CASE REPORT
We present a previously healthy thirteen-year-old male. Parents and siblings were diagnosed with COVID-19. On 04/14/21, he consulted, and was admitted to his hospital of origin with progressive respiratory distress. Chest computed tomography (CT) (Figure 1A) showed massive left pleural effusion and multiple nodular lesions in the right lung. In this context, he was connected to non-invasive mechanical ventilation, empiric antibiotic therapy was started, evacuating thoracocentesis was performed, and a pleural catheter (PC) was placed. Blood tests showed elevated inflammatory markers (C-reactive protein (CRP) 191 mg/L, ferritin 535 ng/ml). In addition, tomographic abdominal and pelvic exploration (Figure 1B) showed a multilobed, heterogeneous pelvic mass. Brain CT was normal. SARS-COV-2 was confirmed by polymerase chain reaction, so dexamethasone was initiated. The patient evolved towards severe respiratory distress and hypoxemia, was connected to invasive mechanical ventilation (IMV), and transferred to the Pediatric Intensive Care Unit (PICU) of the corresponding reference hospital.
Upon transfer, he was described as feverish, pale, tachycardic and hypotensive, requiring norepinephrine, that could be suspended four days later. He presented torpid respiratory evolution with severe ARDS, requiring prone position ventilation and neuromuscular blockade. Discrete initial improvement was observed, but on day 11 of hospital admission (04/25/21), he deteriorated, presenting right pneumothorax, another PC was installed. A new chest CT was performed that ruled out pulmonary thromboembolism. Despite these measures he continued hypoxemic (PaO2/FiO2 50, oxygenation index 29) and lung protective ventilation was impossible to sustain. VV-ECMO was decided.
Etiologic study for the pelvic mass was performed including: beta-human chorionic gonadotropin and alpha-fetoprotein (normal), pleural fluid flow cytometry for malignant hematological diseases (negative) and an ultrasound-guided biopsy of the pelvic mass was made 9 days after hospital admission, which confirmed Ewing’s sarcoma. Protocol chemotherapy was initiated (on day 16 of admission), with our patient already on VV-ECMO.
He continued in critical condition, with suitable perfusion parameters, but without improvement of ARDS. Acute kidney injury developed which, added to fluid overload, required continuous renal replacement therapy through the ECMO circuit for 15 days. He continued with high inflammatory biomarkers (maximum CRP 343 mg/dl); antimicrobial coverage was changed empirically to vancomycin, meropenem, voriconazole and cotrimoxazole. Bronchoalveolar lavage (BAL) was performed and ruled out bacterial, fungal, or viral intercurrence. Due to torpid evolution, compatible with acute fibrinous organizing pneumonia, steroid dosage was increased, changing dexamethasone for methylprednisolone (10 mg/kg daily for 3 days), and maintained subsequently with prednisone in progressively decreasing doses. After that, a decrease in inflammatory parameters was observed but without improvement in respiratory state.
During the third week from admission, he presented new significant respiratory compromise, secondary to ventilator-associated pneumonia due to Candida parapsilosis isolated in a second BAL culture, specific treatment with caspofungin was started. In addition, left pleural effusion increased and right pneumothorax reappeared. This required the installation of a new right PC, and in attempt to improve oxygenation, prone position on ECMO was used for 6 days (from day 22 of admission, 11 on ECMO). For management of the left pleural effusion, fibrinolytic therapy was administered (recombinant tissue plasminogen activator (rt-PA)). A new chest CT scan was performed (Figure 2) that showed bilateral pleural effusion, greater in the right lung, with large organized collections of blood content that produce a mass effect on adjacent pulmonary segments. Due to the patient’s condition, resolution of the pulmonary clot was attempted with pleural administration of rt-PA. He presented partial response, but also bleeding. Therefore, at 44 days from admission and 34 of ECMO, he was taken to the operating room for video-assisted thoracoscopic surgery, where a collection of clots was identified and cleaned at the level of the thoracic cavity, an inflamed-looking lung, especially in the middle lobe, which appeared to be an intraparenchymal hematoma. After the procedure, respiratory improvement was finally observed, but given prolonged IMV, tracheostomy was performed in the PICU, 30 days after admission. He presented progressive improvement, weaning from ECMO was possible, and decannulation was performed after 42 days of VV-ECMO support. Maintained improvement led to IMV weaning after 85 days of hospital admission.
There were no other hematological complications, and they did not present neurological complications, except myopathy of the critical patient.
Our patient continued his treatment with chemotherapy according to protocol. In addition, a rehabilitation program was carried out in the PICU, being able to decannulate tracheostomy on day 118. He was moved to Oncology 2 days later and finally discharged from hospital after 138 days with a Karnofsky score of 70. He is currently undergoing his outpatient controls in Oncology.