Umeå University's logo

Purpose: COVID-19 has been extensively researched; however, the lack of standardized COVID-19 severity categorization in register-based research complicates comparison of studies. The WHO COVID-19 Clinical Progression Scale is a standardized disease severity tool for clinical data, though not adapted to data available in health registries. We aimed to develop and validate such a novel categorization with international applicability.

Methods: The WHO Clinical Progression Scale was translated to a severity index utilizing ICD-and procedure-codes from outpatient, inpatient, intensive care, and mortality registries using the adult Swedish population and SARS-CoV-2 positive-test data (January 2020 – July 2022). Cox proportional hazards were applied to determine whether increasing severity correlates with mortality in COVID-19 patients compared to the population.

Results: The WHO-Scale was translated to ten categories reflecting the increasing need for advanced care, encompassing 8,245,474 individuals including 1,981,946 SARS-CoV-2 infections. Fatal COVID-19 cases were older with more comorbidities. Those receiving mechanical ventilation and ECMO were younger with fewer comorbidities. Among survivors beyond 30 days, 90-day all-cause mortality increased with severity using category zero (no laboratory-verified SARS-CoV-2) as reference. Mortality was lowest for patients without health care adjusted for age, sex, comorbidities and socio-economic variables (adjusted hazard ratio (aHR) 1.18, 95% confidence interval (CI) 1.13–1.22). Those hospitalized >5 days had higher mortality (aHR 5.83, 5.5–6.17). Those requiring ECMO/ ECLS had the highest mortality (aHR 593.54, 317.77–1108.65).

Conclusion: The novel COVID-19 severity index associated with all-cause 90-day mortality and aligned with previous literature. This index will enable comparative studies of COVID-19, which is important for public health policies and development of clinical guidelines. This is an innovative epidemiologic tool with potential applicability in all countries with centralised health registers. The index also has the potential to be used for other infectious diseases and in real-time data for modelling predictions.

BACKGROUND: The quality of registry data is important for epidemiological research. The Swedish inpatient registry (IPR) is a national database with mandatory registration of all hospitalisations since 1987, and since 2007, the medical procedure codes which can be used for grading severity of infectious diseases. However, the completeness of procedure code registration has rarely been studied.

OBJECTIVES: To determine the quality and completeness of procedure codes for ICU admission, mechanical ventilation and extra-corporeal membrane oxygenation (ECMO) in the Swedish IPR utilising the Swedish Intensive Care Registry (SIR) as the gold standard. DESIGN A Swedish nationwide observational study.

SETTING: Covid-19 patients in Sweden who required intensive care in Sweden between March 2020 and August 2022. PATIENTS Covid-19 patients with a laboratory-verified SARS-CoV-2 infection who required ICU admission (n=8992), mechanical ventilation (n=5262) or ECMO (n=29).

MAIN OUTCOME MEASURES: The sensitivity and/or positive predictive values of procedure code registration for ICU, mechanical ventilation, ECMO and Covid-19 diagnosis code registration in the IPR were evaluated using SIR as the reference. Factors associated with low reporting were explored and the dates of ICU admission registration compared between IPR and SIR.

RESULTS: For Covid-19 patients registered in SIR as needing intensive care, mechanical ventilation or ECMO, the completeness of procedure codes in the IPR was 39.7, 78.2 and 100%, respectively. Of the 39.7% with an ICU code in the IPR, the ICU date in the IPR corresponding to the actual ICU admission date was 52.3%. The completeness of ICU registration in the IPR varied from 0.6 to 96.9% between healthcare regions

CONCLUSIONS: Procedure codes for intensive care in the Swedish IPR showed low sensitivity and varied greatly between healthcare regions. This negatively influences their usability for epidemiological research and calls for updated guidelines on coding.

PURPOSE: Individuals with severe liver disease are more vulnerable to severe COVID-19, but the association between chronic hepatitis B virus (HBV) infection and severe COVID-19 remains unclear. This study evaluates this relationship.

METHODS: We analysed nationwide Swedish data from national databases and healthcare registers, identifying laboratory-confirmed COVID-19 cases from February 2020 to April 2021. Chronic HBV infection was classified into cases with and without cirrhosis. Multivariable logistic regression assessed the association between HBV and severe COVID-19, adjusting for demographics, comorbidities, vaccination, and socioeconomic factors.

RESULTS: Among 1,057,174 COVID-19 cases, 2,902 had chronic HBV infection, which was associated with increased risk of severe COVID-19 (adjusted odds ratio [aOR] 1.242, 95% confidence interval [CI] 1.097-1.403). This risk was significantly higher in HBV individuals with cirrhosis (aOR 2.463, CI 1.546-3.892) compared to those without cirrhosis (aOR 1.183, CI 1.039-1.343). While overall COVID-19 mortality was not significantly elevated in the HBV cohort, patients with cirrhosis showed a higher, though nonsignificant, mortality risk (aOR 2.350, CI 0.921-5.203).

CONCLUSION: This nationwide study highlights an increased risk of severe COVID-19 in individuals with chronic HBV, particularly those with cirrhosis. Geographic and socioeconomic factors further influence outcomes. These findings underscore the need to consider HBV status in COVID-19 risk assessments. Future studies should explore these associations in the context of evolving SARS-CoV-2 variants and widespread vaccination.

Background and Aims: Covid-19 is a multiorgan disease affecting the kidney. However, the risk of kidney injury after infection remains unknown. Therefore, this study aimed to determine the risk and time of first ever diagnosed kidney injury following Covid-19, and determine the impact of Covid-19 disease severity on this risk.

Research Questions:

• Is the risk of a first ever kidney injury increased following Covid-19 in a nationwide Swedish whole population setting?
• If so, which patients are at higher risk?

Method: The total Swedish adult population were included in the study from January 1, 2020, to July 26, 2022. Nationwide multi-registry data was used and cross-linked with Personal Identification Numbers. Data was retrieved from the Swedish Inpatient, Outpatient, Covid-19 (SmiNet), Vaccination, Intensive Care, Cancer and Cause of Death Registries. Covid-19 date (exposure) was defined as the first SARS-CoV-2 related date registered in SmiNet based on the date of symptom onset, sample date, diagnosis date or date of report. All ICD-codes (IDC9 and ICD10) used for kidney injury registered since 1987 and 2000 respectively were identified to exclude patients with previous kidney injury. Outcome was defined as all first-time events of kidney injury diagnosis (acute, non-specified and chronic) reported with ICD10 codes post Covid-19 date, during the study period. We used the Self-Controlled Case Series (SCCS) method to determine the incidence rate ratio (IRR) of kidney injury during risk periods up to 6 months after infection. In the SCCS analysis, all individuals with reported Covid-19 (exposure) and first time diagnosed kidney injury (outcome) were included. The adjusted SCCS model was used, which considers deaths in the model.

Results: Among the total 2 426 423 Covid-19 cases, there were 10 351 first kidney injury events diagnosed. In a preliminary analysis, the risk of developing kidney injury after Covid-19 was increased up to 90 days post infection with the highest IRR during the first week (day 1–7) of Covid-19 onset being 56.1 (95% CI 52.5–60). The highest risk was day 0 with nearly 200-fold increased risk, however, due to risk of selection bias (Fonseca-Rodriguez O., 2021) when including day 0, this data is excluded from the first week and should be considered with caution. The IRR was elevated for a longer time for men than for women. For women, the IRR was elevated up until 60 days post infection, compared to 90 days for men. Stratified by age groups, the IRRs were highest in the group aged 51–74 years, compared with those ≤50 years and >74 years. Individuals with higher Covid-19 disease severity were also at higher risk than those with mild infection.

Conclusion: Covid-19 is associated with an increased risk of kidney injury according to this nationwide preliminary analysis, including more than two million Covid-19 cases in Sweden. The risk of a first ever diagnosed kidney injury is elevated up to 90 days after Covid-19, which is later than previously shown. The risk was higher for men than for women and was highest for age group 51–74 years. These results highlight the importance of vaccination to prevent severe Covid-19, and if diseased by Covid-19, follow up to detect kidney injury post Covid-19.

Aims: Doctors have an increased risk of SARS-CoV-2 infection caused by exposure to contagious patients. We aimed to identify which clinical specialities among medical doctors had the highest occupation-related risk of testing positive for SARS-CoV-2, utilizing data for all publicly employed medical doctors in Sweden.

Methods: Data regarding positive SARS-CoV-2 test results and employment for publicly employed doctors in Sweden were divided into three observation periods: 1) 1 February to 31 December 2020, 2) 1 January to 30 June 2021 and 3) 1 July 2021 to 31 March 2022. Individuals were stratified according to occupation clinic and compared with clinical occupations with little to no patient contact. The risk of testing positive for SARS-CoV-2 was estimated using Cox proportional hazards regression, with sex, age and vaccination status as covariates.

Results: The study cohort included all publicly employed doctors in Sweden: 35,028 individuals. In the first period, Infectious Disease doctors had the highest incidence of SARS-CoV-2 positive tests, with an incidence of 20.2 %, compared with 8.7 % in the reference group, and an adjusted hazard ratio of 2.5 (95% confidence interval 2.02–3.04), which decreased during period 2–3. Doctors in Geriatric Medicine had an elevated risk throughout the whole study period.

Conclusions: Our study shows an association between working in a speciality that involves caring for contagious COVID-19 patients, which raises concerns about infection control measures and routines being insufficient to prevent occupational infection in future pandemics.

Introduktion: Behovet av ett globalt perspektiv på hälsa.

Det har gått fem år sedan Global Hälsa – En praktisk guide släpptes. Sedan dess har världen förändrats. Covid-19-pandemin har i grunden påverkat förutsättningarna för den global hälsan och visar på hur svårt det är att isolera sig från globala hälsohot. Hälsokonsekvenserna av klimatförändringarna, liksom hälso- och sjukvårdens klimatpåverkan har tydliggjorts. Fler väpnade konflikter, inklusive kriget i Ukraina, riskerar många år av folkhälsoarbete. I kriser drabbas de fattigaste hårdast. Detta gäller globalt såväl som i Sverige.

I årets halvtidsgenomgång av världens utvecklingsagenda, Agenda 2030 och de globala målen, konstateras att många viktiga framsteg har gjorts, men att dessa hotas av det förändrade världsläget. Ett förnyat fokus på globala hälsofrågor krävs och här är svensk kunskap viktig. Många av de utmaningar som Sverige står inför delar vi dessutom med andra länder, såsom till exempel personalbrist, som leder till stängda vårdplatser och för låg täckning i primärvården. Här kan vi lära av varandra.

Svenska Läkaresällskapet har sedan 2013 aktivt arbetat med globala hälsofrågor, med övertygelsen om att större medvetenhet om global hälsa kan minska konsekvenserna från världens gemensamma utmaningar. Sedan den förra guiden kom ut har läkaresällskapet bidragit till mobilisering och kunskapsspridning om Covid-19 under pandemin, en hybridkonferens om planetär hälsa har hållits med världsledande forskare, och svensk hälso- och sjukvårds möjligheter att stötta den ukrainska befolkningen under pågående krig har lyfts i en webinarie-serie.

Liksom förra gången är guiden framtagen av läkarstudenter och läkare tidigt i karriären under handledning av kommittén för global hälsa. Den är tänkt som ett handfast stöd för de som vill engagera sig för global hälsa – genom klinik, forskning eller folkhälsoarbete och berör bland annat hälso- och sjukvårdens utmaningar i omställningen till ett klimatneutralt samhälle.

Fältets ambition om att skapa alltmer jämlika samarbeten, genom att ifrågasätta äldre beslutsstrukturer, berörs också som en röd tråd genom guiden.

Därför vill vi rikta ett stort tack till de studenter och yngre läkare som med vägledning av projektledarna har möjliggjort denna nya och förbättrade upplaga av guiden!

Tillsammans kan vi verka för förbättrad hälsa, här hemma och utomlands!

Aims: COVID-19 increases the risk of cardiovascular disease, especially thrombotic complications. There is less knowledge on the risk of arrhythmias after COVID-19. In this study, we aimed to quantify the risk of arrhythmias following COVID-19.

Methods and Results: This study was based on national register data on all individuals in Sweden who tested positive for SARS-CoV-2 between 1 February 2020 and 25 May 2021. The outcome was incident cardiac arrhythmias, defined as international classification of diseases (10th revision) codes in the registers as follows: atrial arrhythmias; paroxysmal supraventricular tachycardias; bradyarrhythmias; and ventricular arrhythmias. A self-controlled case series study and a matched cohort study, using conditional Poisson regression, were performed to determine the incidence rate ratio and risk ratio, respectively, for an arrhythmia event following COVID-19.A total of 1 057 174 exposed (COVID-19) individuals were included in the study as well as 4 074 844 matched unexposed individuals. The incidence rate ratio of atrial tachycardias, paroxysmal supraventricular tachycardias, and bradyarrhythmias was significantly increased up to 60, 180, and 14 days after COVID-19, respectively. In the matched cohort study, the risk ratio during Days 1–30 following COVID-19/index date was 12.28 (10.79–13.96), 5.26 (3.74–7.42), and 3.36 (2.42–4.68), respectively, for the three outcomes. The risks were generally higher in older individuals, in unvaccinated individuals, and in individuals with more severe COVID-19. The risk of ventricular arrhythmias was not increased.

1 057 174 exposed (COVID-19) individuals were included in the study as well as 4 074 844 matched unexposed individuals. The incidence rate ratio of atrial tachycardias, paroxysmal supraventricular tachycardias and bradyarrhythmias was significantly increased up to 60, 180 and 14 days after COVID-19, respectively. In the matched cohort study, the risk ratio during day 1-30 following COVID-19/index date was 12.28 (10.79-13.96), 5.26 (3.74-7.42) and 3.36 (2.42-4.68), respectively for the three outcomes. The risks were generally higher in older individuals, unvaccinated individuals and in individuals with more severe COVID-19. The risk of ventricular arrhythmias was not increased.

Conclusion: There is an increased risk of cardiac arrhythmias following COVID-19, and particularly increased in elderly vulnerable individuals, as well as in individuals with severe COVID-19.

Background: COVID-19 is a multiorgan disease. We previously identified COVID-19 as a risk factor for myocardial infarction, stroke (1), venous thromboembolism and bleeding (2). Less evidence exists on the risk of arrhythmias after COVID-19. Previous studies included mainly hospitalized patients with severe COVID-19, and there are no nationwide studies published.

Purpose: The aim of this study was to estimate the risk of atrial tachycardias (atrial fibrillation and atrial flutter) following COVID-19, including all individuals tested positive for SARS-CoV-2 in Sweden, regardless of disease severity.

Method: COVID-19 has been a notifiable disease in Sweden. All individuals in Sweden who were tested positive for SARS-CoV-2 between February 1, 2020 and May 25, 2021 were included in the study. We identified four control individuals for each COVID-19 individual matched on age, sex, and county of residence. Using Personal Identification Numbers, we cross-linked data from national registries: COVID-19 registry; Inpatient and Outpatient Registry; Cause of Death Registry; Prescribed Pharmaceutical Registry and Intensive Care Registry. Outcomes are cardiovascular events, defined using ICD-10 diagnosis codes for atrial fibrillation and atrial flutter in the registries. We performed a ‘’first-ever event’’ analysis, i.e., we excluded individuals with events before the study period. The self-controlled case series (SCCS) method was used to determine the incidence rate ratio (IRR) of a first atrial tachycardia during the risk periods 1-7, 8-14, 15-30, 31-60, 61-90, and 91-180 days after COVID-19. In the matched cohort study (MCS), Poisson regression was performed to calculate the risk ratio (RR) of a first arrhythmia event in the risk period 1-30 days following COVID-19, after adjusting for the effect of confounders, such as cardiac disease, treatment with antiarrhythmics, comorbidities and vaccination status.

Results: 1 057 174 cases and 4 074 844 controls were included in the study. In the SCCS, the risk of first atrial tachycardia was significantly increased up to 60 days following COVID-19. Specifically, during days 1-7 and 8-14 post-COVID-19 the IRRs were approximately 12 and 10 respectively. Similarly, in the MCS the RR for the first atrial tachycardia during day 1-30 post-COVID-19 was approximately 11. The risks were higher in patients with more severe COVID-19; and during the first pandemic wave compared to the second and third wave.

Conclusions: This study suggests that COVID-19 is a risk factor for atrial tachycardias, based on information obtained on all people who tested positive for SARS-CoV-2 in Sweden, regardless of disease severity. These results could impact recommendations on diagnostic and prophylactic strategies against atrial tachycardias after COVID-19. The importance of preventive strategies, such as risk factor control; vaccination to prevent severe COVID-19; and early review of high-risk individuals after COVID-19, is indicated.

Introduction: COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This emerging disease has become a public health emergency worldwide.

Acute Kidney Injury (AKI) secondary to COVID-19 has been described in different studies, but information characterising patients with subsequent AKI is limited. The cause of kidney involvement in COVID-19 is thought to be multifactorial. Cardiovascular comorbidity and predisposing factors (e.g. sepsis and nephrotoxins) are considered as important contributors. The tubular damage has been linked to the cytopathic effects of kidney-resident cells and cytokine storm syndrome. To gain better understanding of the effect of COVID-19 on renal function, large clinical and register based studies have been requested.

The objective of this study was to quantify the risk of acute kidney injury during and after covid-19.

Methods: This was a Swedish prospective cohort study where Generalised Estimating Equation methods (GEE) was used to map the kinetics of kidney injury markers such as serum-creatinine (s-creatinine), cystatin and eGFR for the hospitalised patients in the cohort, comparing patients with moderate and severe COVID-19 during and after the acute infection. Furthermore, we will investigate if patients with kidney dysfunction during COVID-19 have more severe disease outcome compared with the whole cohort, adjusting for age, sex, and comorbidities. We will also compare start values of kidney injury markers with the latest values and count the percentage worsening among all disease severity groups.

Cohort: Approximately 550 COVID-19 patients were recruited to the study following informed and signed consent at 2 Swedish University Hospitals. A case report form was filled in at pre-specified time points, and samples collected consecutively. A database was then created containing dates and information regarding symptoms, laboratory samples, complications, and disease severity (e.g., need of oxygen, intensive care, mechanical ventilation, death).

Results: There was a significant increase in s-creatinine among hospitalised and intensive care unit patients (n=126) during the acute phase of COVID-19 (day 0-6 post disease onset) when compared to the follow up samples after 90 days from disease onset. There was also a decrease in s-creatinine in day 11-21 and 31-70 among hospitalised and intensive care unit COVID-19 patients when compared to the same follow up samples. This analysis was adjusted for age and sex. See figure 1.

Conclusions: Our preliminary results show that s-creatinine was increased during the first days of COVID-19 followed by decreased levels compared to baseline.

The higher levels of s-creatinine day 0-6 of COVID-19 could be an effect of the acute infection, but it could also be caused by other factors such as dehydration or medication. The lower levels of s-creatinine might be caused by dietary changes or loss of muscle mass due to immobilisation during hospitalisation. Knowledge about fluctuations in s-creatinine in COVID-19 patients may be of use for treating physicians.

OBJECTIVE: To quantify the risk of deep vein thrombosis, pulmonary embolism, and bleeding after covid-19.

DESIGN: Self-controlled case series and matched cohort study.

SETTING: National registries in Sweden.

PARTICIPANTS: 1 057 174 people who tested positive for SARS-CoV-2 between 1 February 2020 and 25 May 2021 in Sweden, matched on age, sex, and county of residence to 4 076 342 control participants.

MAIN OUTCOMES MEASURES: Self-controlled case series and conditional Poisson regression were used to determine the incidence rate ratio and risk ratio with corresponding 95% confidence intervals for a first deep vein thrombosis, pulmonary embolism, or bleeding event. In the self-controlled case series, the incidence rate ratios for first time outcomes after covid-19 were determined using set time intervals and the spline model. The risk ratios for first time and all events were determined during days 1-30 after covid-19 or index date using the matched cohort study, and adjusting for potential confounders (comorbidities, cancer, surgery, long term anticoagulation treatment, previous venous thromboembolism, or previous bleeding event).

RESULTS: Compared with the control period, incidence rate ratios were significantly increased 70 days after covid-19 for deep vein thrombosis, 110 days for pulmonary embolism, and 60 days for bleeding. In particular, incidence rate ratios for a first pulmonary embolism were 36.17 (95% confidence interval 31.55 to 41.47) during the first week after covid-19 and 46.40 (40.61 to 53.02) during the second week. Incidence rate ratios during days 1-30 after covid-19 were 5.90 (5.12 to 6.80) for deep vein thrombosis, 31.59 (27.99 to 35.63) for pulmonary embolism, and 2.48 (2.30 to 2.68) for bleeding. Similarly, the risk ratios during days 1-30 after covid-19 were 4.98 (4.96 to 5.01) for deep vein thrombosis, 33.05 (32.8 to 33.3) for pulmonary embolism, and 1.88 (1.71 to 2.07) for bleeding, after adjusting for the effect of potential confounders. The rate ratios were highest in patients with critical covid-19 and highest during the first pandemic wave in Sweden compared with the second and third waves. In the same period, the absolute risk among patients with covid-19 was 0.039% (401 events) for deep vein thrombosis, 0.17% (1761 events) for pulmonary embolism, and 0.101% (1002 events) for bleeding.

CONCLUSIONS: The findings of this study suggest that covid-19 is a risk factor for deep vein thrombosis, pulmonary embolism, and bleeding. These results could impact recommendations on diagnostic and prophylactic strategies against venous thromboembolism after covid-19.