A Summary of Bronchiolitis

Posted on July 13, 2022 by Mandy Peach

A Summary of Bronchiolitis: A review of bronchiolitis, evidence behind various treatment regimens, and suggested admission criteria – A Resident Clinical Pearl

Melanie Johnston, R3

Integrated FMEM, Dalhousie

Reviewed by Dr. Patricia Dutton

Respiratory illnesses are the second most common ED presentation for paediatric patients, particularly during the winter months, in Canada. ^1,2 These paediatric patients with respiratory pathologies are at risk of rapid clinical deterioration; a thorough history and exam with careful attention to respiratory evaluation is critical. Three of the most common paediatric respiratory complaints presenting to the ED include croup, asthma, and bronchiolitis. This pearl will focus on a review of bronchiolitis, its presentation, evaluation, and the evidence behind various treatments.

What is bronchiolitis:

Bronchiolitis is a viral lower respiratory tract infection. It is characterized by obstruction of small airways cause by acute inflammation, swelling/edema, and necrosis of the cells lining the small airways.² Airways are further narrowed by increased mucous production. The most common causes are respiratory syncytial virus (RSV), influenza, rhinovirus, adenovirus, and parainfluenza.² These viruses are transmitted by secretions from the nose/mouth and via respiratory droplets in the air. Co-infection with multiple viruses occurs in 10-30% of hospitalized children.²

Figure 1: Pathophysiology of Bronchiolitis.³

Epidemiology:
RSV season generally begins in November and persists until April. Bronchiolitis generally presents with a first episode of wheezing before the age of 24 months during the winter months.² It is the most common reason for admission to hospital in the first year of life in Canada, and more than one-third of children will be affected by bronchiolitis in their first two years of life.²

Presentation:

Bronchiolitis may present with a wide range of symptoms from mild upper respiratory tract infection symptoms (cough, rhinorrhea, fever) to respiratory distress (tachypnea, wheeze, grunting, indrawing, abdominal breathing, and retractions).⁴ The peak severity of illness usually occurs on day 2-3 of the illness with resolution over 7-10 days.^2,6 Cough can persist in infants for up to three weeks after onset.

Pediatric populations at risk for more serious illness include:
– Age <3 months
– Infants born prematurely (<35 weeks gestation)
– Chronic lung disease
– Congenital heart disease
– Chronic neurological conditions
– Immunodeficiency
– Trisomy 21

Patients with the above risk factors are at risk of rapid clinical deterioration even if presenting early in illness with mild symptoms.^2,5

Diagnosis:

The diagnosis of bronchiolitis is considered to be clinical based on history and physical exam. The illness generally begins with a 2-3 day prodrome of mild URTI symptoms including cough, fever, rhinorrhea. This may progress to tachypnea, wheeze, and signs of respiratory distress.² If respiratory distress is interfering with feeding, there may be signs of dehydration (delayed cap refill, dry mucous membranes, no tears produced with crying). Initial assessment should focus on overall appearance, breathing, and circulation. A tool to assist in establishing a general first impression of the paediatric patients stability is the paediatric assessment triangle. Abnormalities in any domain of the triangle (appearance, work of breathing, circulation) should be noted and factored into initial workup with potential to decompensate, with abnormalities in two domains indicative of potentially serious illness.

Figure 3: Pediatric Assessment Triangle.¹

Signs of respiratory distress to note on exam include:

– Tachypnea
– Intercostal/subcostal retractions
– Accessory muscle use
– Nasal flaring
– Grunting
– Colour change or apnea
– Wheezing
– Low O2 saturation (<90%)

In stratifying the severity of illness in bronchiolitis, the Royal Children’s Hospital of Melbourne has proposed the following chart to assist with assessment:

Figure 4: Stratifying severity of illness in bronchiolitis, adapted from RCHM.⁵

Investigations

Bronchiolitis is considered to be a clinical diagnosis. As such, the majority of patients won’t require any additional investigations. If there is diagnostic uncertainty, then the following investigations may be considered:

Management:

Bronchiolitis is a self-limiting disease with peak severity generally at day 3-4 of illness.^2,5,6 Most children have mild disease and can be managed with supportive care at home. For those ultimately admitted, focus in hospital is on supportive care with assisted feeding, nasal suctioning, and oxygen therapy as needed.

Disposition:

Most children do well and the symptoms will peak by day 3-5 of illness.

Criteria for safe discharge home include:
– O2 > 90-92%
– Adequate oral hydration
– Mild respiratory symptoms
– Access to reliable follow-up care if needed.²

Criteria for hospital admission include:

– Persistent oxygen saturation <92% and requiring supplemental oxygen AND/OR
– Unable to maintain oral hydration (fluid intake 50% of normal), requiring IV or NG fluids AND/OR
– Persistent moderate-severe respiratory distress
– Apnea (observed or reported)
– Children with risk factors for severe disease (see above).²

Admission or a period of observation in the ED can be used to document feeds and monitor vital signs/oxygen status. Other considerations for admission to hospital include social circumstances, comfort of caretaker in managing child at home, distance to healthcare facility in case of deterioration, and the phase of illness.

Resources:

1. Pediatric Respiratory Illnesses, Dr Allan Shefrin. Jan 30, 2020. Accessed at https://criticallevels.ca/2020/01/30/episode-3-paediatric-respiratory-illnesses-dr-allan-shefrin/

Bronchiolitis: Recommendations for diagnosis, monitoring and management of children one to 24 months of age. Canadian Pediatric Society. Friendman, J., Rieder, M., Walton, J. et al. Nov 3, 2014. Accessed at https://emergencymedicinecases.com/wp-content/uploads/filebase/pdf/CPS-guidelines-bronchiolitis.pdf.3. Bronchiolitis. Cleveland Clinic. Accessed online at: https://my.clevelandclinic.org/health/diseases/8272-bronchiolitis
Bronchiolitis, Bottom Line Recommendations. Trekk: Translating Emergency Knowledge for Kids. October 2020. Accessed online at: https://trekk.ca/system/assets/assets/attachments/502/original/2021-01-08-Bronchiolitis_v_3.0.pdf?16106625135. Bronchiolitis, Clinical Practice Guidelines. The Royal Children’s Hospital Melbourne. Accessed online at: https://www.rch.org.au/clinicalguide/guideline_index/Bronchiolitis/
6. Bronchiolitis, Episode 59. Emergency Medicine Cases. Accessed online at https://emergencymedicinecases.com/episode-59-bronchiolitis/

7. Bronchiolitis in children: diagnosis and management. NICE guideline. June 1, 2015. Accessed online at: https://www.nice.org.uk/guidance/ng9/resources/bronchiolitis-in-children-diagnosis-and-management-pdf-51048523717

8. https://www.connectedcare.sickkids.ca/quick-hits/2019/8/29/volume6-efnk4-nyn48-max8h-rczlx (Pediatric assessment triangle)

9. Bronchioitis, accessed online at: https://en.wikipedia.org/wiki/Bronchiolitis.

A Seal Barking… In the ED?? – Croup Management in the Emergency Department

Posted on July 6, 2022 by Mandy Peach

A Seal Barking… In the ED?? – Croup Management in the Emergency Department: A Medical Student Clinical Pearl

Kalpesh Hathi, CC3
MD Candidate, Class of 2023
Dalhousie Medicine New Brunswick

Reviewed by Dr. Jeremy Gross

Copyedited by Dr. Mandy Peach

All case histories are illustrative and not based on any individual.

Case Presentation:

You are the clinical clerk in the ED on a cold Monday, December afternoon. You pick up a chart that describes a 12-month-old baby boy, with a 1-day history of subjective fever of 38.4 C at its highest, respiratory distress, decreased PO intake and mom noting a barking cough.

Vitals: HR: 100 BPM, RR: 45, SpO2: 98% RA, BP: 90/65, Temp: 36.8 C, GCS 15, Wt: 10.2 kg.

You pull out your normal pediatrics vitals chart, and note that aside from a mildly elevated RR, these vitals are within normal limits for this child’s age and the child is afebrile.

What would you want to include in your history and physical?

History:

On history, mom says that the child began having classic URTI symptoms on Sunday (1 day ago) including a cough, rhinorrhea, and increased work of breathing. He also had a temperature of 38.4 C by ear on Sunday. Today, he began having what mom describes as increased work of breathing and a barking seal like cough.

Mom shows you two videos from this morning of the increased work of breathing and the barking-seal like cough:

Example of increased work of breathing (assume this is at home without the monitors attached):

https://www.youtube.com/watch?v=KQTEu1mpRY8&t=3s

As an astute clerk, you look for signs of increased work of breathing including tracheal tug, chest wall indrawing (inter, supra, or subcostal), abdominal breathing, grunting, head bobbing, cyanosis, nasal flaring, pursed lip breathing, and tachypnea.

Example of barking seal-like cough:

https://www.youtube.com/watch?v=UWOrKzgp3Wc

You agree that this sounds classically like a croup presentation.

The rest of the history including pregnancy, family, social, developmental, medications, allergies, and medical is largely unremarkable. The child’s vaccinations are up to date.

Mom is concerned as she feels the child is feeding and drinking less, but they are still having a normal number of wet (~6/day) and dirty (~1/day) diapers.

Physical Exam:

The child appears well in the ED, they are fussy and fighting your exam, they are jumping on the bed and playing with mom, they find comfort in mom, and they are even playing peek-a-boo with the RNs. You currently do not hear the barking seal like cough, nor stridor. They have mild intercostal indrawing, but no other signs of respiratory distress. No cyanosis is present.

Vitals are unchanged from the chart; the RR is still mildly elevated at ~40-45/min.

Resp: Mildly decreased air entry bilaterally, no crackles/wheezes. Mild stridor transmitted from upper respiratory tract upon agitation.

Fluid Status: Moist mucous membranes, fontanelles not bulging or sunken in, skin turgor is normal (no excessive tenting of skin), and when prompted they drink apple juice mixed with water.

You complete a thorough head to toe exam including HEENT, Neuro, Cardio, Abdo, GU, and MSK, aside from some cerumen in the ears and some rhinorrhea, the exam is within normal limits.

Differential Diagnosis [1-3]:

Croup

Bacterial tracheitis

Epiglottitis

COVID-19

Foreign body aspiration

Neoplasm

Hemangioma

Peritonsillar abscess

Retropharyngeal abscess

Acute anaphylaxis reaction

Bronchiolitis

Bronchiolitis and lower respiratory tract infections would present with wheeze rather than stridor [1-3].
Peritonsillar and retropharyngeal abscesses would have a hot potato voice, and potentially a mass on the neck [1-3].
In children <6 months old it is important to consider congenital presentations such as choanal atresia and tracheoesophageal fistula [1-3].
URTI symptoms would not be present in isolated foreign body aspiration but should be considered [1-3].
It is important to differentiate croup from epiglottitis because epiglottitis can lead to rapid deterioration and often requires operating room intubation [1,2]. Drooling suggests epiglottitis whereas cough suggests croup, both have a high sensitivity and specificity for each respective diagnosis [1-3,4].
Bacterial tracheitis the child would look much sicker and more toxic, and this would be represented on vital signs as well [1-3].

Croup:

Croup is a viral illness most commonly caused by parainfluenza virus, it is formally called laryngotracheobronchitis as it is inflammation of upper airway including the larynx, trachea, and bronchi [1,5].

Croup is a common presentation to Canadian emergency departments, most of which will be mild forms of croup, however occasionally hospitalization will be required, and rarely intubation is needed [1,6]

Classically croup will present in children between 6 months – 3 years old, with a 1-2 day history of URTI symptoms followed by a barking cough and stridor [1,7,8]. As this causes inflammation and obstruction of the upper respiratory tract, stridor will be present and often is more pronounced with agitation and at night [1,2]. A low-grade fever may be present, but is not required for the diagnosis, the child will not typically have drooling or dysphagia (if this is present consider epiglottitis) [1-3]. Parents will often be concerned/alarmed by the barking cough sounds.

As with most viral infections, croup is a self-limiting illness and most management is supportive, improvement should be noted within 2-7 days [1,6,7].

The diagnosis of croup is a clinical one of the child meeting the clinical picture outlined above and ruling out other causes with history and physical [1-3]. A radiograph is not needed to diagnose croup however if obtained due to uncertainty, will often show a narrowing of the glottic and subglottic areas in a classic steeple sign [3]. Whereas epiglottitis will show a thumb sign [9].

Picture taken from: https://www.pinterest.ca/pin/541980136386136007/

Picture taken from: https://kidshealth.org/Nemours/en/parents/az-croup.html

Workup of the Patient…

You remember some clinical decision aids for croup management… So, you employ the Westley Scoring System for Croup Severity [10]. As our child has a normal LOC, no cyanosis, stridor with agitation, mildly decreased air entry, and moderate retractions. They receive a Westley Score of 4 = moderate croup.

Mild </= 2

Moderate = 3-7

Severe = >/=8

Picture taken from: https://www.uptodate.com/contents/image/print?imageKey=PEDS%2F100744&topicKey=PEDS%2F6004&rank=1~60&source=see_link&search=croup&utdPopup=true

Based on this you pull out a trusted croup decision aid guide [1,11]:

Taken from: https://cps.ca/documents/position/acute-management-of-croup

In summary:

Mild croup, children will be given oral dexamethasone classically the dose is 0.6 mg/kg of body weight, however literature has shown equal effectiveness with 0.3 mg/kg, therefore some practitioners may opt for this lower in patients with moderate or mild croup [1,11,12]. Parents will be educated, and the child will be discharged home [1,11].

Moderate croup, the child will be given the same dose of dexamethasone and will be observed for 4 hours for improvement and sent home if symptoms have improved [1,11].

Severe croup, the child will be given blow-by O2 if cyanosis present, racemic epinephrine 2.25% (0.5 ml in 2.5 ml of normal saline) OR L-epinephrine 1:1000 5 mL, and the same dose of dexamethasone as above [1,11]. They will be observed for 2 hours and either sent home or admitted based on response [1,11].

Of note… previously aerosolized racemic epinephrine or L-epinephrine was given, however to reduce aerosolized treatments during the COVID-19 pandemic some emergency departments have received special authorization to give a puffer with epinephrine which was previously only approved in the US.

Case Conclusion

As our child had moderate croup and weighs 10.2 kg, they were given 0.3 mg/kg of dexamethasone which was 3.6 mg. We also performed a viral swab, which returns negative for COVID-19, but positive for parainfluenza virus, re-enforcing your diagnosis of croup. They were observed in the ED and quickly improved with no more increased work of breathing, and no stridor at rest. As such they were discharged to the care of their parents, and the parents’ received education on supportive management and indications to re-seek medical care. In fact, the SJRH ED has a handy parent information sheet that you give to the mother, which she is very appreciative of.

References:

Ortiz-Alvarez O, Canadian Pediatric Society, Acute Care Committee. Acute management of croup in the emergency department. J Paediatr Child Health. 2017;22(3):166-9. https://cps.ca/documents/position/acute-management-of-croup#ref1
Sizar O, Carr B. Croup. [Updated 2021 Jul 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. https://www.ncbi.nlm.nih.gov/books/NBK431070/
Smith DK, McDermott AJ, Sullivan JF. Croup: Diagnosis and Management. Am Fam Physician. 2018;97(9):575-80. https://www.aafp.org/afp/2018/0501/p575.html
Tibballs J, Watson T. Symptoms and signs differentiating croup and epiglottitis. J Paediatr Child Health. 2011;47(3):77-82. https://pubmed.ncbi.nlm.nih.gov/21091577/
Rihkanen H, Rönkkö E, Nieminen T, et al. Respiratory viruses in laryngeal croup of young children. J Pediatr 2008;152(5):661–5. https://pubmed.ncbi.nlm.nih.gov/18410770/
Rosychuk RJ, Klassen TP, Metes D, Voaklander DC, Senthilselvan A, Rowe BH. Croup presentations to emergency departments in Alberta, Canada: A large population-based study. Pediatr Pulmonol 2010;45(1):83–91. https://pubmed.ncbi.nlm.nih.gov/19953656/

Johnson DW. Croup. BMJ Clin Evid. 2014. https://pubmed.ncbi.nlm.nih.gov/25263284/
Bjornson CL, Johnson DW. Croup in children. CMAJ. 2013;185(15):1317-23. https://www.cmaj.ca/content/185/15/1317
Takata, Fujikawa, Goto. Thumb sign: acute epiglottitis. BMJ Case Rep. 2016. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4904439/
Yang WC, Lee J, Chen CY, Chang YJ, Wu HP. Westley score and clinical factors in predicting the outcome of croup in the pediatric emergency department. Pediatr Pulmonol. 2017;52(10):1329-34. https://pubmed.ncbi.nlm.nih.gov/28556543/
Toward Optimized Practice. Diagnosis and Management of Croup. Clinical Practice Guideline, January 2008. www.topalbertadoctors.org/download/252/croup_guideline.pdf.
Geelhoed GC, Macdonald WB. Oral dexamethasone in the treatment of croup: 0.15 mg/kg versus 0.3 mg/kg versus 0.6 mg/kg. Pediatr Pulmonol. 1995;20(6):362-8. https://pubmed.ncbi.nlm.nih.gov/8649915

A Case of Smoke Inhalation Injury

Posted on February 14, 2022 by Mandy Peach

A Case of Smoke Inhalation Injury – A Medical Student Clinical Pearl

Emmanuel Hebert

MD Candidate, Class of 2022

Dalhousie Medicine New Brunswick

Reviewed by Dr. Matthew Greer

Copyedited by Dr. Mandy Peach

Case

A 54-year-old Male presents to the emergency room via EMS. He woke up at nighttime to his house on fire. He says he woke up coughing due to the smoke and was able to crawl out of the house while ablaze and called EMS. He was then transported to the hospital. He also reports that his voice is more rough than usual and that he has pain on his back.

Past Medical History: Unremarkable

Medications: No prescriptions medications.

Physical Examination: Patient is seen wearing a non-rebreather mask with an oxygen rate of 12L/min. He appears well and is in no acute distress. He has singed scalp hair and appears flushed. The patient’s vitals are HR-110, BP-125/80, Temp-36.5, O2 sat- 99%. Patient weighs 130 kg. His back appears very red but there are no open lacerations or blisters. There is good air entry bilaterally with no adventitious sounds or wheeze. There is soot in the mouth as far back as can be visualized. The oropharynx is dry and mucous contains soot.

Figure 1: First degree burns on the back.

Initial bloodwork:

WBC: 10×10^9/L
Hgb: 135
Plt: 300×10^9/L
Na: 135
K: 4
Glu: 6
Carboxyhemoglobin: 5%
EtOH: Neg

What is the differential diagnosis of dysphonia?

-Acute laryngitis

-Functional dysphonia

-Tracheal Injury

-Injury to recurrent laryngeal nerve

-Caustic ingestion, smoke inhalation injury, blister chemical agents

-Neck masses (benign and malignant) [5,7]

Smoke Inhalation Upper Respiratory Tract Injury

Definition: Inhalation injury refers to damage to the respiratory tract or lung tissue from heat, smoke, or chemical irritants carried into the airway during inspiration [1].

Damage to the airway can be broken into three different affected zones with their own clinical consequences:

Upper Airway

The leading injury in the upper airway (above the vocal cords) is thermal injury due to heat exchange in the oro- and nasopharynx.
Injuries occurring early include erythema, ulcerations, and edema.
It is for this reason that aggressive fluid resuscitation should be avoided as the edema resulting from the heat transfer, can be compounded with fluid resuscitation, resulting in a further compromised airway. [2]

Tracheobronchial

Injuries to the tracheobronchial system occurs due to the chemical makeup of the smoke. When smoke stimulates the vasomotor and sensory nerve endings, neuropeptides get released which cause bronchoconstriction and vasodilation. Due to this inflammatory response, a loss of plasma proteins and fluid from the intravascular space into the alveoli and bronchioles ensues. This causes alveolar collapse and causes a VQ mismatch resulting in hypoxia. [3]

Parenchymal Injury

Injuries to the parenchyma occur because of the above mechanism resulting in alveolar collapse, which then cause increased transvascular fluid flux, a decrease in surfactant, and a loss of hypoxic vasoconstriction and therefore impaired oxygenation. [3]

Figure 2. Mechanisms of smoke inhalation injury in tracheobronchial area [4]

Management

Patients with smoke inhalation injuries are also at risk for carbon monoxide poisoning. It is for this reason that carboxyhemoglobin is used to assess degree of carbon monoxide toxicity. The treatment for this is 100% oxygen via non-rebreather. Another treatment that can be used is hyperbaric therapy. Choice of hyperbaric therapy should be made in consultation with a hyperbaric specialist and patient must be stable prior to transport. [3]

One of the earliest decisions to make in the management of patients with suspected smoke inhalation injuries is whether to secure the airway. In patient whom the airway is non-patent or there is an obstruction, the decision is easy to either attempt intubation via endotracheal tube or secure a surgical airway. The decision is less straight forward when the patient does not seem to be having any difficulties with ventilation and oxygenation. In the case of smoke inhalation injury, early intubation can be lifesaving. [6] This is due to the delayed fashion of bronchoconstriction in addition to the thermal changes that result from heat/smoke inhalation. Clinical judgement must be used however, to avoid intubating everyone prematurely. There are several red flag symptoms that physicians can use to assess whether a patient with smoke inhalation injury requires prophylactic intubation. [5]

Indications for early intubation:

Signs of airway obstruction: hoarseness, stridor, accessory respiratory muscle use, sternal retraction
Extent of the burn (TBSA burn > 40-50%)
Extensive and deep facial burns
Burns inside the mouth
Significant edema or risk for edema
Difficulty swallowing
Signs of respiratory compromise: inability to clear secretions, respiratory fatigue, poor oxygenation or ventilation
Decreased level of consciousness where airway protective reflexes are impaired
Anticipated patient transfer of large burn with airway issue without qualified personnel to intubate en route

Back to the case:

Due to our patient having progressive hoarseness, as well as soot throughout his oropharynx, the decision was made to secure his airway before it became too difficult to do so. A discussion was had with the patient about the risks and benefits to intubation and sedation while the inflammatory response could take its course and he consented to the procedure. Using rapid sequence intubation, rocuronium, a paralytic was used at a dose of 1mg/kg=130mg and propofol was used as a sedative at 1mg/kg=130mg. Fentanyl was used for analgesia at a dose of 1mcg/kg= 130mcg.

Due to the complexity of intubating a patient with possible impending upper airway collapse, it is important to have the best person available for intubation with one pass and ENT should be consulted so that a surgical airway can be obtained. One should also consider awake intubation due to high risk of upper airway occlusion. With this patient, a video laryngoscope was used to place the endotracheal tube.

Figure 3: Video laryngoscopy of an airway with smoke inhalation injury

During the intubation, it was seen that the tissue surrounding the airway was quite edematous with black soot present as well. This was an impending airway collapse! The endotracheal tube was placed, and the patient was monitored in the ICU overnight. As expected, edema ensued and oropharynx, tongue became edematous. The patient was stabilized on propofol drip over the next 2 days and was extubated on the third day post intubation.

Key Takeaways

Early identification of smoke inhalation injury is critical to survival.
The longer delay of intubation is, the harder it becomes. Consider awake intubation.
Red flag symptoms: Respiratory distress, respiratory depression, or altered mental status, Progressive hoarseness, Supraglottic or laryngeal edema/inflammation on bronchoscopy or NPL, Full thickness burns to face or perioral region, Circumferential neck burns, Major burns over 40-60% of body surface
Early intubation=lower mortality

References:

Woodson CL. Diagnosis and treatment of inhalation injury. In: Total Burn

Care, 4 ed, Herndon DN (Ed), 2009.

Sheridan RL. Fire-Related Inhalation Injury. N Engl J Med 2016; 375:1905.
Rehberg S, Maybauer MO, Enkhbaatar P, et al. Pathophysiology, management and treatment of smoke inhalation injury. Expert Rev Respir Med 2009; 3:283.
Herndon, D. N. (2018). 16. In Total burn care (pp. 174–183). essay, Elsevier.
ABLS Provider Manual. (2019). Ameriburn.org
Cioffi WG, Mason AD Jr, et al. The risk of pneumonia in thermally injured patients requiring ventilatory support. J Burn Care Rehabil 1995; 16:262.
Reiter R, Hoffmann TK, Pickhard A, Brosch S. Hoarseness-causes and treatments. Dtsch Arztebl Int. 2015;112(19):329-337. doi:10.3238/arztebl.2015.0329

A Case of Pneumomediastinum

Posted on January 26, 2022 by Mandy Peach

A Case of Pneumomediastinum: A Medical Student Clinical Pearl

Reviewed by Dr. Maria Kovalik

Copyedited by Dr. Mandy Peach

Nick Ellingwood, Med II

Dalhousie Medicine New Brunswick (DMNB)

Case

A 16 year-old male presented to the emergency department complaining of shortness of breath which started 3 days prior. He stated that he was unable to take a deep breath. The patient described a sore throat with a productive cough. The patient also revealed that he was having some generalized chest tightness which did not radiate and was non-pleuritic. The patient was also experiencing some diarrhea as well as nausea when he eats. The patient denied any abdominal pain, vomiting, dysphagia, or fever. He had no past medical or surgical history and taking no medications.

On Examination:

Vitals: Temp=36.7^oC, HR=126, RR=24, BP=100/62, O₂ Sat=95% The patient was sitting comfortably but did appear to be dyspneic. He was of normal body habitus.

On examination, upon palpation there was crepitus in the lower neck, supraclavicular region, and shoulder region on both sides. There was diffused crackles upon auscultation over the anterior and posterior chest wall. Good air entry into the base of both lungs and no wheezing. There was a normal S1 and S2 with no additional heart sounds or murmurs. Abdomen was soft and non-tender with normal bowel sounds.

A nasopharyngeal swap, chest X-ray, cervical X-ray, CBC, electrolytes, creatinine, urea, random glucose were ordered.

Figure 1. Chest X-ray showing extensive subcutaneous emphysema along the chest wall and lower neck and a pneumomediastinum. There is bilateral perihilar opacities but no pneumothorax or pleural effusion.

Figure 2. Cervical X-rays showing subcutaneous emphysema in the supraclavicular and lower neck regions as well as the retropharyngeal region extending beyond the angle of the mandible.

Etiologies of Pneumomediastinum^1,2:

Acute asthma exacerbations
Covid-19 or other lower respiratory infections
Injury to thoracic cavity or airways from surgery, trauma, inhalation of drugs, or Valsalva maneuvers
Perforated esophagus (Boerhaave syndrome)

Case Continued:

A CT chest was ordered to evaluate the extent of the pneumomediastinum and subcutaneous emphysema and rule out severe etiologies such as esophageal and bronchi rupture which were not present. The nasopharyngeal swap came back negative for Covid-19 but positive for another coronavirus. The bloodwork showed leukocytosis (25×10⁹/L) but was otherwise unremarkable. The diagnosis of pneumomediastinum secondary to coronavirus infection was made.

Pathophysiology:

As seen in Figure 3, a pneumomediastinum can result from air escaping from small alveolar ruptures into the surrounding bronchovascular sheath. Air then travels along a pressure gradient through the bronchovascular sheath to the hilum and builds up in the mediastinum.³ From there, air can freely move subcutaneously to the chest wall, upper limbs, and neck. Less commonly, air will directly escape into the mediastinum from a more central structure such as the upper respiratory tract or the esophagus.

Figure 3. Pathophysiology of pneumomediastinum and subsequent subcutaneous emphysema.

https://www.uptodate.com/contents/image/print?imageKey=PEDS%2F111129&topicKey=6352&search=pneumomediastinum&rank=1~111&source=see_link

Additional Exam Findings:

Hamman’s sign is described as a crunching or rasping sound heard over the precordium that is synchronous with systole and tends to be best heard with the patient in the left lateral decubitus position. This sign can be positive in up to 50% of patients with pneumomediastinum and is specific for pneumomediastinum or pneumopericardium^4,5.

PoCUS Findings:

Firstly, in a pneumomediastinum the visualization of the cardiac structures is commonly obstructed by the presence of an “air gap” which is characterized by diffused A-lines anterior to the heart when in the parasternal and apical views. This can also be present in pneumothorax; however, the key difference is that in a pneumothorax the cardiac structures will be visualize during diastole when the heart dilates and pushes the pleural air to the side. In a pneumomediastinum, the air gap will vary with the respiratory cycle (not the cardiac cycle such as in a pneumothorax) because during inspiration the lungs will expand and push the air in the mediastinum cranially allowing the cardiac structures to be visualized⁶.

There are other clinical tools that can be used to differentiate a pneumomediastinum and a pneumopericardium like ECG changes. However, they can also be easily differentiated using PoCUS because the cardiac structures can’t be visualized in the subxiphoid view in a pneumopericardium. In contrast, the absence of air between the diaphragm, pericardium and myocardium allows the cardiac structure to be visualized in the setting of a pneumomediastinum as seen in Figure 4⁷.

Figure 4. PoCUS images showing a pneumomediastinum where box A (subxiphoid view) shows cardiac structures. The parasternal long (B), parasternal short (C), and apical (D) views all show diffuse A-lines suggesting the presence of the air superficial to the heart. These findings would suggest a pneumomediastinum⁷.

Treatment:

Pneumomediastinum normally follows a benign course and is self-limiting
Some patients undergo bronchoscopy or esophagogram to rule out airway or esophageal injury
Admission is recommended to observe for complications because pneumopericardium and pneumorachis can arise^8,9
Supplemental oxygen is given to help promote gas reabsorption
Simple analgesics are used for pain management as needed

Case Conclusion:

The patient was on 4L/min of oxygen while in hospital, and his symptoms significantly improved. Repeat chest X-ray showed improvement in pneumomediastinum and subcutaneous emphysema and he was discharge after 3 days. A chest X-ray 10 days later showed minimal subcutaneous emphysema, and the patient had no symptoms.

Clinical Pearls:

Pneumomediastinum is rare but something to keep in your differential for chest pain and SOB especially in young thin males
There are some life-threatening etiologies of pneumomediastinum that must be ruled out
There are some specific PoCUS findings for pneumomediastinum that can help with your diagnosis
The treatment for pneumomediastinum is rest, simple analgesics, and oxygen

References:

1: Ojha S, Gaskin J. Spontaneous pneumomediastinum. BMJ Case Rep. 2018;2018:bcr2017222965. Published 2018 Feb 11. doi:10.1136/bcr-2017-222965

2: Spontaneous pneumomediastinum in children and adolescents – UpToDate [Internet]. [cited 2021 Dec 17]. Available from: https://www.uptodate.com/contents/spontaneous-pneumomediastinum-in-children-and-adolescents?search=pneumomediastinum&source=search_result&selectedTitle=1~111&usage_type=default&display_rank=1

3: Ivan Macia, Juan Moya, Ricard Ramos, Ricard Morera, Ignacio Escobar, Josep Saumench, Valerio Perna, Francisco Rivas, Spontaneous pneumomediastinum: 41 cases, European Journal of Cardio-Thoracic Surgery, Volume 31, Issue 6, June 2007, Pages 1110–1114

4: Sahni S, Verma S, Grullon J, Esquire A, Patel P, Talwar A. Spontaneous pneumomediastinum: time for consensus. N Am J Med Sci. 2013 Aug;5(8):460-4. doi: 10.4103/1947-2714.117296. PMID: 24083220; PMCID: PMC3784922.

5: Alexandre AR, Marto NF, Raimundo PHamman’s crunch: a forgotten clue to the diagnosis of spontaneous pneumomediastinumCase Reports 2018;2018:bcr-2018-225099.

6: Ng L, Saul T, Lewiss RE. Sonographic evidence of spontaneous pneumomediastinum. Am J Emerg Med. 2013 Feb;31(2):462.e3-4. doi: 10.1016/j.ajem.2012.08.019. Epub 2012 Nov 15. PMID: 23158605.

7: Zachariah, S., Gharahbaghian, L., Perera, P., & Joshi, N. (2015). Spontaneous pneumomediastinum on bedside ultrasound: case report and review of the literature. The western journal of emergency medicine, 16(2), 321–324. https://doi.org/10.5811/westjem.2015.1.24514

8: Vanzo V, Bugin S, Snijders D, Bottecchia L, Storer V, Barbato A. Pneumomediastinum and pneumopericardium in an 11-year-old rugby player: a case report. J Athl Train. 2013 Mar-Apr;48(2):277-81. doi: 10.4085/1062-6050-48.1.11. Epub 2013 Feb 20. PMID: 23672393; PMCID: PMC3600931.

9: Belotti EA, Rizzi M, Rodoni-Cassis P, Ragazzi M, Zanolari-Caledrerari M, Bianchetti MG. Air within the spinal canal in spontaneous pneumomediastinum. Chest. 2010 May;137(5):1197-200. doi: 10.1378/chest.09-0514. PMID: 20442120.

Department of Emergency Medicine | Saint John

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