A previously healthy 18 year old male was admitted to hospital with a few days history of fever and shortness of breath. Chest X-ray showed bilateral interstitial infiltrates and empirical therapy for presumed community-acquired pneumonia was started. A more thorough history taking revealed symptoms of weight loss, lethargy and swallowing difficulties of three months duration. The patient was in hypoxic respiratory failure and therefore intubated within a few hours of admission. A computed tomography (CT) scan showed widespread nodular infiltrates and signs of an abscess in the mediastinum (Fig. 1). Later CT scans confirmed leakage of contrast medium from the oesophagus to the mediastinum but endoscopy did not reveal any obvious pathology.
The patient was septic on admission and needed high-dose vasopressors. Hemodynamic instability resolved within few days but the respiratory failure did not. The patient received lung-protective mechanical ventilation for 18 days, with intermittent prone positioning. Initial cultures from bronchoalveolar lavage and viral polymerase chain reaction (PCR) assays were negative. Ziehl-Neelsen staining did not reveal acid-fast bacilli on repeated samples of tracheal aspirates. Interferon-gamma release assay (IGRA) for tuberculosis was indeterminable. An extensive work-up regarding infectious, malignant and immunological causes was negative. Antibiotic therapy was expanded and the patient received empirical corticosteroids and immunoglobulins. At last transbronchial biopsies were taken with fiberoptic bronchoscopy guidance. Shortly after that intervention the patient developed bilateral tension pneumothoraces, pneumopericardium and subcutant emphysema (Fig. 2). Despite prompt drainage of both pleura, oxygenation of the patient became critical and veno-venous ECMO therapy was started.
Microscopy of transbronchial biopsies revealed acid-fast bacilli and tuberculosis treatment was initiated with rifampicin, isoniazide, ethambutol and pyrazinamide. The diagnosis of miliary tuberculosis was later confirmed (26 days after admission) when growth of Mycobacterium tuberculosis was detected in samples taken at admission. The bacteria grew in tracheal aspirate, urine and cerebrospinal fluid. Additionally, granulomas were seen in a bone marrow aspirate, liver and lung biopsies. The bacteria was found to be susceptible to all first-line anti-tuberculosis agents. The patient's dysphagia and mediastinal abscess were probably related to tuberculosis in the mediastinum. During the ECMO treatment the patient's lungs developed multiple bullae and he had persistent pneumothoraces where the lungs did not expand despite patent pleural tubes (Fig. 3).
Serum levels of anti-tuberculosis agents were monitored and levels of both isoniazid and rifampicin were repeatedly subtherapeutic despite escalating doses and a change to intravenous administration. After multiple negative samples, acid-fast bacilli were seen in tracheal aspirates on two occasions, four weeks after the start of treatment. During the VV-ECMO treatment, a multi-resistant Pseudomonas aeruginosa and Stenotrophomonas maltophilia were repeatedly cultured from tracheal aspirates. These bacteria were successfully eradicated with a combination therapy of inhaled colistin and tobramycin along with intravenous amikacin, meropenem and ceftazidime/avibactam. As with the anti-tuberculosis agents, serum levels of amikacin were low.
After 45 days on ECMO the patient started to show signs of recovery with increasing lung compliance and re-expansion of the lungs (Fig. 4). He was successfully weaned from ECMO after 50 days. Complications during the ECMO run were thrombocytopenia, minor bleedings from puncture sites and sensory symptoms in lower limbs. The patient stayed a total of 76 days in the ICU. After three months of rehabilitation he was back at home and had resumed previous activities, including sports.
A; CT scan after two weeks on VV-ECMO. Both lungs show numerous bullae and there were persistent bilateral pneumothoraces despite pleural tubes in-situ.