Review of Respiratory Medicine - Volumen 25, Número 2 - June 2025

Case Reports

Pneumomediastinum Associated with Asthma Exacerbation in Adults. Two Case Reports and Literature Review

Neumomediastino asociado a crisis asmática en el adulto. Reporte de dos casos y revisión bibliográfica

ABSTRACT

Background: Pneumomediastinum (PM) is defined as the presence of air in the mediasti­nal cavity. It has been described by Laennec in 1819 as secondary to trauma. Among the non-traumatic causes, asthma exacerbations are included. The following report depicts two pneumomediastinum cases in the context of an asthma crisis. Case 1: 18-year-old male, diagnosed with asthma since childhood. The patient presented with asthma exacerbation, associated with subcutaneous emphysema and pneumomediastinum as a complication. Case 2: 37-year-old male, asthmatic, athlete. He presented with asthma exacerbation, associated with Salmonella bacteremia and pneumomediastinum as a tomographic finding.

Conclusion: The real incidence of pneumomediastinum associated to asthma crisis is currently unknown. It is generally an asymptomatic and self-limited entity, but it must be suspected in patients presenting with dyspnea, subcutaneous emphysema and hypoxemia that doesn’t respond to initial treatment. Controlling asthma exacerbations and monitoring the patient are the main pillars of treatment.

Key words: Pneumomediastinum, Asthma, Air leak síndromes, Subcutaneous emphysema, Hypoxemia, Chest Computed Tomography scan, Macklin effect

RESUMEN

Introducción: Se define como neumomediastino a la presencia de aire en el espacio mediastinal. Este fue descripto en el año 1819 por Laennec, quien lo describió como secundario a trauma. Dentro de las causas no traumáticas se encuentran las exacer­baciones de asma. El siguiente reporte presenta dos casos de neumomediastino en el contexto de crisis asmática. Caso 1: Paciente masculino de 18 años, asmático desde la infancia. Presentó una exacerbación de asma asociada a un enfisema subcutáneo y neumomediastino como complicación. Caso 2: Paciente masculino de 37 años, as­mático y deportista. Presentó una exacerbación de asma y cuadro de bacteriemia por Salmonella, con hallazgo tomográfico de neumomediastino.

Conclusión: Se desconoce la incidencia real del neumomediastino asociado a crisis asmática. Suele ser una entidad asintomática y autolimitada, pero debe sospecharse en pacientes con disnea, enfisema subcutáneo e hipoxemia refractaria al tratamiento inicial. El manejo de la exacerbación de asma y el monitoreo son los pilares del tratamiento.

Palabras clave: Neumomediastino, Asma, Síndromes de fuga de aire, Enfisema subcutáneo, Hipoxemia, Tomografía computarizada de tórax, Efecto Macklin

INTRODUCTION

Pneumomediastinum (PM), also known as medi­astinal emphysema, is defined as the presence of air in the mediastinum. It is rarely diagnosed, and its incidence in asthmatic patients ranges in the literature from 0.3% in pediatric patients¹ to 11% in adults². It occurs due to an air leak from the air­way or, less commonly, from the digestive tract into the thoracic cavity, and falls within the spectrum of air-leak syndromes (ALS). ALS are a possible complication during asthma exacerbations, with PM being the most commonly recognized.³ The objective of this report is to present two cases of PM associated with asthma crisis, highlighting the clinical presentation, diagnosis, and progression of both patients.

Case 1

A 18-year-old male patient, non-smoker, con­sulted the emergency department with a 7-day history of non-productive cough and dyspnea, which progressed to mMRC grade III/IV over the last 48 hours. As relevant medical history, he re­ported being diagnosed with asthma at the age of 11. He had no previous hospitalizations and was self-medicating with one inhaler of salbutamol as needed, 100 μg/dose per month (total doses = 200). He denied using corticosteroids and stated that he had not received follow-up care for his condition from the pulmonology department.

The patient was admitted to a public hospital for 48 hours due to hypoxemia associated with asthma crisis. During hospitalization, a non-contrast chest computed tomography (CT) scan was performed (Figure 1), confirming the presence of pneumo­mediastinum extending to the base of the neck, associated with subcutaneous emphysema in the anterior chest wall.

He was prescribed systemic and inhaled corti­costeroids, along with bronchodilator therapy. He showed partial clinical improvement.

The patient was referred to our center. He was admitted alert, afebrile, normotensive, with a heart rate of 100 beats/min, and good ventilatory mechan­ics. He presented with tachypnea (30 breaths/min) and oxygen saturation of 90% on room air (FiO₂ 21%). On physical examination, there was moder­ate bilateral air entry with generalized mostly ex­piratory wheezing. Subcutaneous emphysema was evident on bilateral palpation of the upper pectoral, supraclavicular, and cervical regions.

Admission laboratory tests showed leukocytosis of 20,520/mm³. An arterial blood gas on room air was performed, revealing hypoxemia with respira­tory insufficiency (PaO₂ 55 mmHg), normocapnia (PaCO₂ 43 mmHg), pH 7.40, HCO₂ 26 mEq/L, base excess 0.8, and elevated lactate (2.4 mmol/L).

The patient was given oxygen therapy at 2 L/ min, and achieved an oxygen saturation of 96%, along with bronchodilators and inhaled and sys­temic corticosteroids, following the institutional protocol for asthma exacerbation. He was hospital­ized for monitoring of the pneumomediastinum. He showed significant clinical and oxygen satu­ration improvement. He was discharged 5 days later, and continued treatment and follow-up in outpatient specialty clinics.

Case 2

37-year-old male patient, high-performance ath­lete, currently on inhaled treatment with two (2) daily doses of budesonide/formoterol, 160 μg/4.5 μg. He reports having received three doses of the COVID-19 vaccine. He came to our emergency department with a 5-day history of headache and fever of 38.6 °C, associated with asthenia and mMRC grade I/II dyspnea that began in the last 24 hours. As relevant medical history, he reports having participated in mountain running at an altitude of 2,000 meters in the north of the country earlier this month, and at the time of consultation, he was presenting with diarrhea and vomiting with a 20-day history. Due to the fever and dyspnea, a nasopharyngeal swab for COVID-19 with PCR (polymerase-chain reaction) testing and a chest CT scan were performed. The PCR test result was negative, but the chest CT scan revealed PM (Figure 2). The patient was hospitalized based on the CT finding and his symptoms, and two blood culture samples were requested.

On admission, the patient was normotensive, with a low-grade fever of 37 °C, tachycardia (110 beats/min), and oxygen saturation of 97% on room air. On physical examination, the patient showed good ventilatory mechanics; bilateral air entry was clear, with no added sounds. The abdomen was soft, depressible, and non-tender. Venous blood samples were taken for routine laboratory testing, which showed no abnormalities. Salmonella spp. was iso­lated in the blood cultures (positive in 2/2 samples), so intravenous ceftriaxone treatment was initiated based on sensitivity, for 7 days. Oxygen therapy and budesonide/formoterol were also indicated for exacerbation of the respiratory condition.

The case was interpreted as PM secondary to asthma exacerbation, along with Salmonella bacteremia in the context of traveler’s diarrhea. However, vomiting or high altitude could not be ruled out as probable causes of PM.

After seven days, a follow-up chest CT was performed, showing a reduction in the pneumo­mediastinum and absence of pleuro-pulmonary alterations. Apart from the initial dyspnea, no other asthma-related symptoms were observed during hospitalization. The patient’s symptoms improved, and the patient was discharged. He is currently under follow-up treatment in the outpa­tient specialty clinic.

DISCUSSION

Two cases of PM secondary to asthma exacerba­tion are presented. The first PM reports date back to 1819, when Laennec described the condi­tion as secondary to trauma. Since then, various classifications have been proposed; the division into primary PM (spontaneous, without apparent cause) and secondary PM is currently the most widely accepted. The latter is further subdivided into traumatic and non-traumatic. Some of the most common non-traumatic causes are: the use of mechanical ventilation (iatrogenic PM) and the presence of underlying lung diseases, such as asthma.

Asthma crises can produce complex clinical symptoms; in some cases, patients present with dyspnea and hypoxemia as a consequence of ALS.⁴ The physiopathological process of this entity is explained by alveolar rupture, secondary to hyper­inflation caused by the airflow obstruction typical of asthma. Coughing and other unintentional Val­salva maneuvers –such as the force exerted during vomiting or defecation– worsen the symptoms by indirectly increasing intrapulmonary pressure.

The Macklin effect describes the cascade of events that lead to the development of PM: ini­tially, the rupture of the marginal alveoli causes an air leak into the interstitium, known as interstitial lung emphysema.⁵ From this site, air travels along the bronchovascular tree, through the perivascular and peribronchial sheaths, reaching the hilum and, finally, the mediastinal space. The latter communicates directly with the retropharyngeal and submandibular spaces; therefore, the finding of subcutaneous emphysema at the cervical level should raise suspicion that the patient has an associated PM.⁶ In addition, the pressure exerted by free air in the cavity can lead to the rupture of the mediastinal pleura and invasion of air into the pleural space, resulting in a pneumothorax. On the other hand, from the mediastinum, air dis­sects the muscular and adipose planes, which can result in the development of pneumopericardium or pneumorrhachis. The downward extension of air to the periaortic or periesophageal area can lead to pneumoperitoneum or pneumoretroperito­neum. All of these air leaks are known as air-leak syndromes (ALS); pneumomediastinum is one of the most common.

Thus, asthma exacerbations contribute to the development of PM. Case 1 illustrates an exacerbation typical of patients with poor con­trol of their underlying disease. The absence of anti-inflammatory therapy was the triggering factor for the onset of the crisis, which led to the appearance of PM due to the physiopathological process described above. On the other hand, Case 2 describes a patient with good asthma control, whose exacerbation was likely due to a history of engaging in mountain sports or to the septicemia. It is also unknown whether the high altitude could have contributed to the development of PM. Al­though the association is not yet clear, cases have been reported of non-asthmatic patients without predisposing factors who develop spontaneous PM at high altitude.⁷ Furthermore, the Valsalva maneuvers typical of vomiting and diarrhea can­not be ruled out as potential causes or aggravating factors of PM.

In both patients, the PM diagnosis was made based on chest CT images, which are considered the reference standard for diagnosing this condition. Chest X-rays are useful, but to a lesser extent, since interstitial lung emphysema and nearly one-third of PM cases are not always evident on such imaging.^{8, 9}

Patients with PM are often asymptomatic; therefore, the condition must be confirmed with imaging. However, certain findings in the patient’s history or physical examination may point toward the PM diagnosis, such as dyspnea or chest pain of varying intensity, hypoxemia refractory to oxygen therapy, or palpation of subcutaneous emphysema, as observed in Case 1. To a lesser extent, dyspha­gia and dysphonia have been reported in patients who, due to compression of mediastinal structures, experience displacement of the esophagus and trachea, respectively.

There are no pathognomonic signs, but the literature highlights one sign that could identify patients suffering from PM: the Hamman’s sign,¹⁰ which describes the auscultation of crackles over the precordial area concomitant with the cardiac systole, usually when the patient is in the left lateral decubitus or seated position. This occurs as a result of air accumulation between the peri­cardium and the anterior chest wall.

Regarding the management of PM, it depends on the clinical status of each patient, but cases usually resolve spontaneously. Treatment is based on the immediate correction of the underlying cause, oxygen therapy as needed, rest, and hospi­tal monitoring. The latter is necessary to prevent or anticipate the appearance of complications associated with PM, such as pneumothorax, pneu­mopericardium, or tension PM that compromises circulation. Barotrauma should be considered as a possible complication in patients requiring mechanical ventilation. Analgesics may be admin­istered if needed, and both Valsalva maneuvers and risk factors for developing PM after hospital discharge should be avoided. In this regard, edu­cation and follow-up of the asthmatic patient are essential for the prevention of exacerbations and, ultimately, air-leak syndromes.

CONCLUSIONS

The actual incidence of PM associated with asthma exacerbations is currently unknown, as only iso­lated cases are reported in medical literature. Pos­sibly the absence of specific signs and symptoms makes it an underdiagnosed and underestimated condition.

Although its course is generally benign and self-limited, exceptional severe cases have been described.¹¹ It is essential to maintain clinical suspicion of PM when evaluating asthma exac­erbations. Timely diagnosis should be consid­ered, as PM in the context of an asthma crisis is an indication for hospital admission. These patients should be monitored to anticipate the development of other ALS and potential severe complications.

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