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Bali Journal of Anesthesiology ; 6(2):125-126, 2022.
Article in English | EMBASE | ID: covidwho-20244660
Bali Journal of Anesthesiology ; 5(4):282-283, 2021.
Article in English | EMBASE | ID: covidwho-20244029
Bali Journal of Anesthesiology ; 6(4):201-209, 2022.
Article in English | Scopus | ID: covidwho-2201686


Hundreds of surgeries are postponed every day during the global COVID -19 pandemic. The hospital and clinicians are in dilemma scheduling elective procedures during the pandemic. The current study was designed to evaluate postoperative pulmonary complications and mortality in COVID-19 patients in a systematic review and meta-analysis of globally published peer-reviewed literatures. A systematic literature search was conducted using the selection criteria in five databases. A quality assessment was made with a validated Newcastle-Ottawa Scale. The meta-analysis worked as a generic inverse variance meta-analysis. A total of 308 articles were identified from different databases and 5 articles with a total 1408 participants were selected for evaluation after successive screenings. The meta-analysis revealed a high global rate of postoperative mortality among COVID-19 patients, as high as 23% (95% CI: 15 to 26), and high postoperative pulmonary complications including pneumonia and acute respiratory distress syndrome. The 30-days mortality rate and prevalence of pulmonary complications were high. There was one death for every five COVID-19 patients undergoing surgical procedures, indicating the need for mitigating strategies to decrease perioperative mortality, transmission to healthcare workers, and non-COVID-19 patients. Larger samples and/or multicenter trials are needed to explore the perioperative mortality dan morbidity rate of patients with COVID-19 undergoing surgeries, and in particular, factors with the highest impact on perioperative mortality. There should be a clinical guideline to determine when to operate or not to operate on patients with COVID-19 for elective and emergency surgeries. © 2022 National Journal of Clinical Anatomy ;Published by Wolters Kluwer - Medknow.

Critical Care and Shock ; 25(3):129-134, 2022.
Article in English | EMBASE | ID: covidwho-1912935


Due to its expression by macrophages, galectin-3 is among the most recently studied biomarkers. It is likely involved in the inflammatory process that leads to remodeling and eventually fibrosis of organs such as the heart, brain, and kidneys. Coronavirus disease 19 (COVID-19) infection causes excessive inflammatory reactions in the whole body, playing a role in the development of fibrosis due to the activation of the galectin-3-macrophage-fibroblast axis. Heart failure or cardiac dysfunction occurred not only due to pro-inflammatory activation but also due to the overactivation of sympathetic nerves and failure of the respiratory system. The latter increases. the possibility of direct infection or necrosis of the heart due to the heart-lung interaction observed in our pilot study. Forty-five intensive care unit (ICU) patients were recruited consecu-tively in this study to be observed their galectin-3 and troponin I levels. This pilot study demonstrates the correlation between galectin-3 as a proinflammatory biomark-er and troponin I as a definitive biomarker for direct heart injury and highlights its potential use in COVID-19 patients. With the assessment of appropriate biomarkers such as cardiac fibro-sis markers, possible worsening of cardiac conditions in COVID-19 patients treated in the ICU can be detected in its early stages.

Bali Journal of Anesthesiology ; 6(2):125-126, 2022.
Article in English | Scopus | ID: covidwho-1893099
Bali Journal of Anesthesiology ; 4(4):152-155, 2020.
Article in English | Scopus | ID: covidwho-1471079


Coronaviruses have caused several global challenges for health-care providers all over the world. The notorious SARS-CoV-2 could attack the lower respiratory tract and trigger the immune systems to release massive number of immune cells and pro-inflammatory cytokines and cause immunopathology consequences called cytokine release syndrome. These pro-inflammatory cytokines and other immune cells caused lung injury and severe acute respiratory distress syndrome in COVID-19 (CARDS) and multiple organ failure. There are still many intertwined immune responses that not yet been discovered in SARS-CoV-2 infections. Targeted and specific cell therapy would be reasonable and considered safer to be employed in patients who present with comorbidities and at risk of complications. © 2020 Bali Journal of Anesthesiology ;Published by Wolters Kluwer-Medknow.

Bali Journal of Anesthesiology ; 5(3):219-220, 2021.
Article in English | Scopus | ID: covidwho-1471064
Bali Journal of Anesthesiology ; 5(3):208-211, 2021.
Article in English | Scopus | ID: covidwho-1471063


Mortality rate in COVID-19 is mainly contributed to respiratory failure caused by intractable acute respiratory distress syndrome (ARDS). However, the direct cause could be caused by diffusion failure or probably pulmonary embolism. Increased central venous pressure (CVP) will ensue in higher pulmonary vascular resistance and in turn would increase pulmonary arterial pressure. Coagulopathy is a common feature of severe acute respiratory syndrome coronavirus 2 infection, and an increase in D-dimer is the most common finding. These factors lead to thrombosis and finally embolism. We observed 14 intensive care unit-admitted COVID-19 patients suffered from CARDS from March to May 2020. We measured their CVP and D-dimer values and pulmonary embolism severity index (PESI) scores to search for possible associations. Only CVP and PESI scores were statistically significant between those three parameters (P < 0.005). Lack of regular D-dimer samples and measurements due to limited resources could be one of potential causes, which contributes to the insignificant value. Further investigations with larger samples should be advised. © 2020 Bali Journal of Anesthesiology ;Published by Wolters Kluwer-Medknow.

Nephrology ; 25(SUPPL 4):31-32, 2020.
Article in English | EMBASE | ID: covidwho-1093771


Background: Several regiments have been proposed to overcome COVID-19 pandemic in our developing country. Many are still in trials, while some of them could not be run due to limited resources. Our proposed sensible management consists of combining low PEEP (less than 15cmH2O) and negative fluid balance by maintaining low CVP 0-4cmH2O. This will reduce risk of overload, congestive kidney failure and eventually acute kidney injury (AKI). Objectives: We would like to reduce outcome of AKI of COVID-19 ICU survivors by titrating low PEEP and implementing negative fluid balance by maintaining low CVP with continuous furosemide titrated dose. Methods: We titrated daily PEEP, CVP, fluid balance, and creatinine clearance of admitted critically ill COVID-19 survivors to evaluate optimum PEEP, CVP, safe range of fluid balance and creatinine clearance. We also maintained low CVP with continuous furosemide between 2-10 mg/kg/hour. Results: Daily observations of our three survivors resulted in values which considered low but still preserve lung and kidney function. As we may see below (Figure 1), patient A, B, and C were maintained in low PEEP ranges from 7-12cmH2O, less than 15cmH2O to maintain adequate driving pressure and dynamic compliance. They were also targeted in low CVP 0-4cmH2O (Figure 2) (highest peak was in patient C with 12, but soon decreased with diuretics). Cumulative balance was widely ranged, mainly targeted to negative values, in accordance with patient's condition and creatinine clearance. Negative balance did not aggravate kidney function, otherwise it helped to reduce congestive kidney caused by pre-ICU overload and inflammatory process in COVID-19 (Figure 3&4). Conclusions: To ensure highest critical care for patients at this time of uncertain therapeutic agents, we would rather optimize basic principles of filtration target organs such lung and kidney by using low PEEP and implementing negative fluid balance.