Review of Respiratory Medicine - Volumen 22, Número 2 - June 2022

Case Reports

Neumomediastino espontáneo en un paciente con COVID-19
Spontaneous Pneumomediastinum in a Patient with COVID-19

Autor : Anci Alvarez Cynthia1, Cid Candelaria1, Solavallone Vanina1, Quiroga Carla1, Rosales Zoe1, Barada Claudia1

1Clinical Medicine Service,, Hospital Santa Isabel de Hungría. Guaymallén, Mendoza, Argentina.

Correspondencia : Cynthia Anci Alvarez E-mail: ancicynthiaantonella@gmail.com

ABSTRACT

Patients infected with SARS-CoV2 show various manifestations consistent with the multiorgan impact of this virus in the system of the human being. However, pulmonary conditions are the most predominant: from slight ground glass infiltrates to severe in­volvement of pulmonary parenchyma. Pneumomediastinum is a rare expression that only occurs in 1% of patients. We present the case of a critically ill male patient with COVID-19 who develops pneumomediastinum without pneumothorax.

Key words: COVID-19, Pneumomediastinum, Spontaneous pneumomediastinum, Ham­man’s syndrome

RESUMEN

Los pacientes infectados por SARS-CoV2 presentan manifestaciones variadas con­secuentes con el impacto multiorgánico de este virus en la economía del ser humano. Sin embargo, las afecciones pulmonares son las predominantes, dado que abarcan desde sutiles infiltrados en “vidrio esmerilado” hasta un gran compromiso del parén­quima pulmonar. El neumomediastino es una expresión rara que se presenta tan solo en un 1% de los pacientes. Presentamos el caso de un paciente varón con COVID-19 crítico que desarrolla neumomediastino sin neumotórax.

Palabras claves: COVID-19, Neumomediastino, Neumomediastino espontáneo, Síndrome de Hamman

Recibido: 09/16/2021

Aceptado: 11/07/2021

INTRODUCTION

The spontaneous pneumomediastinum (SP), also known as “Hamman’s syndrome” was first described in 1939. It is defined as the presence of air in the mediastinum generated by alveolar rupture and air exit from the bronchial tree. It may also reach the subcutaneous cellular tissue, the peritoneum or the rachidial canal. The Hamman’s sign is the perception of a crackling sound synchro­nous with the heartbeat in the anterior thorax aus­cultation. It is a rare disease mostly associated with chronic pulmonary diseases, such as asthma or COPD (chronic obstructive pulmonary disease)1-7. One of its multiple triggering factors is the Valsal­va maneuver generated by respiratory infectious processes5-7. This would justify finding this condi­tion in patients with COVID-19 showing intense, difficult-to-control cough. Other situations that could favor this condition are those related to the use of invasive mechanical ventilation (IMV) and non-invasive mechanical ventilation (NIMV), as for example the high-flow nasal cannula (HFNC), although those situations usually come with a pneumothorax2, 3, 5.

We present the case of a male patient who deve­loped SP without pneumothorax, in the context of SARS-CoV2 infection and use of HFNC.

 

CASE REPORT

59-year-old male patient who had started to have fever up to 39°C six days before consultation. High temperature associated with myalgia was measured and confirmed with a thermometer and was partially lowered with parace­tamol. For that reason, and in the context of being close contact of a SARS CoV2 positive patient, a rt-PCR (reverse transcription-polymerase chain reaction) was performed, with positive result. The patient had dyspnea, functional class II-III, 48 hours before hospital admission. He attended the on-call service, where a chest computed tomography (CT) confirmed bilateral ground glass infiltrates, and the physical examination showed desaturation, after which it was decided that he should be hospitalized. It is important to mention es­sential AHT and obesity degree 1 as relevant patient history. Moreover, the patient had received one dose of the Sputnik V vaccine the day before the onset of symptoms. The physical examination on admission showed the following results: BP (blood pressure): 110/70 mmHg, HR (heart rate): 81 lpm, RR (respiratory rate): 18 rpm, SatO2 96%-97% with nasal cannula at 4 L/min, T°: 36.9 °C, BMI (body mass index): 35 kg/m2. The respiratory assessment confirmed good ventilatory mechanics, generalized hypoventilation associated with isolated bilateral crepitant rales. As for the cardiovascular system: S1 and S2 normal heart sounds with clear silent phases, with no signs of pump failure. Supplementary tests: lymphocytopenia, thrombocytopenia, increase in LDH (lactate dehydrogenase), ferritin, PCR and IL-6. The patient also showed acute renal failure. Arterial blood gas: pH 7.43, pCO2: 31.6 mmHg, pO2: 66.9 mmHg, HCO3: 20.8 mmol/L, EB (excess-base): –2.4 mmol/L, SO2 (AA): 93.7% Table 1 shows laboratory tests taken on admission, and their evolution during hospitalization. Chest CT done on admission: ground glass confluent areas and associated areas of consolidation that compromise both pulmo­nary fields in a diffuse way, attributed to moderate COVID-19 bilateral pneumonia (according to the criteria of the Chest CT Severity Score). Two-dimensional transthoracic Doppler echocardiography: LV (left ventricular) concentric remodeling with left atrial enlargement and mild enlargement of right cavities; unchanged valves; enlargement of aortic root; preser­ved global motility; LVEF (left ventricular ejection fraction): 70%; PSP (pulmonary systolic pressure): 44 mmHg; normal diastolic relaxation pattern. The patient was categorized on admission as a moderate case of COVID-19 according to the established criteria of the WHO (World Health Organization), and began treatment with oxygen therapy, dexamethasone in doses of 8 mg/day by endovenous route (which he underwent for 10 days) and pharmacologic thromboprophylaxis. 48 hours after admission, worsening of respiratory failure was confirmed. It was decided that a dose of tocilizumab of 8 mg/ kg of weight had to be given to the patient (according to the protocol of the Institution) and he had to use a HFNC. Diphen­hydramine and codelase syrup plus inhaled budesonide were indicated because the patient showed persistent dry cough. Due to HFNC weaning failure and progression of respiratory failure, 13 days after admission and 19 days since the onset of symptoms, the patient was transferred to the intensive care unit (ICU). As soon as he was admitted to the ICU, the patient underwent a chest CT angiography that showed signs of pneumomediastinum, and absence of tomographic signs compatible with acute pulmonary thromboembolism (PTE); in the pulmonary parenchyma, patchy and confluent areas of interstitial-alveolar infiltrates with tendency to consolidate, associating overlapping linear images that form a crazy paving pattern compatible with severe tomographic pulmonary in­volvement (Figure 1). It is worth mentioning that no invasive thorax procedures had been performed before in this patient. The patient stayed 4 days in the ICU; no IMV or vasopressor requirement. Due to the presence of the pneumomediastinum, the patient was evaluated by the chest surgery service, which adopted a watchful waiting approach. The patient returned to clinical medicine, where he weaned from the HFNC after a total of 15 days. 24 days post-hospital admission, the patient was discharged, with indication of home oxygen therapy and outpatient follow-up visits. Follow-up CT done 30 days after discharge confirmed the complete resolution of the pneumo­mediastinum (Figure 2).

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Figure 1. Chest CT angiography
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Figure 2. Chest CT after 30 days.

DISCUSSION

The main target of the SARS-CoV2 infection is the respiratory system, and it can affect it in va­rious ways. In hospitalized patients, it is common to observe large involvement of the pulmonary parenchyma by ground glass infiltrates confirmed by CT, but this infection also affects pulmonary vascularization with manifestations such as PTE in a not insignificant percentage8. The possibility of developing a pneumothorax is around 1% and may rise to 6% in critical cases9. The development of the pneumomediastinum is not very common (1%) and has been observed more frequently in young male adults. In severe pneumonia of viral etiology, the alveolus tends to break due to the condition of the alveolar membrane caused by the infectious involvement of type I and II pneu­mocytes7. The factors that could trigger the SP could be due to Valsalva maneuvers produced by excessive coughing in salvos generating alveolar damage and air leak (Macklin effect)1, 5-9.

The literature also mentions other conditioning factors associated with the development of nons­pontaneous pneumomediastinum, such as the use of IMV or HFNC1-4, 6-10.

In the case of the HFNC, there are some studies about pneumomediastinum, but it is generally accompanied by pneumothorax2, 3, 9. In our patient, there wasn’t a SP-associated pneumothorax, so we guided our etiologic suspicion towards the Valsalva maneuvers produced by uncontrolled coughing.

The SP that occurs in patients with a SARS-CoV2 infection usually shares some clinical cha­racteristics according to scientific reports, as for example suffering a severe or critical disease with large involvement of pulmonary parenchyma and the presence of cough as leading symptom2, 7, 9.

Once the SP is established, the most common clinical manifestations are usually intense thora­cic pain and dyspnea. The physical examination confirms a crackling sound in the subcutaneous cellular tissue when emphysema is added3-5, 7-9. This wasn’t the case of our patient, in whom it was incidentally detected through a chest CT an­giography, encouraged by his difficulty in weaning from the HFNC, which has been described in other clinical cases5.

As supplementary methods, chest X-ray is the most available worldwide, but the SP may go unnoticed if lateral view is not requested. This method is difficult in patients with IMV, due to the technique itself and the need to transfer the patient to other hospital areas. Currently, the CT has become relevant and is the most reliable study for diagnostic confirmation7.

It is very important to suggest differential diagnoses, such as the pneumothorax, acute myo­cardial infarction, PTE, neuromuscular diseases or Boerhaave syndrome (spontaneous esophageal perforation), and those should be considered as possible complications in SARS CoV2 infection4, 6, 8.

With regard to the prognosis, it is a low-mortality disease, except for the cases where it is associated with pneumothorax, a situation in which it rises to 33%. There aren’t any confirmatory studies, but this condition could be associated with a higher mortality rate in patients with severe COVID-19, thus the existence of this condition must warn the physicians about the potential severity of the symptoms.1, 6, 8, 9 The common treatment of choice is observation and follow-up of the patient, pain control and oxygen therapy, not requiring surgical intervention in most reported cases1, 4, 6-8.

There is limited literature on this condition. Most publications are clinical cases or case reports, so we think it is of fundamental importance to add suitable studies to determine associated factors and prognosis1, 2, 6, 7, 9, 10.

CONCLUSION

In short, the SP is a low-frequency entity in SARS-CoV2 infection, with benign behavior in most cases; nevertheless, it should be discarded in patients with progression of hypoxemia or refrac­tory hypoxemia. High clinical suspicion related to imaging confirmation will allow us to choose the correct management of the disease. Improving its diagnosis will let us know its real incidence and optimize treatments.

ANNEX

Table 1. Laboratory test during hospitalization
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Conflict of interest

The authors declare that there is no conflict of interest.

REFERENCES

1. García-Villarreal F, Palacios-Mendoza EB. Neumomedi­astino espontáneo asociado con COVID-19. Med Int Méx. 2021; 37: 296-99.

2. Rubiera Ponga C, Pelayo Quispe-Mauricio A, Sánchez- Carpintero Abad M. Neumomediastino masivo en paciente COVID-19. Arch Bronconeumol. 2021; 57: 42.

3. Vela Colmenero RM, Pola Gallego de Guzmán MD, Molina de la Torre MC. Neumomediastino y neumotórax espontá­neo en neumonía bilateral por COVID-19. Med Intensiva. 2020; 44: 591-2.

4. Macia I, Moya J, Ramos R et al. Spontaneous pneumome­diastinum: 41 cases. EJCTS. 2007; 31: 1110-4

5. López Zúñiga M, López Zúñiga D, Martínez Colmenero J, et al. Neumomediastino espontáneo en pacientes con COVID-19. Emergencias 2020; 32: 290-9.

6. Sotelo-Jiménez P, Moyano-Navarro E, Tipacti-Rodríguez F, Milla-Bravo C. Neumomediastino espontáneo en un pa­ciente con COVID-19, reporte de caso. Rev Fac Med Hum. Abril 2021; 21: 445-8.

7. Bolaños-Morales F, Santibáñez-Salgado JA, Guadarrama- Pérez C, Herrera-Zamora JJ, Armas-Zárate FJ, Santillán- Doherty PJ. Neumomediastino espontáneo en pacientes COVID-19. Serie de casos. Gac Med Mex. 2021; 157: 116-20.

8. Parra Gordo M, Buitrago Weiland G, Grau Garcíac M, Are­naza Choperena G. Aspectos radiológicos de la neumonía COVID-19: evolución y complicaciones torácicas. Radiología 63. 2021; 74-88.

9. Pérez-López KP, Moreno-Madrigal LG. Neumotórax y neumomediastino espontáneos en pacientes con neumonía por COVID-19. Med Int Méx. 2021; 37:1 52-6.

10. Fernández-Raga S, Fidalgo-Navarro A, Bernardo-Cofiño J. Neumomediastino espontáneo en neumonitis por corona­virus evolucionada. Med Clin (Barc). 2020; 155: 421.

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