Post-Sepsis Syndrome

Sepsis survivorship is increasing, but many survivors develop post-sepsis syndrome, marked by high early readmission rates and new-onset conditions, notably recurrent infections, cardiovascular, psychiatric, and kidney disease. Persistent physical, cognitive, and psychological sequelae may further impair daily functioning. Emerging evidence suggests lasting immune dysregulation, likely interacting with mitochondrial dysfunction, immunosuppression, endothelial injury, low-grade inflammation, and microbiome disruption. While evidence for targeted postdischarge interventions remains limited and yields mixed results, much can still be done. Several strategies can begin during hospitalization, and after discharge a primary-care-centered, risk-stratified follow-up pathway may support recovery and reduce readmissions and complications.

Key points

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Post-sepsis syndrome (PSS) is common after sepsis regardless of severity, but remains underrecognized and poorly standardized.
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Long-term morbidity and mortality are not confined to critically ill patients, and all sepsis survivors show substantial risk of rehospitalization, new disease, and long-term health impairments.
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Emerging evidence in PSS points to persistent immune dysregulation involving immunosuppression, (neuro)inflammation, mitochondrial/endothelial dysfunction, and microbiome disruption.
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Overlap with post-acute infection syndromes, including long COVID, suggests shared features in pathogenesis and thus opportunities for cross-field learning.
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A pragmatic, primary-care–centered, risk-stratified follow-up model could be feasible, but needs further evaluation.

Abbreviations

ADL	activities of daily living
AKI	acute kidney injury
BBB	blood–brain barrier
CLP	cecal ligation and puncture
DAMP	damage-associated molecular pattern
GP	general practitioner
HMGB1	high-mobility group box 1
ICU	intensive care unit
IL	interleukin
MDSC	myeloid-derived suppressor cell
PAIS	post-acute infection syndrome
PPI	proton pump inhibitor
PSS	post-sepsis syndrome
PTSD	post-traumatic stress disorder
SAE	septic-associated encephalopathy

Introduction

The global burden of sepsis, known as a dysregulated host response to an infection leading to organ dysfunction, is rising. Recent estimates report 166 million sepsis cases annually, accounting for approximately 31.5% of all global deaths. With medical advancements in quality of care, in-hospital mortality from sepsis has declined, substantially increasing the number of sepsis survivors. Due to the aging population, a rise in chronic conditions, and increased antibiotic resistance, this number is expected to increase even further in the coming years. Patients who survive their initial sepsis episode frequently experience long lasting medical, cognitive, and psychological sequelae. These complications following sepsis have long been underrecognized, despite their substantial impact on long-term health and quality of life. So far, standardized care pathways and coordinated approaches to support patients after sepsis and improve long-term outcomes have not been widely implemented.

Patients surviving their initial sepsis episode face an increased long-term risk of rehospitalization and mortality after hospital discharge. ^,^,^,^, Approximately 1 in 5 sepsis patients are readmitted within 30 days after discharge, increasing up to three-quarters within the first year. Compared to patients hospitalized for infection without organ dysfunction, sepsis survivors have a 10.4% higher absolute risk of late mortality, with excess mortality persisting up to 1 year. Although these sequelae are often discussed as part of post–intensive care syndrome (PICS), many affected sepsis survivors were never admitted to the intensive care unit (ICU). ^,^,^, After adjustment for prior health status, the association between sepsis and subsequent disabilities persists, suggesting that sepsis itself may initiate or accelerate a process of long-term health deterioration rather than merely unmask pre-existing disease. ^,

Although post-sepsis syndrome (PSS) currently lacks a standardized case definition, it refers to the constellation of physical, cognitive, and/or psychological impairments that develop after survival from sepsis, persist beyond the acute recovery phase, and cannot be explained by pre-existing conditions. ^, The underlying mechanisms of long-term sequalae after sepsis remain poorly understood and are hypothesized as a complex interplay between a patient’s pre-sepsis health status, the individual clinical course of the disease, severity and source of the infection, comorbidities, availability of health care resources care, and so on. The recently updated surving sepsis campaign guidelines have stressed the urgent need for post hospital evaluation, management and rehabiliation after hospitalization for sepsis. To date, the lack of evidence-based treatment guidelines for PSS is regarded as one of the most urgent research priorities in sepsis. This article synthesizes current evidence and key knowledge gaps on long-term sequelae specifically attributable to PSS rather than critical illness survivorship more broadly. It proposes a primary care–oriented framework for postdischarge follow-up and identifies priorities for prevention and targeted intervention.

Clinical sequelae

A considerable proportion of readmissions are for diagnoses that may be preventable with earlier outpatient recognition and management, implying that hospital readmissions alone underestimate the overall burden, as emerging sequelae may be managed in primary care or outpatient settings. Consistent with this, up to three-quarters of sepsis survivors develop at least one new medical, cognitive, or psychological diagnosis after discharge, and approximately 1 in 6 develop severe, persistent long-term impairments ( Fig. 1 ). While clinical outcomes are primarily derived from observational studies rather dan randomized controlled trials (RCTs), possibly resulting in residual confounding, the association between sepsis and clinical sequelae is firmly established across international literature.

Alt text begins. A conceptual graph shows health status over time from pre-sepsis through sepsis to post-sepsis, with recovery, long-term impairment, or new disease trajectories. Alt text provided by Elsevier. — Fig. 1

Sepsis Survivors Are More Prone to Disease and Rehospitalization

Reinfection

Recurrent sepsis is reported as the leading readmission diagnosis, accounting for approximately 29% to 52% of early readmission across studies on sepsis survivors. ^,^, In an age-matched and sex-matched analysis, individuals who survived a severe sepsis admission had over 8 times higher risk of experiencing recurrent severe sepsis compared to the general population. A French nationwide study further showed that readmission with recurrent sepsis regardless of severity is strongly associated with 1-year mortality, alongside age and comorbidity burden. In this study, factors associated with recurrent sepsis included malignancy, renal disease, older age, and longer length of hospital stay, whereas rehospitalization for recurrent sepsis was lower in ICU admitted patients without septic shock. Approximately two-thirds of patients readmitted for sepsis within 90 days experience sepsis recurrence at the same site of infection as their initial hospitalization. However, microbiological data indicate that in roughly half of these cases the episode represents a newly acquired infection rather than an ongoing primary infection.

Cardiovascular disease

Sepsis is a clinically meaningful, nontraditional cardiovascular risk factor as shown in pooled results from several studies. ^, Rehospitalization for cardiovascular disease has been reported in approximately 3.5% of sepsis survivors within 30 days, while heart failure-related readmissions occur in 1.5% by 30 days and 2.9% by 90 days. New-onset heart failure after sepsis is the most common cardiovascular complication (8.6%), followed by stroke (4.9%) and myocardial infarction (2.4%). One in 4 ICU sepsis survivors without pre-existing cardiovascular disease developed new, acute cardiovascular events. This corresponds to a 1.9 fold increased risk compared to matched controls, a risk magnitude similar to traditional factors such as smoking, diabetes, and hypercholesterolemia.

Large population-based cohorts consistently show sustained long-term cardiovascular risk after sepsis, regardless of ICU admission. An US administrative cohort of more than 8 million sepsis survivors showed higher cardiovascular mortality and rehospitalization than propensity score–matched, hospitalized non-sepsis controls over up to 12 years of follow-up, with the strongest association for heart failure hospitalization (adjusted hazard ratio [HR] 1.51). Consistently, a Taiwanese cohort of more than 93,000 sepsis survivors showed increased risks of cardiovascular events ranging from HR 1.14 to HR 1.42, compared to propensity score-matched, hospitalized non-sepsis controls. Risk of all-cause mortality (HR, 1.95) and major adverse events (HR 1.27) were highest within 1 year and persisted for more than 5 years. Notably, ICU admission was associated with higher all-cause mortality, but did not increase the risk of major cardiovascular disease.

Psychiatric disease

Post-sepsis psychiatric disease represents a frequent and clinically relevant component of PSS, encompassing depression, anxiety, and posttraumatic stress disorder (PTSD). Approximately one-quarter of sepsis survivors develop a new psychiatric diagnosis, with depression being the most common disorder, affecting 16.2% of patients without a prior history of depression. While longitudinal data suggest that the prevalence of PTSD and anxiety tend to decrease over time, depressive symptoms often persist or increase, indicating divergent recovery trajectories. Persistent post-sepsis depression is independently associated with excess long-term mortality, as shown across multiple cohorts. ^, Notably, a nationwide cohort study in Korea reported a 5-year all-cause mortality of 46.2% among patients with post-sepsis depression, corresponding to a 1.29 fold increased risk compared to matched controls.

Kidney disease

Acute renal failure is a relatively frequent readmission diagnosis after severe sepsis, accounting for 3.3% of readmissions compared to 1.2% in matched non-sepsis hospitalizations. Approximately 4.5% of early unplanned readmissions after sepsis are attributed to acute kidney injury (AKI). Although much of the literature on sepsis-associated AKI focuses on critically ill cohorts, evidence supports that the pathophysiological impact of sepsis on renal function contributes to sustained renal complications in a broad sepsis population. A retrospective cohort study of 1636 patients with sepsis admitted to the ward and ICU reported a high AKI incidence of 61% at admission. Among survivors with sepsis-associated AKI and available follow-up, 19% progressed to chronic kidney disease within 1 year, unrelated to AKI stage at presentation.

Cancer

Cancer increases the risk of sepsis, but growing evidence suggests this relationship may be bidirectional. ^, Beyond malignancy as a predisposing factor, sepsis has been linked to a higher subsequent cancer incidence than in the general population. In a Swedish nationwide study of 18,550 one-year ICU sepsis survivors, the incidence rate ratio for a new cancer diagnosis ranged from 1.31 to 1.74 depending on sex, relative to the general population. However, this association may be partly explained by residual confounding and surveillance bias and requires further confirmation.

Sepsis Survivors Suffer From Long-Term Health Impairments

Cognitive impairment

Sepsis survivors can experience substantial and persistent impact on cognitive function. During acute illness, many patients develop septic-associated encephalopathy (SAE), an umbrella term for sepsis-related acute brain dysfunction ranging from mild confusion to delirium and coma. SAE, particularly when complicated by delirium, has been linked to adverse long-term cognitive outcomes such as attention, memory, and executive functioning. An ICU-based, prospective cohort study found neuropsychological impairment in 34% of sepsis survivors 6 months after discharge. Additionally, a prospective cohort study including all sepsis survivors showed an increase in moderate to severe cognitive impairment of 10.6% after sepsis, persisting for up to 8 years of follow-up even after accounting for baseline cognitive status. Sepsis has also been associated with a faster decline in cognitive performance compared to pre-sepsis slopes. Poorer cognitive performance was further associated with greater activities of daily living (ADL) dependence and reduced survival.

Functional decline

A considerable proportion of sepsis survivors experience persistent limitations in daily activities. In a large longitudinal cohort study involving 1194 ICU and ward patients in the United States, severe sepsis was associated with the acquisition of approximately 1 to 2 new ADL or instrumental ADL limitations among patients without prior functional impairment. While partial recovery of physical function is commonly observed during 6 to 12 months of follow-up, functional performance often remains below population norms and does not consistently return to pre-sepsis levels. In line with these findings, sepsis survivors demonstrate reduced tolerance to physical exertion, reflecting impaired exercise capacity during recovery. ^, Furthermore, in a prospective survey study, sepsis survivors reported a significant increase in sensory, digestive, breathing, chest pain, and musculoskeletal problems. Fatigue is a prominent feature of PSS and is reported by approximately 67.8% of sepsis survivors at 6 months after hospitalization. Mental health problems are also frequent, as illustrated by a large population-based German cohort study that reported mental health impairment in 54.8% of patients within the first year following sepsis hospitalization.

Proposed mechanisms

The pathogenesis of PSS remains poorly defined; however, proposed contributing mechanisms include chronic low-grade inflammation, persistent immunosuppression, mitochondrial dysregulation, endothelial dysfunction, and microbiome disruption ( Fig. 2 ). Notably, many of these mechanisms are not unique to sepsis: they overlap substantially with etiopathogenesis proposed for post-acute infection syndromes (PAIS; Box 1 ).

Alt text begins. A three column infographic outlines proposed post sepsis syndrome mechanisms, related clinical sequelae, and corresponding management strategies. Alt text provided by Elsevier. — Fig. 2

Box 1

Post-sepsis syndrome in the context of post-acute infection syndromes: from infection to impaired recovery

Post-acute infection syndromes (PAIS) have moved to the forefront since the COVID-19 pandemic, largely driven by recognition of post-COVID syndrome (long COVID). However, persistent post-infectious symptoms have been described across multiple pathogens well before COVID-19, including Epstein–Barr virus, Coxiella burnetii , and Borrelia burgdorferi . Across PAIS, symptom profiles are heterogeneous yet strikingly overlapping. Fatigue is the most frequently reported symptom. An important feature of post-COVID syndrome is post-exertional malaise: a delayed and disproportionate worsening of symptoms following physical or cognitive effort. Cognitive dysfunction, myalgia, muscle weakness, and arthralgia are consistently reported in post-COVID syndrome, post-treatment Lyme disease syndrome, and Q-fever fatigue syndrome. Similar symptom clusters such as fatigue, reduced exercise tolerance, and cognitive impairment are also prominent in PSS.

Beyond clinical overlap, biological hypotheses suggest shared underlying mechanisms. Persistent immune activation, driven by residual pathogen components or sustained autoimmunity, has been proposed across PAIS. Neuroinflammation, as well as epigenetic and metabolic reprogramming, have been described after both sepsis and SARS-CoV-2 infection. The overlap in symptoms and proposed mechanisms raises the question whether these conditions should be considered distinct entities, or instead represent the same spectrum after infection. If so, synergies from PSS and PAIS research should be increasingly utilized.

Immune Dysregulation

Chronic low-grade inflammation

The most commonly proposed mechanism behind PSS is persistent immune dysregulation, characterized by ongoing inflammation alongside immunosuppression following acute sepsis. Prospective cohort studies have identified persistent elevation of inflammatory markers, including interleukin (IL)-6, IL-10, and high-sensitivity C-reactive protein (CRP) at discharge and up to 1 year after sepsis in a subgroup of survivors. ^, Persistent elevation of proinflammatory cytokines is associated with long-term mortality and readmissions, particularly from cardiovascular disease and cancer. ^, Persistent inflammation after sepsis may also be mediated by damage-associated molecular patterns (DAMPs), particularly high-mobility group box 1 (HMGB1). Elevated plasma HMGB1 levels have been reported following sepsis and may contribute to sustained innate immune activation by acting as a potent DAMP, modulating neuroinflammatory signaling. Persistently elevated HMGB1 levels were associated with memory impairment lasting up to 4 weeks after sepsis.

Neuroinflammation may be amplified by blood–brain barrier (BBB) disruption after sepsis, as shown in MRI studies in patients with sepsis, potentially facilitating central nervous system exposure to circulating inflammatory mediators. Cerebral ischemia and systemic inflammation during sepsis can promote BBB permeability and microglial activation, leading to sustained cytokine production and further compromise of BBB integrity. ^, Together, these processes provide a potential mechanistic link between systemic immune dysregulation and long-term neurologic sequelae in PSS.

Immunosuppression

Immunosuppression is hypothesized as a key component of PSS and may contribute to the increased susceptibility to recurrent infections after sepsis. Several mechanisms have been proposed to underlie sustained post-sepsis immunosuppression, including epigenetic reprogramming of both innate and adaptive immune cells. Experimental data support the concept that epigenetic reprogramming affects innate immune cells after sepsis. In a murine cecal ligation and puncture (CLP) model, repressive epigenetic modifications at inflammatory gene promoters persisted after recovery up to 4 weeks after sepsis. In addition, persistently reduced expression of monocytic human leukocyte antigen (mHLA)–DR, a key molecule for antigen presentation, has also been observed in sepsis survivors for up to 2 months after discharge and was independently associated with reinfection and mortality.

Adaptive immune dysregulation further contributes to sustained immunosuppression after sepsis. In a prospective cohort study, low absolute lymphocyte counts 4 days after sepsis onset were independently associated with increased 28-day and 1-year mortality and a higher risk of secondary infections. In parallel, regulatory T cells remain expanded for 5 to 10 months following sepsis hospitalization, potentially shifting to an immunoregulatory milieu which may impair antitumor immune surveillance. Myeloid-derived suppressor cells (MDSCs), which can inhibit T-cell activation and antigen-presenting cell function, have also been reported to expand for at least 4 weeks following sepsis and are clinically associated with secondary infections. ^, Functional evidence, although limited, is consistent with these cellular changes. In a small translational study using ex vivo whole-blood stimulation months to years after sepsis, survivors showed reduced cytokine responses to immune challenges, including lower IL-6 and tumor necrosis factor (TNF) after zymosan stimulation and diminished IL-10 production following lipopolysaccharide (LPS) stimulation. Taken together, these findings suggest impaired responsiveness to secondary immune challenges involving both innate and adaptive pathways in sepsis survivors. However, the extent to which these observations directly contribute to clinical outcomes such as secondary infections remains uncertain, with findings largely based on circulating markers that may not capture, among other factors, relevant immune processes at local sites of infection and damaged organs.

Mitochondrial Dysfunction

Mitochondrial dysfunction is hypothesized to play a central role in the metabolic alterations associated with PSS. Sepsis induces persistent mitochondrial abnormalities which can cause incomplete mitochondrial recovery and defective homeostatic mechanisms. These alterations may sustain low-grade inflammation through DAMP release and compromise immune-cell bioenergetics, leading to reduced cytokine responsiveness. ^, Immunometabolic perturbations have further been linked to immunoregulatory phenotypes, including upregulation of programmed death-ligand 1 (PD-L1) and persistent metabolic impairment in circulating MDSCs months after sepsis. ^, The extent to which sepsis-induced mitochondrial damage is reversible remains uncertain. Experimental data indicate that mitochondrial DNA damage can persist for several days after resolution of acute sepsis and that impaired mitochondrial quality control may hinder full metabolic recovery. In a translational two-stage longitudinal study, mitochondrial-related pathways were the only pathways consistently enriched at both 7 days and 6 months after ICU discharge. Detailed functional analyses demonstrated that this was accompanied by impaired oxidative phosphorylation, accumulation of dysfunctional mitochondria, and defective mitophagy in skeletal muscle, collectively driving sustained post-sepsis muscle weakness. Notably, complementary evidence from murine CLP models shows that mitochondrial-targeting synthetic tetrapeptide SS-31 prevented post-sepsis skeletal muscle weakness after inducing sepsis. Mitochondrial dysregulation may therefore represent a common pathway linking immunometabolic imbalance to impaired recovery after sepsis.

Endothelial Dysfunction

Sepsis triggers cardiovascular complications through demand ischemia, endothelial injury, procoagulant states, and inflammatory plaque destabilization. Inflammatory mediators released during sepsis have been shown to accelerate atherosclerosis through endothelial injury and activation. ^, Persistent vascular inflammation may destabilize pre-existing plaques and promotes atherothrombotic events well-beyond hospital discharge. Elevated inflammatory and endothelial activation markers have been linked to increased cardiovascular risk months to years after sepsis. Although not focused on sepsis, a prospective study showed that elevated cardiac and endothelial biomarkers in patients hospitalized with community-acquired pneumonia were independently associated with both early and 30-day cardiovascular events after adjustment for pre-existing cardiovascular disease.

A potential unifying mechanism is accelerated vascular aging, also referred to as premature endothelial senescence, occurring irrespective of age. This state is characterized by loss of endothelial regenerative capacity and sustained endothelial activation, leading to a proinflammatory and prothrombotic vascular state. ^, Experimental rat CLP models demonstrate sepsis-induced premature senescence in aortic tissue, peaking 3 months after the septic insult. Comparable senescence-like endothelial responses have been described in humans following acute respiratory distress syndrome (ARDS) and AKI, conditions frequently associated with sepsis and linked to subsequent chronic organ dysfunction. ^,

Microbiome Disruption

The gut microbiome is increasingly recognized as an important contributing factor in sepsis, influencing susceptibility, disease onset, and recovery. During hospitalization for sepsis, the gut microbiome is highly vulnerable to disruption due to both the underlying disease and treatments patients receive. In particular, antibiotic therapy frequently induces intestinal loss of commensal microbes causing impaired gut barrier integrity, facilitating translocation of microbial products and increasing susceptibility to secondary infections. In addition, depletion of commensal microbes reduces colonization resistance, allowing overgrowth of pathobionts. Enterococcus domination, in particular, has been linked to higher infection risk and mortality in ICU patients, and anti-anaerobic antibiotic exposure has been associated with increased mortality in sepsis. Gut microbiome disruption after sepsis is not limited to bacteria, a prospective cohort study examined the mycobiome dysbiosis in ICU sepsis patients 2 to 3 weeks after discharge. Compared to healthy controls, sepsis survivors had gut dysbiosis characterized by reduced diversity of the mycobiome, with an increase of pathogenic fungi such as Candida and loss of commensal fungi. Strategies to restore the gut microbiota after sepsis, such as prebiotics, probiotics, and synbiotics, are promising but require confirmation in well-designed clinical studies. The PAM-ICU trial is currently evaluating postdischarge supplementation with pasteurized Akkermansia muciniphila to support gut microbiota restoration and immune recovery in ICU sepsis survivors (ClinicalTrials.gov: NCT07295353 ).

Management of post-sepsis syndrome

Prevention of Post-Sepsis Syndrome During Hospitalization

Most current sepsis guidelines primarily focus on reducing short-term mortality, while providing limited guidance on preventing long-term morbidity and PSS. Fluid management appears particularly relevant for neurologic recovery: although conservative fluid strategies may shorten length of stay, they have been associated with worse late cognitive outcomes, potentially due to impaired cerebral perfusion. Stress ulcer prophylaxis is commonly achieved with proton pump inhibitors (PPIs); however, PPIs may adversely affect the gut microbiome by increasing gastric pH and have been associated with higher rates of secondary infections. Delirium during sepsis is strongly associated with subsequent cognitive impairment, and longer delirium duration is associated with poorer cognitive outcome. Multicomponent delirium prevention bundles, which include avoidance or minimization of deliriogenic medications, have been associated with reduced incidence and duration of delirium in hospitalized patients.

Post-discharge Rehabilitation

Evidence supporting post-discharge interventions is emerging but remains limited, especially high-quality studies including ward-treated sepsis remain scarce. A recent systematic review summarizing 14 post-acute intervention studies reports overall improvements in long-term outcomes after hospitalization for sepsis, particularly successful for programs emphasizing physical rehabilitation, mental health support, and care coordination. Rehabilitation programs were associated with improved long-term survival up to 10 years after sepsis, while care coordination was linked to reductions in mortality and hospital readmissions. Large observational data show improved long-term survival after rehabilitation for both ICU and non-ICU treated sepsis patients. A German retrospective cohort including 83,974 sepsis-associated hospitalizations showed significantly improved 5-year survival among sepsis patients discharged to rehabilitation facilities compared to matched sepsis patients discharged home or to self-care. More recently, the Sepsis Transition and Recovery (STAR) trial randomized 3548 sepsis patients to a nurse-led transitional care program focused on medication review, identification of new disabilities, and surveillance of treatable conditions. Although the intervention did not reduce 90 day readmissions compared with usual care, it was associated with lower 90-day mortality. In contrast, another RCT of a nurse navigator-led, multicomponent transition program in 691 sepsis survivors reported reductions in both 30-day mortality and readmission rates.

The Role of Primary Care Postdischarge

The majority of PSS complaints do not lead to hospital readmission and are seen and managed in primary and outpatient care settings. Approximately 40 to 42% causes of early readmission are potentially preventable, such as exacerbation of underlying chronic diseases (chronic obstructive pulmonary disease [COPD], asthma, heart failure), medication updates, and functional decline. Even though there are large differences in primary care organization and delivery throughout the world, the main focus is on the continuum from health promotion and disease prevention to treatment, rehabilitation, and palliative care, all of which should be accessible, continuous, and close to people’s everyday environment. In hierarchical primary care models, general practitioners (GPs) are the cornerstone of the health system and typically maintain long-standing relationships with patients and have detailed knowledge of local support services. This positions them in a central role to coordinate post-sepsis care and implement individualized prevention strategies. Several randomized trials have evaluated broader transitional care approaches for a longer time period. A German RCT of 143 ICU sepsis survivors receiving structured primary care management showed no improvement in mental health–related quality of life at 6 or 24 months, but did demonstrate better physical functioning and ADL at 6 months. ^,

Primary care can already implement several pragmatic, risk-stratified strategies ( Box 2 , Fig. 3 ). As recurrent infections represent the leading cause of rehospitalization after sepsis, targeted prevention deserves particular attention. This includes optimization of vaccination status, hygiene counseling, nutritional support, and patient and caregiver education. Aspiration pneumonia is among the most frequent causes of readmission following severe sepsis. Dysphagia is a well-recognized risk factor for aspiration-related pulmonary infection and is very common after sepsis. ^, Early swallow screening, dietary modification, and referral to speech and language therapy have reduced pneumonia risk in other high-risk populations, suggesting a plausible opportunity for prevention in sepsis survivors as well.

Box 2

Risk stratification in post-sepsis syndrome

Structured transitional care alone has not consistently reduced morbidity or mortality, suggesting that post-sepsis management likely requires individualized, risk-specific interventions rather than generic care coordination. One explanation may be the marked heterogeneity among sepsis survivors. A large retrospective observational study identified early survivorship phenotypes based on clinical characteristics at hospital discharge that were associated with differential risks of 30-day readmission and mortality. Extending this concept to longer-term recovery trajectories, a large retrospective cohort study identified distinct post-sepsis subtypes using a parsimonious algorithm incorporating Charlson Comorbidity Index, length of stay, and discharge destination. These subtypes predicted 3-month mortality, 6-month, and 12-month quality of life, and limitations in activities of daily living, though not readmission risk. This indicates that clinical phenotyping may help identify patients who require intensified follow-up, an approach that should be prospectively validated and implemented in future care pathways.

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Tags: Critical Care Clinics Volume 42 Issue 4

Sep 27, 2026 | Posted by drzezo in CRITICAL CARE | Comments Off

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Post-Sepsis Syndrome

Key points

Introduction

Clinical sequelae