Clinical outcomes and quality of life of COVID-19 survivors: A follow-up of 3 months post hospital discharge.

BACKGROUND: Over 66 million people worldwide have been diagnosed with COVID-19. Therefore, understanding their clinical evolution beyond hospital discharge is essential not only from an individual standpoint, but from a populational level. OBJECTIVES: Our primary aim was to assess the impact of COVID-19 on health-related quality of life (HRQoL) 3 months after hospital discharge. Additionally, we screened for anxiety and depression and assessed important clinical outcomes. METHODS: This was a single-center cohort study performed in Sao Paulo (Brazil), in which participants were contacted by telephone to answer a short survey. EQ-5D-3L was used to assess HRQoL and clinical data from patients' index admission were retrieved from medical records. RESULTS: We contacted 251 participants (59.8% males, mean age 53 years old), 69.7% of which had presented with severe COVID-19. At 3 months of follow-up, 6 patients had died, 51 (20.3%) had visited the emergency department again and 17 (6.8%) had been readmitted to hospital. Seventy patients (27.9%) persisted with increased dyspnoea and 81 had a positive screening for anxiety/depression. Similarly, patients reported an overall worsening of EQ-5D-3L single summary index at 3 months compared to before the onset of COVID-19 symptoms (0.8012 (0.7368 - 1.0) vs. 1.0(0.7368 - 1.0), p < 0.001). This affected all 5 domains, but especially pain/discomfort and anxiety/depression. Only female sex and intensive care requirement were independently associated with worsening of HRQoL. CONCLUSION: Patients hospitalized for COVID-19 frequently face persistent clinical and mental health problems up to 3 months following hospital discharge, with significant impact on patients' HRQoL.

Influence of brain death and associated trauma on solid organ histological characteristics.

PURPOSE: To evaluate histopathological alterations triggered by brain death and associated trauma on different solid organs in rats. METHODS: Male Wistar rats (n=37) were anesthetized with isoflurane, intubated and mechanically ventilated. A trepanation was performed and a balloon catheter inserted into intracraninal cavity and rapidly inflated with saline to induce brain death. After induction, rats were monitored for 30, 180, and 360 min for hemodynamic parameters and exsanguinated from abdominal aorta. Heart, lung, liver, and kidney were removed and fixed in paraffin to evaluation of histological alterations (H&E). Sham-operated rats were trepanned only and used as control group. RESULTS: Brain dead rats showed a hemodynamic instability with hypertensive episode in the first minute after the induction followed by hypotension for approximately 1 h. Histological analyses showed that brain death induces vascular congestion in heart (p<0.05), and lung (p<0.05); lung alveolar edema (p=0.001), kidney tubular edema (p<0.05); and leukocyte infiltration in liver (p<0.05). CONCLUSIONS: Brain death induces hemodynamic instability associated with vascular changes in solid organs and compromises most severely the lungs. However, brain death associated trauma triggers important pathophysiological alterations in these organs.

Influence of brain death and associated trauma on solid organ histological characteristics / Influência da morte encefálica e do trauma associado nas características histológicas de órgãos sólidos

PURPOSE: To evaluate histopathological alterations triggered by brain death and associated trauma on different solid organs in rats. METHODS: Male Wistar rats (n=37) were anesthetized with isoflurane, intubated and mechanically ventilated. A trepanation was performed and a balloon catheter inserted into intracraninal cavity and rapidly inflated with saline to induce brain death. After induction, rats were monitored for 30, 180, and 360 min for hemodynamic parameters and exsanguinated from abdominal aorta. Heart, lung, liver, and kidney were removed and fixed in paraffin to evaluation of histological alterations (H&E). Sham-operated rats were trepanned only and used as control group. RESULTS: Brain dead rats showed a hemodynamic instability with hypertensive episode in the first minute after the induction followed by hypotension for approximately 1 h. Histological analyses showed that brain death induces vascular congestion in heart (p<0.05), and lung (p<0.05); lung alveolar edema (p=0.001), kidney tubular edema (p<0.05); and leukocyte infiltration in liver (p<0.05). CONCLUSIONS: Brain death induces hemodynamic instability associated with vascular changes in solid organs and compromises most severely the lungs. However, brain death associated trauma triggers important pathophysiological alterations in these organs.

OBJETIVO: Avaliar as alterações histopatológicas desencadeadas pela morte encefálica e pelo trauma associado em diferentes órgãos sólidos em ratos. MÉTODOS: Ratos Wistar machos (n=37) foram anestesiados com isoflurano, entubados e mecanicamente ventilados. Foi realizada trepanação e um cateter foi inserido na cavidade intracraniana e insuflado rapidamente para induzir morte encefálica. Após a indução, os ratos foram monitorados por 30, 180 e 360 min para parâmetros hemodinâmicos e exsanguinados pela aorta abdominal. Coração, pulmão, fígado e rim foram removidos e fixados em parafina para avaliação de alterações histológicas (H&E). Ratos falso-operados foram apenas trepanados e usados como grupo controle. RESULTADOS: Ratos com morte encefálica apresentaram instabilidade hemodinâmica com episódio hipertensivo no primeiro minuto após a indução seguido de hipotensão por aproximadamente 1 hora. Análises histológicas demonstraram que a morte encefálica induz congestão vascular no coração (p<0,05) e pulmão (p<0,05); edema alveolar (p=0,001); edema tubular (p<0,05); e infiltrado leucocitário no fígado (p<0,05). CONCLUSÕES: A morte encefálica induz instabilidade hemodinâmica associada com mudanças vasculares em órgãos sólidos e compromete mais severamente os pulmões. Contudo, o trauma associado à morte encefálica desencadeia importantes alterações fisiopatológicas naqueles órgãos.