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1.
Nat Med ; 28(6): 1141-1148, 2022 06.
Article in English | MEDLINE | ID: covidwho-1900513

ABSTRACT

Research and practice in critical care medicine have long been defined by syndromes, which, despite being clinically recognizable entities, are, in fact, loose amalgams of heterogeneous states that may respond differently to therapy. Mounting translational evidence-supported by research on respiratory failure due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection-suggests that the current syndrome-based framework of critical illness should be reconsidered. Here we discuss recent findings from basic science and clinical research in critical care and explore how these might inform a new conceptual model of critical illness. De-emphasizing syndromes, we focus on the underlying biological changes that underpin critical illness states and that may be amenable to treatment. We hypothesize that such an approach will accelerate critical care research, leading to a richer understanding of the pathobiology of critical illness and of the key determinants of patient outcomes. This, in turn, will support the design of more effective clinical trials and inform a more precise and more effective practice at the bedside.


Subject(s)
COVID-19 , SARS-CoV-2 , Critical Care , Critical Illness , Humans , Syndrome
2.
Crit Care Clin ; 38(3): 473-489, 2022 Jul.
Article in English | MEDLINE | ID: covidwho-1878083

ABSTRACT

Initial reporting suggested that kidney involvement following COVID-19 infection was uncommon but this is now known not to be the case. Acute kidney injury (AKI) may arise through several mechanisms and complicate up to a quarter of patients hospitalized with COVID-19 infection being associated with an increased risk for both morbidity and death. Mechanisms of injury include direct kidney damage predominantly through tubular injury, although glomerular injury has been reported; the consequences of the treatment of patients with severe hypoxic respiratory failure; secondary infection; and exposure to nephrotoxic drugs. The mainstay of treatment remains the prevention of worsening kidney damage and in some cases they need for renal replacement therapies (RRT). Although the use of other blood purification techniques has been proposed as potential treatments, results to-date have not been definitive.


Subject(s)
Acute Kidney Injury , COVID-19 , Acute Kidney Injury/etiology , Acute Kidney Injury/therapy , COVID-19/complications , COVID-19/therapy , Humans , Renal Replacement Therapy , SARS-CoV-2
3.
Lancet Diabetes Endocrinol ; 10(2): 97-98, 2022 02.
Article in English | MEDLINE | ID: covidwho-1569157
4.
Blood Purif ; 51(1): 47-54, 2022.
Article in English | MEDLINE | ID: covidwho-1186414

ABSTRACT

INTRODUCTION: Uncontrolled systemic inflammation may occur in severe coronavirus disease 19 (COVID-19). We have previously shown that endotoxemia, presumably from the gut, may complicate COVID-19. However, the role of endotoxin adsorbent (EA) therapy to mitigate organ dysfunction in COVID-19 has not been explored. METHODS: We conducted a retrospective observational study in COVID-19 patients who received EA therapy at the King Chulalongkorn Memorial Hospital, Bangkok, Thailand, between March 13 and April 17, 2020. Relevant clinical and laboratory data were collected by inpatient chart review. RESULTS: Among 147 hospitalized COVID-19 patients, 6 patients received EA therapy. All of the 6 patients had severe COVID-19 infection with acute respiratory distress syndrome (ARDS). Among these, 5 of them were mechanically ventilated and 4 had complications of secondary bacterial infection. The endotoxin activity assay (EAA) results of pre-EA therapy ranged from 0.47 to 2.79. The choices of EA therapy were at the discretion of attending physicians. One patient was treated with oXiris® along with continuous renal replacement therapy, and the others received polymyxin B hemoperfusion sessions. All patients have survived and were finally free from the mechanical ventilation as well as had improvement in PaO2/FiO2 ratio and decreased EAA level after EA therapy. CONCLUSIONS: We demonstrated the clinical improvement of severe COVID-19 patients with elevated EAA level upon receiving EA therapy. However, the benefit of EA therapy in COVID-19 ARDS is still unclear and needs to be elucidated with randomized controlled study.


Subject(s)
COVID-19/therapy , Endotoxemia/therapy , Hemoperfusion/methods , SARS-CoV-2 , Acute Kidney Injury/etiology , Acute Kidney Injury/therapy , Adsorption , COVID-19/complications , Critical Care/methods , Endotoxemia/etiology , Female , Heparin/administration & dosage , Humans , Male , Membranes, Artificial , Middle Aged , Polymyxin B/administration & dosage , Renal Replacement Therapy , Respiratory Distress Syndrome/etiology , Retrospective Studies , Treatment Outcome
5.
Nephrol Dial Transplant ; 35(10): 1652-1662, 2020 10 01.
Article in English | MEDLINE | ID: covidwho-1059488

ABSTRACT

As of 15 August 2020, Coronavirus disease 2019 (COVID-19) has been reported in >21 million people world-wide and is responsible for more than 750,000 deaths. The occurrence of acute kidney injury (AKI) in patients hospitalized with COVID-19 has been reported to be as high as 43%. This is comparable to AKI in other forms of pneumonia requiring hospitalization, as well as in non-infectious conditions like cardiac surgery. The impact of AKI on COVID-19 outcomes is difficult to assess at present but, similar to other forms of sepsis, AKI is strongly associated with hospital mortality. Indeed, mortality is reported to be very low in COVID-19 patients without AKI. Given that AKI contributes to fluid and acid-base imbalances, compromises immune response and may impair resolution of inflammation, it seems likely that AKI contributes to mortality in these patients. The pathophysiologic mechanisms of AKI in COVID-19 are thought to be multifactorial including systemic immune and inflammatory responses induced by viral infection, systemic tissue hypoxia, reduced renal perfusion, endothelial damage and direct epithelial infection with Severe Acute Respiratory Syndrome Coronavirus 2. Mitochondria play a central role in the metabolic deregulation in the adaptive response to the systemic inflammation and are also found to be vital in response to both direct viral damage and tissue reperfusion. These stress conditions are associated with increased glycolysis and reduced fatty acid oxidation. Thus, there is a strong rationale to target AKI for therapy in COVID-19. Furthermore, many approaches that have been developed for other etiologies of AKI such as sepsis, inflammation and ischemia-reperfusion, have relevance in the treatment of COVID-19 AKI and could be rapidly pivoted to this new disease.


Subject(s)
Acute Kidney Injury/etiology , Betacoronavirus , Coronavirus Infections/complications , Glomerular Filtration Rate/physiology , Kidney/physiopathology , Pandemics , Pneumonia, Viral/complications , Acute Kidney Injury/physiopathology , COVID-19 , Coronavirus Infections/epidemiology , Humans , Pneumonia, Viral/epidemiology , SARS-CoV-2
6.
Kidney Int ; 98(6): 1370-1372, 2020 12.
Article in English | MEDLINE | ID: covidwho-1023693
7.
Intensive Care Med Exp ; 8(1): 72, 2020 Dec 07.
Article in English | MEDLINE | ID: covidwho-962367

ABSTRACT

BACKGROUND: When severe, COVID-19 shares many clinical features with bacterial sepsis. Yet, secondary bacterial infection is uncommon. However, as epithelium is injured and barrier function is lost, bacterial products entering the circulation might contribute to the pathophysiology of COVID-19. METHODS: We studied 19 adults, severely ill patients with COVID-19 infection, who were admitted to King Chulalongkorn Memorial Hospital, Bangkok, Thailand, between 13th March and 17th April 2020. Blood samples on days 1, 3, and 7 of enrollment were analyzed for endotoxin activity assay (EAA), (1 → 3)-ß-D-glucan (BG), and 16S rRNA gene sequencing to determine the circulating bacteriome. RESULTS: Of the 19 patients, 13 were in intensive care and 10 patients received mechanical ventilation. We found 8 patients with high EAA (≥ 0.6) and about half of the patients had high serum BG levels which tended to be higher in later in the illness. Although only 1 patient had a positive blood culture, 18 of 19 patients were positive for 16S rRNA gene amplification. Proteobacteria was the most abundant phylum. The diversity of bacterial genera was decreased overtime. CONCLUSIONS: Bacterial DNA and toxins were discovered in virtually all severely ill COVID-19 pneumonia patients. This raises a previously unrecognized concern for significant contribution of bacterial products in the pathogenesis of this disease.

9.
Nat Rev Nephrol ; 16(12): 747-764, 2020 12.
Article in English | MEDLINE | ID: covidwho-872710

ABSTRACT

Kidney involvement in patients with coronavirus disease 2019 (COVID-19) is common, and can range from the presence of proteinuria and haematuria to acute kidney injury (AKI) requiring renal replacement therapy (RRT; also known as kidney replacement therapy). COVID-19-associated AKI (COVID-19 AKI) is associated with high mortality and serves as an independent risk factor for all-cause in-hospital death in patients with COVID-19. The pathophysiology and mechanisms of AKI in patients with COVID-19 have not been fully elucidated and seem to be multifactorial, in keeping with the pathophysiology of AKI in other patients who are critically ill. Little is known about the prevention and management of COVID-19 AKI. The emergence of regional 'surges' in COVID-19 cases can limit hospital resources, including dialysis availability and supplies; thus, careful daily assessment of available resources is needed. In this Consensus Statement, the Acute Disease Quality Initiative provides recommendations for the diagnosis, prevention and management of COVID-19 AKI based on current literature. We also make recommendations for areas of future research, which are aimed at improving understanding of the underlying processes and improving outcomes for patients with COVID-19 AKI.


Subject(s)
Acute Kidney Injury/therapy , Acute Kidney Injury/virology , COVID-19/complications , COVID-19/therapy , Renal Replacement Therapy/methods , Acute Kidney Injury/diagnosis , Acute Kidney Injury/pathology , Anticoagulants/therapeutic use , Consensus , Humans , Risk Factors , SARS-CoV-2
11.
Blood Purif ; 50(1): 17-27, 2021.
Article in English | MEDLINE | ID: covidwho-381787

ABSTRACT

Critically ill COVID-19 patients are generally admitted to the ICU for respiratory insufficiency which can evolve into a multiple-organ dysfunction syndrome requiring extracorporeal organ support. Ongoing advances in technology and science and progress in information technology support the development of integrated multi-organ support platforms for personalized treatment according to the changing needs of the patient. Based on pathophysiological derangements observed in COVID-19 patients, a rationale emerges for sequential extracorporeal therapies designed to remove inflammatory mediators and support different organ systems. In the absence of vaccines or direct therapy for COVID-19, extracorporeal therapies could represent an option to prevent organ failure and improve survival. The enormous demand in care for COVID-19 patients requires an immediate response from the scientific community. Thus, a detailed review of the available technology is provided by experts followed by a series of recommendation based on current experience and opinions, while waiting for generation of robust evidence from trials.


Subject(s)
COVID-19/therapy , Continuous Renal Replacement Therapy/methods , Critical Illness/therapy , Extracorporeal Membrane Oxygenation/methods , Hemoperfusion/methods , Multiple Organ Failure/therapy , COVID-19/blood , COVID-19/complications , Continuous Renal Replacement Therapy/instrumentation , Critical Illness/epidemiology , Cytokines/blood , Cytokines/isolation & purification , Equipment Design , Extracorporeal Membrane Oxygenation/instrumentation , Hemoperfusion/instrumentation , Humans , Multiple Organ Failure/blood , Multiple Organ Failure/etiology
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