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J Rehabil Med Clin Commun ; 3: 1000044, 2020.
Article in English | MEDLINE | ID: covidwho-1197496


Platypnea-orthodeoxia syndrome, characterized by dyspnoea and arterial desaturation while upright, is a rare complication of acute respiratory distress syndrome. We report here 2 patients with COVID-19 pneumonia, who were diagnosed with platypnea-orthodeoxia syndrome during commencement of rehabilitation, 18 and 9 days respectively after admission to the intensive care unit. Both patients presented with normocapnic hypoxaemia. One patient required mechanical ventilation with supplemental oxygen during intensive care, while the other required high-flow nasal oxygen therapy. The manifestations of platypnea-orthodeoxia syndrome were most prominent during physiotherapy, when verticalization was attempted, and hindered further mobilization out of bed, including ambulation. This report describes the clinical manifestations of platypnea-orthodeoxia syndrome and the rehabilitative strategies carried out for these 2 patients. The platypnea-orthodeoxia syndrome in these patients resolved after 65 and 22 days respectively from the day of detection. This report highlights this potentially under-recognized phenomenon, which may be unmasked during rehabilitation of patients with COVID-19 pneumonia. Good functional outcomes were achieved with a combination of verticalization training with supplemental oxygen support, respiratory techniques training and progressive endurance and resistance training, whilst awaiting resolution of the platypneaorthodeoxia syndrome.

Lancet Respir Med ; 9(4): 360-372, 2021 04.
Article in English | MEDLINE | ID: covidwho-1045088


BACKGROUND: Mechanical ventilation in intensive care for 48 h or longer is associated with the acute respiratory distress syndrome (ARDS), which might be present at the time ventilatory support is instituted or develop afterwards, predominantly during the first 5 days. Survivors of prolonged mechanical ventilation and ARDS are at risk of considerably impaired physical function that can persist for years. An early pathogenic mechanism of lung injury in mechanically ventilated, critically ill patients is inflammation-induced pulmonary fibrin deposition, leading to thrombosis of the microvasculature and hyaline membrane formation in the air sacs. The main aim of this study was to determine if nebulised heparin, which targets fibrin deposition, would limit lung injury and thereby accelerate recovery of physical function in patients with or at risk of ARDS. METHODS: The Can Heparin Administration Reduce Lung Injury (CHARLI) study was an investigator-initiated, multicentre, double-blind, randomised phase 3 trial across nine hospitals in Australia. Adult intensive care patients on invasive ventilation, with impaired oxygenation defined by a PaO2/FiO2 ratio of less than 300, and with the expectation of invasive ventilation beyond the next calendar day were recruited. Key exclusion criteria were heparin allergy, pulmonary bleeding, and platelet count less than 50 X 109/L. Patients were randomly assigned 1:1, with stratification by site and using blocks of variable size and random seed, via a web-based system, to either unfractionated heparin sodium 25 000 IU in 5 mL or identical placebo (sodium chloride 0·9% 5 mL), administered using a vibrating mesh membrane nebuliser every 6 h to day 10 while invasively ventilated. Patients, clinicians, and investigators were masked to treatment allocation. The primary outcome was the Short Form 36 Health Survey Physical Function Score (out of 100) of survivors at day 60. Prespecified secondary outcomes, which are exploratory, included development of ARDS to day 5 among at-risk patients, deterioration of the Murray Lung Injury Score (MLIS) to day 5, mortality at day 60, residence of survivors at day 60, and serious adverse events. Analyses followed the intention-to-treat principle. There was no imputation of missing data. The trial is registered with the Australian and New Zealand Clinical Trials Register, number ACTRN12612000418875 . FINDINGS: Between Sept 4, 2012, and Aug 23, 2018, 256 patients were randomised. Final follow-up was on Feb 25, 2019. We excluded three patients who revoked consent and one ineligible participant who received no intervention. Of 252 patients included in data analysis, the mean age was 58 years (SD 15), 157 (62%) were men, and 118 (47%) had ARDS. 128 (51%) patients were assigned to the heparin group and 124 (49%) to the placebo group, all of whom received their assigned intervention. Survivors in the heparin group (n=97) had similar SF-36 Physical Function Scores at day 60 compared to the placebo group (n=94; mean 53·6 [SD 31·6] vs 48·7 [35·7]; difference 4·9 [95% CI -4·8 to 14·5]; p=0·32). Compared with the placebo group, the heparin group had fewer cases of ARDS develop to day 5 among the at-risk patients (nine [15%] of 62 patients vs 21 [30%] of 71 patients; hazard ratio 0·46 [95% CI 0·22 to 0·98]; p=0·0431), less deterioration of the MLIS to day 5 (difference -0·14 [-0·26 to -0·02]; p=0·0215), similar day 60 mortality (23 [18%] of 127 patients vs 18 [15%] of 123 patients; odds ratio [OR] 1·29 [95% CI 0·66 to 2·53]; p=0·46), and more day 60 survivors at home (86 [87%] of 99 patients vs 73 [73%] of 100 patients; OR 2·45 [1·18 to 5·08]; p=0·0165). A similar number of serious adverse events occurred in each group (seven [5%] of 128 patients in the heparin group vs three [2%] of 124 patients in the placebo group; OR 2·33 [0·59 to 9·24]; p=0·23), which were a transient increase in airway pressure during nebulisation (n=3 in the heparin group), major non-pulmonary bleeding (n=2 in each group), haemoptysis (n=1 in the heparin group), tracheotomy site bleeding (n=1 in the heparin group), and hypoxaemia during nebulisation (n=1 in the placebo group). INTERPRETATION: In patients with or at risk of ARDS, nebulised heparin did not improve self-reported performance of daily physical activities, but was well tolerated and exploratory outcomes suggest less progression of lung injury and earlier return home. Further research is justified to establish if nebulised heparin accelerates recovery in those who have or are at risk of ARDS. FUNDING: Rowe Family Foundation, TR and RB Ditchfield Medical Research Endowment Fund, Patricia Madigan Charitable Trust, and The J and R McGauran Trust Fund.

Critical Care/methods , Heparin/administration & dosage , Respiration, Artificial/adverse effects , Respiratory Distress Syndrome/epidemiology , Activities of Daily Living , Administration, Inhalation , Adult , Aged , Australia/epidemiology , Double-Blind Method , Female , Hemoptysis/chemically induced , Hemoptysis/epidemiology , Heparin/adverse effects , Hospital Mortality , Humans , Hypoxia/chemically induced , Hypoxia/epidemiology , Incidence , Male , Middle Aged , Nebulizers and Vaporizers , Placebos/administration & dosage , Placebos/adverse effects , Respiratory Distress Syndrome/diagnosis , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/prevention & control , Self Report/statistics & numerical data , Severity of Illness Index , Survivors/statistics & numerical data , Time Factors , Treatment Outcome
Nutrients ; 12(12)2020 Dec 07.
Article in English | MEDLINE | ID: covidwho-967092


There are limited proven therapies for COVID-19. Vitamin C's antioxidant, anti-inflammatory and immunomodulating effects make it a potential therapeutic candidate, both for the prevention and amelioration of COVID-19 infection, and as an adjunctive therapy in the critical care of COVID-19. This literature review focuses on vitamin C deficiency in respiratory infections, including COVID-19, and the mechanisms of action in infectious disease, including support of the stress response, its role in preventing and treating colds and pneumonia, and its role in treating sepsis and COVID-19. The evidence to date indicates that oral vitamin C (2-8 g/day) may reduce the incidence and duration of respiratory infections and intravenous vitamin C (6-24 g/day) has been shown to reduce mortality, intensive care unit (ICU) and hospital stays, and time on mechanical ventilation for severe respiratory infections. Further trials are urgently warranted. Given the favourable safety profile and low cost of vitamin C, and the frequency of vitamin C deficiency in respiratory infections, it may be worthwhile testing patients' vitamin C status and treating them accordingly with intravenous administration within ICUs and oral administration in hospitalised persons with COVID-19.

Ascorbic Acid Deficiency/drug therapy , Ascorbic Acid/therapeutic use , COVID-19/drug therapy , Respiratory Tract Infections/drug therapy , Sepsis/drug therapy , Vitamins/therapeutic use , Administration, Intravenous , Administration, Oral , Anti-Inflammatory Agents/therapeutic use , Ascorbic Acid Deficiency/complications , COVID-19/complications , COVID-19/virology , Chemotherapy, Adjuvant , Critical Care , Hospitalization , Humans , Immunologic Factors/therapeutic use , Intensive Care Units , Nutritional Status , Pandemics , Respiration, Artificial , Respiratory Tract Infections/etiology , Respiratory Tract Infections/virology , SARS-CoV-2 , Sepsis/etiology , Sepsis/virology