![]() See Table 2 for systematic breakdown of lab markers and risk factors Progressive elevation of cardiac troponins, hepatic enzymes, and serum creatinine, along with advanced lymphocytopenia and increased neutrophils Laboratory markers and clinical indications of severe disease 16, 20, 22, 23 ![]() Less frequently involved: renal, endocrine, gastrointestinal, or integumentary Respiratory, cardiovascular, neurologic, MIS, hematological Respiratory, renal (AKI), hematological (thromboembolism) Systems commonly involved 16, 17, 19, 21 Sequelae mediated by hospitalization interventionsĬommon symptoms 3, 4, 5, 6, 7, 16, 17, 18, 19, 20įever, dry cough, and shortness of breath >50% of patientsįatigue, pneumonia, myalgias, headache, thromboembolic conditions, and MIS Inflammatory and metabolic changes to parenchyma, and supporting structures during initial infection Prolonged activation of type 1 interferons and endothelial cell damage lead to thromboembolic eventsĭecrease in lymphocytes may allow for viral particles to persist, resulting in excessive inflammation that can increase symptom severity and need for ICU admission Microvascular dysfunction via endothelial damageĭysregulation of the innate immune system with lymphopenia Immune-mediated dysregulation of RAAS pathway Pathophysiology 9, 10, 11, 12, 13, 14, 15ĭirect viral toxicity via ACE2/TMPRSS2 expressing cells (alveolar epithelial type II cells, heart, kidneys, gastrointestinal tract, lung tissue, and nasal olfactory cells) ![]() The presence of long-term effects presents another reason for vaccination against COVID-19. This review serves as a guideline for effective management based on current evidence, but clinicians should modify recommendations to reflect each patient's unique needs and the most up-to-date evidence. Interdisciplinary monitoring with holistic management that considers nutrition, physical therapy, psychological management, meditation, and mindfulness in addition to medication will allow for the early detection of post-acute COVID-19 sequelae symptoms and prevent long-term systemic damage. The preliminary evidence on the pulmonary, cardiovascular, neurological, hematological, multisystem inflammatory, renal, endocrine, gastrointestinal, and integumentary sequelae show that COVID-19 continues after acute infection. All studies discussed in this text are from adult populations unless specified (as with multisystem inflammatory syndrome in children). Only peer-reviewed studies in English published by Jwere considered for inclusion. A PubMed search was completed using variations on the term post-acute COVID-19. Recent literature on the long-term health consequences of COVID-19 discusses the need for a comprehensive understanding of the multisystemic pathophysiology, clinical predictors, and epidemiology to develop and inform an evidence-based, multidisciplinary management approach. Our understanding of COVID-19 is constantly progressing, giving better insight into the heterogeneous nature of its acute and long-term effects. From December 2019 to July 2021, this virus has infected nearly 200 million people and led to more than 4 million deaths. ![]() Coronavirus disease 2019 (COVID-19) is the third deadly coronavirus infection of the 21st century that has proven to be significantly more lethal than its predecessors, with the number of infected patients and deaths still increasing daily.
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