https://www.medrxiv.org/content/10.1101 ... 20248903v1At 6-month follow-up after hospitalisation due to COVID-19 disease, patients displayed a wide array of neurological symptoms, being fatigue (34%), memory/attention (31%), and sleep disorders (30%) the most frequent. Subjects reporting neurological symptoms were affected by more severe respiratory SARS-CoV-2 infection parameters during hospitalisation. At neurological examination, 37.4% of patients exhibited neurological abnormalities, being cognitive deficits (17.5%), hyposmia (15.7%) and postural tremor (13.8%) the most common. Patients with cognitive deficits at follow-up were comparable for age, sex and pre-admission comorbidities but experienced worse respiratory SARS-CoV-2 infection disease and longer hospitalisation. Conclusions: long term neurological manifestations after hospitalization due to COVID-19 infection affects one third of survivors. Multiple neurological abnormalities including mild cognitive impairment are associated with severity of respiratory SARS-CoV-2 infection.
Covid-19 discussion, bring your own statistics
Postacute COVID-19: An Overview and Approach to Classification
https://academic.oup.com/ofid/article/7 ... 09/5934556
https://academic.oup.com/ofid/article/7 ... 09/5934556
How COVID-19 Attacks The Brain And May Cause Lasting Damage
https://www.npr.org/sections/health-sho ... ing-damage
https://www.npr.org/sections/health-sho ... ing-damage
https://www.thelancet.com/journals/lanc ... 8/fulltext6-month consequences of COVID-19 in patients discharged from hospital: a cohort study
At 6 months after acute infection, COVID-19 survivors were mainly troubled with fatigue or muscle weakness, sleep difficulties, and anxiety or depression. Patients who were more severely ill during their hospital stay had more severe impaired pulmonary diffusion capacities and abnormal chest imaging manifestations, and are the main target population for intervention of long-term recovery.
Article summarizes likely long-term effects of Covid on the brain and central nervous system: https://alz-journals.onlinelibrary.wile ... /alz.12255
https://www.medrxiv.org/content/10.1101 ... 1.full.pdfAbstract
Objectives: The epidemiology of post-COVID syndrome (PCS) is currently undefined. We quantified rates of organ-specific impairment following recovery from COVID-19 hospitalisation compared with those in a matched control group, and how the rate ratio (RR) varies by age, sex, and ethnicity.
Design: Observational, retrospective, matched cohort study.
Setting: NHS hospitals in England.
Participants: 47,780 individuals (mean age 65 years, 55% male) in hospital with COVID-19 and discharged alive by 31 August 2020, matched to controls on demographic and clinical characteristics.
Outcome measures: Rates of hospital readmission, all-cause mortality, and diagnoses of respiratory, cardiovascular, metabolic, kidney and liver diseases until 30 September 2020.
Results: Mean follow-up time was 140 days for COVID-19 cases and 153 days for controls. 766 (95% confidence interval: 753 to 779) readmissions and 320 (312 to 328) deaths per 1,000 person- years were observed in COVID-19 cases, 3.5 (3.4 to 3.6) and 7.7 (7.2 to 8.3) times greater, respectively, than in controls. Rates of respiratory, diabetes and cardiovascular events were also significantly elevated in COVID-19 cases, at 770 (758 to 783), 127 (122 to 132) and 126 (121 to 131) events per 1,000 person-years, respectively. RRs were greater for individuals aged <70 than ≥70 years, and in ethnic minority groups than the White population, with the biggest differences observed for respiratory disease: 10.5 [9.7 to 11.4] for <70 years versus 4.6 [4.3 to 4.8] for ≥70 years, and 11.4 (9.8 to 13.3) for Non-White versus 5.2 (5.0 to 5.5) for White.
Conclusions: Individuals discharged from hospital following COVID-19 face elevated rates of multi- organ dysfunction compared with background levels, and the increase in risk is neither confined to the elderly nor uniform across ethnicities. The diagnosis, treatment and prevention of PCS require integrated rather than organ- or disease-specific approaches. Urgent research is required to establish risk factors for PCS.
Regarding the above 313614 people have been admitted to hospital in the UK already. It seems like there may be circa 100 000 people with chronic long term conditions that have required another stay in hospital. I expect that there will be many more who are affected but didn’t need to go to hospital.
https://www.medrxiv.org/content/10.1101 ... 21249950v1Abstract
Neurologicaland psychiatric sequelae of COVID-19 have been reported, butthere are limited data on incidence rates and relative risks.
Using retrospective cohort studies and time-to-event analysis, we estimated the incidence of ICD-10 diagnosesin the 6 months after a confirmed diagnosis of COVID-19: intracranial haemorrhage;ischaemic stroke;Parkinsonism;Guillain-Barré syndrome;nerve/nerve root/plexus disorders;myoneural/muscle disease;encephalitis;dementia;mood, anxiety, and psychotic disorders;substance misuse;and insomnia. Data were obtained from the TriNetX electronic health records network (over 81 million patients). We compared incidences with those in propensityscore-matched cohorts of patients with influenza or other respiratory infections using a Cox model. We investigated the effect on incidence estimates of COVID-19 severity, as proxied by hospitalization and encephalopathy (including delirium and related disorders).
236,379 patients survived a confirmed diagnosis of COVID-19. Among them, the estimatedincidence of neurologicalor psychiatric sequelae at 6 months was 33.6%, with 12.8% receiving their first such diagnosis.Most diagnostic categorieswere commoner after COVID-19 than afterinfluenza or other respiratory infections(hazard ratios from 1.21 to 5.28), including stroke, intracranial haemorrhage, dementia, and psychotic disorders.Findings were equivocal for Parkinsonism and Guillain-Barré syndrome. Amongst COVID-19 cases, incidences and hazard ratios for most disorders were higher in patients who had been hospitalized,and markedly so in those who had experienced encephalopathy. Results were robust to sensitivity analyses, including comparisons against an additional four index health events.
The study provides evidence for substantial neurologicaland psychiatric morbidityfollowing COVID-19infection.Risks were greatest in, but not limited to,those who had severe COVID-19. The information can help in service planning and identification of research priorities.
https://www.medrxiv.org/content/10.1101 ... 21251619v1Results Six months after the infection, 67% of the study participants reported at least one symptom as a consequence of COVID-19. Exertional dyspnea (30% of participants), fatigue (25%) and diminished sense of taste/smell (19%) were the most common individual symptoms. At least one symptom, exertional dyspnea, and fatigue were reported more often after a severe acute illness, but diminished sense of taste/smell was unrelated to acute severity. Age group and sex did not associate with the frequency of symptoms at 6 months. Conclusions Based on this study, the prevalence of COVID-19-related symptoms 6 months after the infection is high. Some bias for overestimation may have affected this result. Nevertheless, ′long COVID′ requires attention in medical care and a better scientific understanding.
https://jamanetwork.com/journals/jama/f ... o.linkedin
Although direct infection like this can occur, many experts now believe that systemic inflammation originating from the infected lungs or blood vessels, not myocyte infection, explains most myocardial injury findings among patients hospitalized with COVID-19. Immune cell messengers called cytokines circulating through the body could induce heart muscle inflammation. Systemic inflammation could also trigger arrhythmias and destabilize coronary plaques, leading to plaque rupture and type 1 myocardial infarction (MI), or heart attack—the most common cause of elevated troponins.
A recent study involving Rhesus macaques supports the role of systemic inflammation. Researchers at Emory University led by cardiologist Rebecca Levit, MD, discovered more scar tissue in the hearts of monkeys they infected with SARS-CoV-2 two weeks prior than in an uninfected control group. Yet they detected no virus or white blood cells in the infected monkeys’ hearts.
“We hypothesize that support cells in the heart, fibroblast, may be responding to the systemic inflammation,” Levit said in an email. “The activation of these cells may lead to fibrosis.”
Additionally, several other COVID-19 manifestations could injure the heart muscle, including an oxygen supply-and-demand imbalance in the heart (type 2 MI), blood clots, sepsis, stress-induced cardiomyopathy, and multisystem inflammatory syndrome. Troponin levels could also represent COVID-19 severity because a critical illness can hasten preexisting cardiovascular disease.
Sorting out the source of myocardial injury could steer treatments to safeguard the heart. Going forward, novel research tools like stem cell–derived cardiovascular cells will be used to model how SARS-CoV-2 infection causes cardiac damage. Researchers have begun to infect these lab-grown cells to understand the precise mechanisms of heart cell injury.
https://jamanetwork.com/journals/jamane ... le/2776560
In this cohort of individuals with COVID-19 who were followed up for as long as 9 months after illness, approximately 30% reported persistent symptoms. A unique aspect of our cohort is the high proportion of outpatients with mild disease. Persistent symptoms were reported by one-third of outpatients in our study, consistent with a previously reported study,4 in which 36% of outpatients had not returned to baseline health by 14 to 21 days following infection. However, this has not been previously described 9 months after infection.
Consistent with existing literature, fatigue was the most commonly reported symptom.2-4 This occurred in 14% of individuals in this study, lower than the 53% to 71%2-4 reported in cohorts of hospitalized patients, likely reflecting the lower acuity of illness in our cohort. Furthermore, impairment in HRQoL has previously been reported among hospitalized patients who have recovered from COVID-19; we found 29% of outpatients reported worsened HRQoL.5
Notably, 14 participants, including 9 nonhospitalized individuals, reported negative impacts on ADLs after infection. With 57.8 million cases worldwide, even a small incidence of long-term debility could have enormous health and economic consequences.6
Study limitations include a small sample size, single study location, potential bias from self-reported symptoms during illness episode, and loss to follow-up of 57 participants. To our knowledge, this study presents the longest follow-up symptom assessment after COVID-19 infection. Our research indicates that the health consequences of COVID-19 extend far beyond acute infection, even among those who experience mild illness. Comprehensive long-term investigation will be necessary to fully understand the impact of this evolving viral pathogen.
https://www.thelancet.com/journals/lanr ... 0/fulltext
Delayed-onset myocarditis following COVID-19
A multisystem inflammatory syndrome occurring several weeks after SARS-CoV-2 infection and that can include severe acute heart failure has been reported in children (MIS-C).1, 2 In adults with acute severe heart failure, we have identified a similar syndrome (MIS-A) and describe presenting characteristics, diagnostic features, and early outcomes. Our data also complement reports of MIS-A.3
https://www.medrxiv.org/content/10.1101 ... 21252329v1Long COVID neuropsychological deficits after severe, moderate or mild infection
Background: There is growing awareness that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can include long-term neuropsychological deficits, even in its mild or moderate respiratory forms. Methods: Standardized neuropsychological, psychiatric, neurological and olfactory tests were administered to 45 patients (categorized according to the severity of their respiratory symptoms during the acute phase) 236.51 (SD: 22.54) days post-discharge following SARS-CoV-2 infection. Results: Deficits were found in all the domains of cognition and the prevalence of psychiatric symptoms was also high in the three groups. The severe performed more poorly on long-term episodic memory and exhibited greater anosognosia. The moderate had poorer emotion recognition, which was positively correlated with persistent olfactory dysfunction. The mild were more stressed, anxious and depressed. Conclusion: The data support the hypothesis that the virus targets the central nervous system (and notably the limbic system), and support the notion of different neuropsychological phenotypes.