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).
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
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.