Spontaneous Pneumothorax After Rupture of the Cavity as the Initial Presentation of Tuberculosis in the Emergency Department

Background

Pneumothorax is defined as the presence of gas in the pleural space. A spontaneous pneumothorax typically occurs without history of chest trauma and can be classified as secondary or primary when it occurs in an individual with or without underlying lung disease, respectively [1]. Spontaneous pneumothorax can be secondary to a wide variety of lung diseases. Spontaneous pneumothorax secondary to pulmonary tuberculosis can occur in cases of residual fibrosis with retractions and bullae [2].

The estimated incidence of spontaneous pneumothorax associated with active pulmonary tuberculosis is only approximately 1–2%. Other pulmonary infections, such as necrotizing bacterial pneumonias and particularly Pneumocystis jiroveci pneumonia in patients with acquired immunodeficiency syndrome (AIDS), are associated with spontaneous pneumothorax [3].

Latent tuberculosis infection is characterized by an adaptive and specific immune response to Mycobacterium tuberculosis (MTB) complex antigens, with no evidence of clinically active TB. The microorganisms that cause latent infection can persist in an inactive phase for several decades, even during the entire life of the host; however, in approximately 5% of all infected individuals, the latent infection progresses to active replication and causes TB disease [4].

Patients with severe tuberculosis who require admission to the ICU typically present with acute respiratory failure, severe/sepsis, and shock/septic, and with multiple organ dys-function. Patients with acute respiratory failure due to pulmonary involvement most often present with severe radiographic alterations involving the lung lobes [5].

Here, we report the case of a patient with spontaneous pneumothorax due to a possible rupture of a tuberculous cavity with acute respiratory failure in the Emergency Department.

Case Report

LABORATORY EXAMS:

Complete blood count analysis revealed: leukocytes 14 200 mm³, hemoglobin 8.9 g/dl, hematocrit 28.9%, mean corpuscular volume (MCV) 77 fl/red cell, mean concentration of hemoglobin (MCH) 23, 7 picograms/cell, mean cell hemoglobin concentration (MCHC) 30.6 grams/deciliter, red blood cell count 374 mm³, platelets 166 000 mm³, Monocytes (%) 3.2, eosinophils (%) 1.4, lymphocytes (%) 3.9, neutrophils (%) 91.3, and basophils (%) 0.2.

Biochemical analysis revealed: glucose 114.3 mg/dl; electrolytes sodium 141 meq/L, potassium 3.2 meq/L, chlorine 111 meq/L, calcium 7.9 meq/L, BUN 15 mg/dl, and creatinine 0.9 g/dl. During his initial admission, the patient received specific treatment for severe community-acquired pneumonia with ampicillin/sulbactam plus clarithromycin. The antifimic treatment with primary scheme (rifampicin-isoniazid, pyrazinamide, and ethambutol) was started immediately after the positive result for tuberculous mycobacteria was obtained from bronchoalveolar lavage.

BRONCHOSCOPY FINDINGS:

The patient underwent a bronchoscopy at 24 h, in which a sharp pale palate mucosa and areas of erythematous stippling and cavitary image in the apical segment of the right upper lobe were noted. Bronchioloalveolar lavage (BAL) and bronchial brushing of the site of injury were performed and samples were taken for cultures of mycobacteria and fungi (Figure 3).

MICROBIOLOGICAL DIAGNOSTICS:

Results were obtained at 4 h after performing the bronchos-copy using a molecular biology technique with the use of MALDI-TOF mass spectrometry (Brucker Daltonics) and by additional phenotypic tests (Optochin and Vitek 2). These results were determined using a disc diffusion method according to CLSI recommendations [6] with detection of Pseudomonas aeruginosa and Klebsiella pneumonia and with mechanism of resistance to KPC (producing strains of carbapenemase) and GeneXpert MTB/RIF System for detection of Mycobacterium tuberculosis determined without resistance to rifampicin examination in straw. Ziehl-Neelsen (IN) staining for the identification of bacillus acid-resistant alcohol was positive in alveolar bronchial lavage.

Conventional cultures of bronchioloalveolar lavage (BAL) fluid confirmed the presence of Pseudomonas aeruginosa and Klebsiella pneumonia with carbapenemases resistance mechanism, and the KPC type enzyme previously reported with the use of MALDI-TOF mass spectrometry and by additional phenotypic analysis. The Löwenstein-Jensen culture method was positive at 4 weeks. Colistin treatment was administered at an initial dose of 300 mg followed by 100 mg every 8 h plus 500 mg of nebulized amikacin every 12 h.

On day 10, a new CT scan of the thorax control showed complete resolution of the pneumothorax with the presence of an interstitial pattern, more left pulmonary cavern and pleural effusion, and a small amount of bilateral right predominance. The patient presented with hemodynamic instability on day 13 of hospitalization, requiring an increased dose of vasopressor and inotropic support with norepinephrine and dobutamine. An episode of atrial fibrillation with rapid reverse ventricular response was noted, and the patient died on day 13.

Discussion

Secondary spontaneous pneumothorax usually occurs as a complication of the underlying lung disease. The diseases most commonly associated with this entity are obstructive pulmonary disease, cystic fibrosis, cavitated cancers, necrotizing pneumonia, Pneumocystis pneumonia, and tuberculosis [7]. Under these conditions, the lung tissue is hyper-dis-tended and the pulmonary alveoli in hyper-aeration can come into contact with the pleural cavity and rupture. The existence of lung caverns in contact with the intrapleural space can also cause secondary pneumothorax.

Destruction of the pulmonary parenchyma with loss of the metalloproteinase matrix is the main characteristic of pulmonary tuberculosis [8]. Cavities appear when large granulomas with central liquefaction and erosions with discharge of their contents in the underlying airway are produced. Most studies that report larger cavities after the initial presentation of the disease suggest an acute presentation event in pulmonary tuberculosis [7]. In addition, the amount of adjacent fibrosis is not correlated with the age of the lesion, and the cavities are generally observed adjacent to extensive zones of condensation [9]. Regardless of its location in the pulmonary lobe of the tuberculous cavities, in the vast majority of cases it has a subpleural localization; however, there is little evidence of cavitary rupture or pneumothorax as the initial presentation of severe respiratory insufficiency [10].

Our patient presented to the Emergency Department with a spontaneous pneumothorax, probably due to the rupture of a cavity, most likely of tuberculous origin, without ruling out the possibility of multidrug-resistant polymicrobial association. However, another potentially associated factor is the presence of other microorganisms that cause lung cavities, such as Klebsiella pneumoniae and Pseudomonas aeruginosa, which are common causes of community-acquired pneumonia in patients with chronic structural lung lesions. However, the presence of multiple pulmonary cavities that cause coalescence and gangrene in the lung parenchyma [9] was not observed in the bronchoscopy of our patient, although this result does not rule out the possibility of participation of these bacteria in the genesis of pneumothorax due to cavitary rupture.

Studies show that the extension of cavitation is a very dynamic process, with preferential formation in sites of high mechanical stress near the necrotic granuloma, suggesting that mechanical stress can weaken the underlying lung tissue, with subsequent air entrapment and cavity expansion [11]. Our patient had a ruptured cavity that caused a spontaneous pneumothorax and acute respiratory failure with immediate transfer to the ICU for management of respiratory failure and pneumothorax drainage.

The literature describes the association of tuberculosis and pneumothorax in various circumstances associated with miliary tuberculosis [12], as well as in some cases with remnant cavitary lesions that become visible after the drainage of pneumothoraxes, some of them reported retrospectively [14] and with diagnosis based on radiographs of the cavity after expansion of the pneumothorax, while other cases have been reported in children [15].

We present a case in which the pneumothorax presented by initial rupture of a cavity, probably of tuberculous origin, without ruling out the possibility of polymicrobial association of multidrug-resistant polymicrobial association. Rapid and timely diagnosis is made possible by rapid performance of bronchoscopic visualization and the processing of samples in the laboratory with results obtained 4 h after bronchoscopy using a molecular biology technique, as well as by additional phenotypic tests and the GeneXpert MTB/RIF system for the detection of Mycobacterium tuberculosis [6].

However, in patients with Pseudomonas aeruginosa and Klebsiella pneumonia with carbapenemases resistance mechanism, the KPC type enzyme is the main cause of progression to septic shock and death.

Conclusions

We report the case of a 65-year-old man with a history of valvuloplasty approximately 3 years ago, who came to our Emergency Department due to acute respiratory failure (ARF) and was admitted to the ICU due to poor ventilatory mechanics. The unusual complications such as secondary pneumothorax resulted from primary parenchymal disease with cavity formation. Mycobacterium tuberculosis was confirmed by polymerase chain reaction (PCR) (GeneXpert MTB/RIF) and culture. Chest tube drainage allows for rapid expansion and resolution, but in a polymicrobial infection with carbapenemases resistance mechanism, the KPC type enzyme is the main cause of progression to septic shock and death.