ABSTRACT
Rationale: We aim to describe the clinical characteristics and outcomes of patients who received Tocilizumab for COVID-19 pneumonia at our institution between March 20 and October 26, 2020. Methods: In this single center, retrospective, observational study, we identified 55 adults admitted with COVID-19 pneumonia who received Tocilizumab. Demographic data, symptoms, laboratory values, treatments, and clinical outcomes were collected. Data was compared between those who received Tocilizumab and all patients admitted with COVID-19. Primary outcome was 28-day mortality. Secondary outcomes included role of concomitant steroid use and change in eosinophil counts, ferritin, AST, CRP and D-Dimer values. Results: Of the 589 patients admitted with COVID-19 pneumonia, 55 received Tocilizumab as part of their treatment course. Patient demographics of those who received Tocilizumab include a mean age of 58 years with 73% male, 51% with diabetes, and 58% with hypertension. 4/55 (7.3%) were immunocompromised. Common presenting symptoms on admission were fever (62%), cough (78%) and dyspnea (89%). 35/55 (64%) were admitted to the ICU during their hospitalization;their mean P/F ratio was 127. Tocilizumab was administered on average admission day 4 (1-19). A second dose was given to 17 (31%) of patients, with 11 given the following day. Average hospital length of stay (LOS) postadministration was 17 days. Average white blood cell (WBC) count on day of Tocilizumab administration was 11, with an absolute lymphocyte count of 0.96. Mean IL-6 on hospital admission was 48.3. Two days post Tocilizumab administration there was a peak in ferritin, percent eosinophils, and AST. Both two-and five-day post-Tocilizumab CRP levels decreased while D-Dimer increased (Table 1). All Tocilizumab patients received antibiotics. In addition, three received hydroxychloroquine, 16 Remdesivir, and 51 convalescent plasma. 31 (56%) received steroids. On Day 2, those who did not receive steroids had, on average, more than double the percent of eosinophils in their blood (3.21% vs 1.53%). This difference decreased by Day 5. In time period of interest, COVID-19 admission mortality was 63/589 (10.6%) and 40/77 (52%) for mechanically ventilated patients. For Tocilizumab recipients, 25/55 patients were mechanically ventilated and 12/25 (48%) died. Overall, 28-day mortality was 11/55 (20%), with hospital mortality up to 16/55 (29%). This was similar to our larger cohort ICU mortality of 29.3%. Conclusion: Tocilizumab recipients in our cohort had a mortality similar to overall COVID ICU mortality. It appeared to be well tolerated except for an increase in eosinophilia if with no concomitant steroid use.
ABSTRACT
Introduction: Post-extubation stridor, or inspiratory noise following extubation, is frequently observed in patients post-extubation, due to laryngeal edema secondary to airway manipulation. Post-extubation stridor is of increasing concern during the COVID-19 pandemic, as risk for re-intubation and consequent poor outcome is high. We present a case of post-extubation stridor due to tracheal mucus plugging in the setting of COVID-19 pneumonia. Case Presentation: A 61-year-old female diagnosed with COVID-19 pneumonia, right lower lobe pulmonary embolus, and left lung pneumothorax with chest tube experienced a nontraumatic intubation and 13 days of ventilatory support due to respiratory failure. Four days following extubation patient developed stridor and increased oxygen requirement. Patient was given racemic epinephrine 0.5mL x two doses and IV solumedrol 40mg BID x four doses, maintaining oxygen saturation >91% on BiPAP. Direct visualization under flexible laryngoscopy showed small granulation tissue in posterior commissure and concretions and dried mucus in the trachea. The following day, patient displayed worsening stridor, hoarseness, and respiratory difficulty. Bronchoscopy versus tracheoscopy was considered. CT chest displayed moderate debris within the proximal trachea. Due to concern for airway compromise with bronchoscopy, patient underwent laryngoscopy and tracheoscopy with tracheal plug removal by airway forceps. Stridor and hoarseness improved following procedure;oxygen requirements declined in following two-three days leading to discharge. Discussion: Post-extubation stridor can occur in nearly 10% of intensive care unit patients, frequently due to laryngeal edema. In the present case, our patient underwent steroid and racemic epinephrine therapy to address this possible cause with no clinical improvement. Chest CT was performed for further characterization, which discovered moderate debris within the proximal trachea. We hypothesize the tracheal debris accumulation was due to illness with COVID-19, prolonged intubation, and a weak cough unable to clear airway secretions. Previous studies have shown that COVID-19 pneumonia causes bilateral diffuse alveolar damage with fibromyxoid exudates leading to excessive airway mucus. This excess mucus leads to increased airway resistance and decreased alveolar gas exchange. Weakness after critical illness and prolonged intubation likely contributed to our patient's inability to clear these secretions, leading to tracheal accumulation, increased oxygen requirement, and stridor. Bronchoscopy and/or intubation in patients with tracheal debris may be detrimental due to endotracheal tube obstruction or mucus plug mobilization into distal bronchi and subsequent respiratory failure. Therefore, it is important to maintain a broad differential diagnosis while assessing stridor after extubation, particularly in patients with COVID-19 pneumonia.