Long-Term Effects of COVID-19

Abstract

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. From December 2019 to July 2021, this virus has infected nearly 200 million people and led to more than 4 million deaths. Our understanding of COVID-19 is constantly progressing, giving better insight into the heterogeneous nature of its acute and long-term effects. 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. A PubMed search was completed using variations on the term post-acute COVID-19. Only peer-reviewed studies in English published by July 17, 2021 were considered for inclusion. All studies discussed in this text are from adult populations unless specified (as with multisystem inflammatory syndrome in children). 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. 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. 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. The presence of long-term effects presents another reason for vaccination against COVID-19.

Figure 1

Pathophysiology of pulmonary, cardiac, neurological, hematological, renal, gastrointestinal, integumentary, and endocrine effects of post-acute coronavirus disease 2019 and its subsequent clinical manifestations.^,,,,,, , , , , , , , , , , , , , , , BBB = blood brain barrier; ACE = angiotensin-converting enzyme; ACE2 = angiotensin-converting enzyme 2; AKI = acute kidney injury; APOL1 = apolipoprotein L1; COVID-19 = coronavirus disease 2019; DAMP = damage-associated molecular patterns; DKA = diabetic ketoacidosis; ECM = extracellular matrix; HIF-1 = hypoxia-inducible factor 1; HPA = hypothalamic-pituitary-adrenal; IL = interleukin; PAMP = pathogen-associated molecular pattern; PNS = peripheral nervous system; TGF = tumor growth factor; TMPSSR2 = type 2 transmembrane protein; TNF = tumor necrosis factor.

Figure 2

Multisystem inflammatory syndrome in children (MIS-C) by the numbers. Epidemiological images derived from the Centers for Disease Control and Prevention data on 4018 reported cases of MIS-C as of June 2, 2021. Disease classifications from 570 MIS-C case reports from March 2 to July 18, 2020. Percentages by race and ethnicity may exceed 100%. Multiple race identities could be selected. Race/ethnicity data were not reported for 276 of 4018 cases. Percentages of Asian, NH/OPI, and AI/NA were rounded up to 1%. AI = American Indian; ARDS = acute respiratory distress syndrome; NA = Native Alaskan; NH = Native Hawaiian; OPI = Other Pacific Islander; rt-PCR = real-time polymerase chain reaction; SOB = shortness of breath.