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.