults since advent of the Hib vaccine. Whether this is due to increased recognition or prevalence is unknown.⁷

This patient exhibits many of the signs and symptoms characteristic of adult epiglottitis, including sore throat, odynophagia, dysphagia, muffled voice, stridor and drooling. Arguments against epiglottitis include the recent dental procedure that preceded the onset of symptoms and the significant swelling of the submandibular and sublingual tissue, which are not characteristic of epiglottitis. Worth noting, however, is that epiglottitis can be a cause of Ludwig’s angina, so indeed may be present. As such, it cannot be ruled out.

The prehospital treatment for adult epiglottitis mirrors that of pediatric epiglottitis. The patient should be allowed to sit upright and given humidified oxygen as needed, and providers should pay particular attention to the airway in anticipation of impending obstruction. If airway obstruction is imminent, ETI should be performed or a surgical airway secured as a last resort. Further management in the ED will include IV antibiotic and steroid administration.

Another cause of stridor, and one that can also lead to Ludwig’s angina, is retropharyngeal abscess, an infection in the fascia located behind the pharynx, extending from the base of the skull to the bifurcation of the trachea. Infection in this space can displace the soft tissue of the posterior pharynx anteriorly into the airway, in worst cases obstructing the airway. Significant edema of the neck and the development of stridor are much more common in children than adults.⁹ More common symptoms in adult patients include sore throat, fever, torticollis (tipping the head to one side while turning the chin to the other) and dysphagia. Retropharyngeal abscess may have been the cause of Ludwig’s angina in this patient, but is most likely not the sole cause of his stridor, as the significant swelling of the submandibular and sublingual tissues are not characteristic of the disease.

Prehospital treatment of retropharyngeal abscess consists of placing the patient in a position of comfort, which will likely be lying supine and not sitting upright. Sitting upright causes the swollen tissues of the posterior pharynx to shift forward into the airway, resulting in pain and increased dyspnea. Lying supine allows the tissues to displace posteriorly, out of the airway. Administer oxygen via an appropriate delivery device if hypoxia is present. If the airway or ventilation is compromised, ventilate the patient with a BVM and BLS airway adjuncts (preferably NPA) and ETI utilized as necessary. Additional treatment in the ED will include initiation of IV antibiotic treatment and possible surgical intervention.

Conclusion

The development of stridor in any patient is a serious, potentially life-threatening event. While identification of the cause of stridor via the differential diagnosis process is important, of more importance is the identification and management of an impending airway compromise. Some key elements to remember are:

• The presence of stridor indicates that some degree of airway obstruction has occurred.

• Based on the etiology of the stridor, proper positioning of the patient can help with airway maintenance.

• Perform BVM ventilation if breathing rate or tidal volume becomes inadequate.

• ALS providers should perform ETI only if total airway obstruction is imminent.

References

1. Lustig LR, Schindler JS. Chapter 8: Ear, Nose, & Throat Disorders. In: Papadakis MA, McPhee SJ, Current Medical Diagnosis & Treatment 2013. New York: McGraw-Hill, 2013.

2. CDC. Haemophilus influenza type b. The Pink Book: Course Textbook, 12th ed., second printing, May 2012, www.cdc.gov/vaccines/pubs/pinkbook/hib.html#trends.

3. Manno M. Chapter 166: Pediatric Respiratory Emergencies: Upper Airway Obstruction and Infections. In: Marx J, Hockberger R, Walls R, Rosen’s Emergency Medicine, 7th ed. Mosby, 2010.

4. Hebert RB, Bose S, Mace SE. Cricothyrotomy and Transtracheal Jet Ventilation. In: Roberts JR, Hedges JR, Custalow CB, Clinical Procedures in Emergency Medicine, 5th ed. Saunders Elsevier, 2010.

5. Gunn JD. Chapter 119: Stridor and Drooling. In: Tintinalli JE, et al, Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed. New York: McGraw-Hill, 2011.

6. Saifeldeen K, Evans R. Ludwig’s angina. Emerg Med J 2004; 21: 242–43.

7. Melio FR. Chapter 73: Upper Respiratory Tract Infections. In: Marx J, Hockberger R, Walls R, Rosen’s Emergency Medicine, 7th ed. Mosby, 2010.

8. Barakate MS, et al. Ludwig’s angina: Report of a case and review of management issues. Ann Otol Rhinol Laryngol 2001; 110: 453.

9. Shah RN, Cannon TY, Shores CG. Chapter 241: Infections and Disorders of the Neck and Upper Airway. In: Tintinalli JE, et al, Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed. New York: McGraw-Hill, 2011.

Scott R. Snyder, BS, NREMT-P, is the EMT program director for the San Francisco Paramedic Association. Contact him at scottrsnyder@me.com.

Sean M. Kivlehan, MD, MPH, NREMT-P, is an emergency medicine resident at the University of California, San Francisco and a former New York City paramedic. Contact him at sean.kivlehan@gmail.com.

Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT, is performance improvement coordinator for Vitalink/Airlink in Wilmington, NC, and a lead instructor for Wilderness Medical Associates. Contact him at kcollopy@colgatealumni.org.