Sepsis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2], Parth Vikram Singh, MBBS[3]

Synonyms and keywords: sepsis syndrome; septic shock; septicemia

Sepsis is a condition characterized by a whole-body inflammatory state caused by infection. Septic shock is a serious medical condition caused by decreased tissue perfusion and oxygen delivery as a result of infection and sepsis. It can cause multiple organ failure and death. Its most common victims are children, immunocompromised individuals, and the elderly. This is because their immune systems cannot cope with the infection as well as those of full-grown adults.^[1]

The immunological response that causes sepsis is a systemic inflammatory response causing widespread activation of inflammation and coagulation pathways. This may progress to dysfunction of the circulatory system and, even under optimal treatment, may result in the multiple organ dysfunction syndrome and eventually death. A subclass of distributive shock, shock refers specifically to decreased tissue perfusion resulting in end-organ dysfunction. Dysregulated immune response remains the cornerstone of pathophysiology, involving both excessive inflammation and subsequent immunosuppression. Cytokines TNFα, IL-1β, interferon γ, IL-6 released in a large scale inflammatory response results in massive vasodilation, increased capillary permeability, decreased systemic vascular resistance, and hypotension. Hypotension reduces tissue perfusion pressure and thus tissue hypoxia ensues. Excessive inflammation is now recognized to include cytokine storm, formation of neutrophil extracellular traps (NETs), and emergency myelopoiesis. In parallel, an immunosuppressive phase develops, characterized by lymphopenia, expansion of MS1 monocytes, and T-cell exhaustion.

Recent work has also highlighted metabolic failure as a key contributor to immunoparalysis, with impaired glycolysis and oxidative phosphorylation in immune cells leading to inadequate host defense. Finally, in an attempt to offset decreased blood pressure, ventricular dilatation and myocardial dysfunction will occur.

Microvascular injury further amplifies tissue damage. Endothelial glycocalyx shedding leads to barrier loss, microvascular thrombosis, and inflammation, while complement overactivation exacerbates endothelial and organ injury.

Heterogeneity is increasingly recognized: gene expression and molecular profiling are uncovering distinct subtypes of sepsis with different immune signatures and therapeutic responses, such as macrophage activation–like syndrome.^{[2][3][4][5][6][7]}

In rough order of severity, these are bacteremia or fungemia; septicemia; sepsis, severe sepsis or sepsis syndrome; septic shock; refractory septic shock; multiple organ dysfunction syndrome, and death.

The process of infection by bacteria or fungi can result in systemic signs and symptoms that are variously described. The condition develops as a response to certain microbial molecules which trigger the production and release of cellular mediators, such as tumor necrosis factors (TNF); these act to stimulate immune response.^[8][9][10]

Sepsis must be differentiated from other syndromes presnting with fever, hypotension such as the acute bacterial endocarditis, myocardial ring abscess, subacute bacterial endocarditis and bacterial meningitis.^[11][12][13]

The hospitalization rate of those with a principal diagnosis of septicemia or sepsis more than doubled from 2000 through 2008. During the same period, the hospitalization rate for those with septicemia or sepsis as a principal or as a secondary diagnosis increased by 70% from 221 to 377 for every 100,000 people. Reasons for these increases may include an aging population with more chronic illnesses, greater use of invasive procedures, immunosuppressive drugs, chemotherapy, transplantation, and increasing microbial resistance to antibiotics.^[14]

Globally, the burden of sepsis remains very high, with an estimated 48.9 million cases and 11 million deaths annually. Importantly, about 85% of these cases occur in low- and middle-income countries (LMICs), particularly in sub-Saharan Africa.^[15]

Factors responsible for increased risk of sepsis may include an aging population with more chronic illnesses; greater use of invasive procedures, immunosuppressive drugs, chemotherapy, and transplantation; and increasing microbial resistance to antibiotics. Other patients population at increased risk are ICU admits, immunocompromised, bacteremic, with community acquired pneumonia, and with genetic predisposition.^[16][14][14]

There are many complications associated with sepsis, especially because it is a systemic phenomenon. Sepsis is a severe condition, and the prognosis of the patient will depend greatly on the condition and overall health of the patient. Many factors, such as age, hosts immune response, site of infection, type of infection, appropriate antibiotic therapy, and restoration of circulation of perfusion contribute to the overall prognosis.^{[17][18] [19][20][21][22] [23]}

Symptoms of sepsis are often related to the underlying infectious process. When the infection crosses into the bloodstream the resulting symptoms of sepsis occur fever, chills, and rigors, confusion, anxiety, difficulty breathing, fatigue and malaise, nausea and vomiting.^[24][25][1]

The physical examination of sepsis shows findings of the causative system as well as some generalized features.^[26][27]

The international guideline committee for diagnosis of septic shock recommends obtaining appropriate cultures that may include at least two blood cultures, urine, cerebrospinal fluid, wounds, respiratory secretions, or other body fluid cultures before antimicrobial therapy is initiated. If such cultures do not cause significant delay in antibiotic administration, then other tests that may be done include blood gases, kidney function tests, platelet count, white blood cell count, blood differential, fibrin degradation products, and peripheral smear.^[28][1]

Improved detection using molecular tools (e.g., plasma metagenomics) is increasing pathogen identification rates. Transcriptome- and proteome-based diagnostic tools have also been approved, though their clinical impact is still untested.^[15]

Sepsis-3 remains the dominant definition for adults, whereas the Phoenix 2024 criteria are now recommended for pediatrics.^[15]

There are no specific chest X-ray findings associated with sepsis but may show the features consistent with the primary source of infection.

There are no specific CT findings associated with sepsis but may show the features consistent with the primary source of infection.

There are no specific MRI findings associated with sepsis but may show the features consistent with the primary source of infection.

There are no specific echocardiography or ultrasound finidngs associated with sepsis but may show the features consistent with the primary source of infection.

According to IDSA, “Surviving Sepsis Campaign” guidelines, the management protocol for sepsis include screening for high-risk patients; taking bacterial cultures soon after the patient arrived at the hospital; starting patients on broad-spectrum intravenous antibiotic therapy before the results of the cultures are obtained; identifying the source of infection and taking steps to control it (e.g., abscess drainage); administering intravenous fluids to correct a loss or decrease in blood volume; and maintaining glycemic (blood sugar) control.^{[14][29][30][31][32][33][34][34][35][36][37][38][39]}

Surgical intervention is not recommended for the management of sepsis itself but may be essential as part of source control (e.g., abscess drainage, removal of infected devices).

Prevent infections that can lead to sepsis by cleaning scrapes and wounds and getting regular vaccination against infections that cause sepsis can help in the prevention of sepsis.^[40]

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Sepsis currently has differing definitions as shown in the table below. These definitions were compiled from the three following sources:

1) Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock (2016)

2) Center of Medicare and Medicaid Services (CMS) (2015/2016)

3) The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) from 2016

This table is based on the 2019 published table by the Wisconsin Chapter of American College of Emergency Physicians.

• Surviving Sepsis Campaign
• Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2] ; Aditya Ganti M.B.B.S. [3]; Parth Vikram Singh, MBBS[4]

Synonyms and keywords: sepsis syndrome; septic shock; septicemia

The immunological response that causes sepsis is a systemic inflammatory response causing widespread activation of inflammation and coagulation pathways. This may progress to dysfunction of the circulatory system and, even under optimal treatment, may result in the multiple organ dysfunction syndrome and eventually death. A subclass of distributive shock, with shock referring specifically to decreased tissue perfusion resulting in end-organ dysfunction. Cytokines TNFα, IL-1β, interferon γ, IL-6 released in a large scale inflammatory response results in massive vasodilation, increased capillary permeability, decreased systemic vascular resistance, and hypotension. Hypotension reduces tissue perfusion pressure and thus tissue hypoxia ensues. Finally, in an attempt to offset decreased blood pressure, ventricular dilatation and myocardial dysfunction will occur. ^{[1][2][3][4][5]}

• Sepsis is defined as a collection of physiologic responses by the immune system in response to an infectious agent.
• Sepsis results when an infectious insult triggers a localized inflammatory reaction that resulting in systemic symptoms of fever or hypothermia, tachycardia, tachypnea, and either leukocytosis or leukopenia.
• The clinical course of sepsis depends on the type and resistance of the infectious organism, the site and size of the infecting insult, and the genetically determined or acquired properties of the host’s immune system.
• The pathogenesis of sepsis can be discussed as follows ^{[2][3][4][5][6]}

• The immune system is activated by pathogen entry which is facilitated by contamination of tissue either by surgery or infection, foreign body insertion (catheters) and in an immunocompromised state.
• Products of activation include
  • Bacterial cell wall products such as lipopolysaccharide
  • Binding to host receptors, including Toll-like receptors (TLRs).
• Toll-like receptors are found in leukocytes and macrophages, and endothelial cells.
• These have specificity for different bacterial, fungal, or viral products.
• TLRs are associated with a predisposition to shock with gram-negative organisms.
• Activation of the innate immune system results in a complex series of cellular and humoral responses.

• Immune response includes the release of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-alpha and interleukins 1 and 6 along with reactive oxygen species, nitric oxide (NO), proteases, and pore-forming molecules, which bring about activation of immune cells and bacterial killing.
• Nitrous oxide is responsible for vasodilatation and increased capillary permeability and has been implicated in sepsis-induced mitochondrial dysfunction.
• The complement system gets activated which mediates activation of leukocytes, attracting them to the site of infection (phagocytes, cytotoxic T lymphocytes),
• Complement system also helps as a mediator for antigen-presenting cells and B lymphocytes
• This response by complement system helps the B lymphocyte to produce memory cells in case of future infection and is responsible for the increased production and chemotaxis of more T helper cells.
• In modern understanding, this immune cascade represents a dysregulated host response rather than a balanced defense. Excessive inflammation manifests as cytokine storm, neutrophil–endothelial traps (NETs), and emergency myelopoiesis, while immunosuppression occurs in parallel, marked by lymphopenia, MS1 monocyte expansion, and T-cell exhaustion. At the same time, impaired glycolysis and oxidative phosphorylation in immune cells contribute to metabolic failure and sustained immunoparalysis.

• The vascular endothelium plays a major role in the host’s defense to an invading organism, but also in the development of sepsis.
• Activated endothelium not only allows the adhesion and migration of stimulated immune cells but becomes porous to large molecules such as proteins, resulting in the tissue edema.
• Alterations in the coagulation systems include an increase in procoagulant factors, such as plasminogen activator inhibitor type I and tissue factor, and reduced circulating levels of natural anticoagulants, including antithrombin III and activated protein C (APC), which also carry anti-inflammatory and modulatory roles.
• Additionally, microvascular injury is now recognized as a critical process: endothelial glycocalyx shedding disrupts the vascular barrier, promotes thrombosis, and amplifies inflammation, while complement overactivation further exacerbates tissue damage and organ dysfunction.

• Through vasodilatation (causing reduced systemic vascular resistance) and increased capillary permeability (causing extravasation of plasma), sepsis results in relative and absolute reductions in circulating volume.
• A number of factors combine to produce multiple organ dysfunctions.
• Relative and absolute hypovolemia are compounded by reduced left ventricular contractility to produce hypotension.
• Initially, through an increased heart rate, cardiac output increases to compensate and maintain perfusion pressures, but as this compensatory mechanism becomes exhausted, hypoperfusion and shock may result.
• Impaired tissue oxygen delivery is exacerbated by pericapillary edema.
• It makes oxygen to diffuse a greater distance to reach target cells.
• There is a reduction of capillary diameter due to mural edema and the procoagulant state results in capillary microthrombus formation.

• Decreased blood flow through capillary beds, resulting from a combination of shunting of blood through collateral channels and an increase in blood viscosity secondary to loss of red cell flexibility.
• As a result, organs become hypoxic, even with increased blood flow.
• These abnormalities result in lactic acidosis, cellular dysfunction, and multiorgan failure.
• Cellular energy levels fall as metabolic activity begins to exceed production.
• However, cell death appears to be uncommon in sepsis, implying that cells shut down as part of the systemic response.
• This could explain why relatively few histologic changes are found at autopsy, and the eventual rapid resolution of severe symptoms, such as complete anuria and hypotension, once the systemic inflammation resolves.
• Importantly, heterogeneity is increasingly recognized: molecular profiling and gene expression studies have revealed distinct sepsis subtypes, some resembling macrophage activation–like syndromes, which may respond differently to targeted therapies.

There are no genetic conditions associated with sepsis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]

The process of infection by bacteria or fungi can result in systemic signs and symptoms that are variously described. In rough order of severity, these are bacteremia or fungemia; septicemia; sepsis, severe sepsis or sepsis syndrome; septic shock; refractory septic shock; multiple organ dysfunction syndrome, and death. The condition develops as a response to certain microbial molecules which trigger the production and release of cellular mediators, such as tumor necrosis factors (TNF); these act to stimulate immune response.^[1]

Sepsis is a life-threatening condition, if left untreated it results in death.

Sepsis is caused by a bacterial infection that can begin anywhere in the body. Common places where an infection might start include:

• The bowel (usually seen with peritonitis)
• The kidneys (upper urinary tract infection or pyelonephritis)
• The lining of the brain (meningitis)
• The liver or the gall bladder (cholecystitis)
• The lungs (bacterial pneumonia)
• The skin (cellulitis)
• In children, sepsis may accompany infection of the bone (osteomyelitis).
• In hospitalized patients, common sites of infection include intravenous lines, surgical wounds, surgical drains, and sites of skin breakdown known as bedsores (decubitus ulcers).

Common organisms responsible for sepsis includes:^[2][3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]

Sepsis must be differentiated from other syndromes such as the acute bacterial endocarditis, myocardial ring abscess, subacute bacterial endocarditis and bacterial meningitis.^[1]

Sepsis must be differentiated from other causes of shock and fever based on clinical and hemodynamic findings.

Abbreviations: CO: cardiac output, CVP: central venous pressure, PAD: pulmonary artery diastolic pressure. PAS: pulmonary artery systolic pressure, RVD: right ventricular diastolic pressure.RVS: right ventricular systolic pressure. SVO2: systemic venous oxygen saturation, SVR: systemic vascular resistance.

Other non-infectious causes of systemic inflammatory response syndrome (SIRS) that must be considered include:

• Postoperative recovery
• Penetrating trauma
• Burns
• Transplant rejection
• Hyperthyroidism
• Addisonian crisis
• Blood product transfusion reactions
• Serum sickness
• Immunizations
• CNS infarction or hemorrhages
• Leukemia
• Malignant hyperthermia
• Neuroleptic malignant syndrome
• Serotonergic syndrome
• Delirium tremens
• Metformin lactic acidosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]; Parth Vikram Singh, MBBS[3]

Synonyms and keywords: sepsis syndrome; septic shock; septicemia

The hospitalization rate of those with a principal diagnosis of septicemia or sepsis more than doubled from 2000 through 2008. During the same period, the hospitalization rate for those with septicemia or sepsis as a principal or as a secondary diagnosis increased by 70% from 221 to 377 for every 100,000 people. Reasons for these increases may include an aging population with more chronic illnesses, greater use of invasive procedures, immunosuppressive drugs, chemotherapy, transplantation, and increasing microbial resistance to antibiotics.^[1]

• It is the tenth most common cause of death overall according to data from the Center for Disease Control and Prevention.^{[2] [1]}
• The hospitalization rate of those with a principal diagnosis of septicemia or sepsis more than doubled from 2000 through 2008, increasing from 116 to 240 per 100,000 population.
• During the same period, the hospitalization rate for those with septicemia or sepsis as a principal or as a secondary diagnosis increased by 70% from 221 to 377 for every 100,000 people.
• Reasons for these increases may include an aging population with more chronic illnesses, greater use of invasive procedures, immunosuppressive drugs, chemotherapy, transplantation, and increasing microbial resistance to antibiotics.^[3] Increased coding of these conditions due to greater clinical awareness of septicemia or sepsis^[4] may also have occurred during the period studied.
• On a global scale, the burden of sepsis remains high, with an estimated 48.9 million cases and 11 million deaths annually, of which nearly 85% occur in low- and middle-income countries (LMICs), particularly in sub-Saharan Africa.^[5]

• Only 2% of hospitalizations in 2008 were for septicemia or sepsis, yet they made up 17% of in-hospital deaths.
• In-hospital deaths were more than eight times as likely among patients hospitalized for septicemia or sepsis (17%) compared with other diagnoses (2%). In addition, those hospitalized for septicemia or sepsis were one-half as likely to be discharged home, twice as likely to be transferred to another short-term care facility, and three times as likely to be discharged to long-term care institutions, compared to those with other diagnoses.
• Sepsis may be the cause for up to 50% of hospital deaths^[6][7].

• For those under age 65, 13% of those hospitalized for septicemia or sepsis died in the hospital, compared with 1% of those hospitalized for other conditions.^[1]
• For those aged 65 and over, 20% of septicemia or sepsis hospitalizations ended in death compared with 3% for other hospitalizations.
• Sepsis is common and also more dangerous in elderly, immunocompromised, and critically ill patients.

• More common in African Americans compared to other races in the United States.

• In the United States, sepsis is the leading cause of death in non-coronary ICU patients.

• It is a major cause of death in intensive care units worldwide, with mortality rates that range from 20% for sepsis to 40% for severe sepsis to > 60% for septic shock.
• It occurs in 1%–2% of all hospitalizations, accounts for as much as 25% of intensive care unit (ICU) bed utilization, and its disproportionate impact on LMICs underscores global health inequities.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]

Synonyms and keywords: sepsis syndrome; septic shock; septicemia

Common risk factors in the development of sepsis include elderly people with more chronic illnesses; greater use of invasive procedures, immunosuppressive drugs, chemotherapy, and transplantation; and increasing microbial resistance to antibiotics. Other patients population at increased risk are ICU admits, immunocompromised, bacteremic, with community acquired pneumonia, and with genetic predisposition.^[1][2]

Common risk factors in the development of sepsis are

• Increased age (age >65 years)
• Immunosuppression
• Bacteremia
• Community acquired pneumonia
• Genetic predisposition
• Underlying malignancy
• Hemodialysis
• Alcoholism
• Diabetes mellitus
• Recent surgery or other invasive procedures
• Skin injury
• Indwelling lines or catheters
• Intravenous drug misuse
• Pregnancy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]; Parth Vikram Singh, MBBS[3]

Synonyms and keywords: sepsis syndrome; septic shock; septicemia

There are many complications associated with sepsis, especially because it is a systemic phenomenon. Sepsis is a severe condition, and the prognosis of the patient will depend greatly on the condition and overall health of the patient. Many factors, such as age, hosts immune response, site of infection, type of infection, appropriate antibiotic therapy, and restoration of circulation of perfusion contribute to the overall prognosis.^{[1][2] [3][4][5][6] [7]}

No universal diagnostic test for sepsis yet exists, and studies suggest that nearly one-third of patients treated for bacterial sepsis are later found to have a noninfectious illness.^[8]

If left untreated sepsis can lead to multiorgan failure and eventually death. Even in survivors, high rates of cognitive dysfunction, functional decline, and inability to return to work (e.g., 40% in a Norwegian study) are reported. Persistent immune dysregulation after sepsis is strongly correlated with late mortality.

• Disseminated intravascular coagulation (DIC) can be the result of sepsis.
• Acute tubular necrosis (ATN) leading to acute renal failure, can be the result of hypoperfusion of the kidneys in sepsis (i.e. not enough blood gets to the kidney and they stop working properly). Acute kidney injury occurs in about 30% of patients and about 5% of patients need renal replacement therapy.^[1]
• Arrhythmia is an abnormal heart rhythm; it can be the result of sepsis.
• Ileus or ischemic colitis can be the result (hypoperfusion) or cause of sepsis.
• Multiple organ dysfunction syndrome can be the result of sepsis.
• Meningitis, infection of the tissue that covers the brain and spinal cord, can be a complication or cause of sepsis.
• Osteomyelitis is an infection of the bone; it can be the cause or result of sepsis.
• Endocarditis, infection of the inner surface of heart which is in contact with blood, can also be a complication or cause of sepsis.
• Pyaemia — causes abscesses.

The serum lactate level may be more predictive of outcomes than the serum bicarbonate^[9].

Transitional care interventions, including structured follow-up and multidisciplinary support, have been shown to improve survival and recovery after sepsis (Kowalkowski 2022).^[10]

Mortality can be estimated with the MEDS (Mortality in Emergency Department Sepsis)score. More complicated scores such as the Apache, Sequential Organ Failure Assessment (SOFA), and Logistic Organ Dysfunction System (LODS) can be used as well.^[4][5][6]

The components and their scores for the MEDS are described in the following table

The total score will be added up and that total will correlate to the mortality percentage with a 95% confidence interval. The following are the point ranges associated with various mortality percentages.

• 0-4 points total – 0.6% mortality rate
• 5-7 points total – 5% mortality rate
• 8-12 points total – 19% mortality rate
• 13-15 points total – 32% mortality rate
• 15+ points total – 40% mortality rate

The area under the receiver operating characteristic curve for the MEDs score is 0.92.^[4]

Approximately 12% of of patients with sepsis progress to septic shock within 48 hours. Among variables studied (which did not include procalcitonin, predictors of progression to septic shock were:^[3]

• Nonpersistent hypotension
• Bandemia at least 10%
• Lactate at least 4.0 mmol/L
• Past medical of coronary artery disease
• Female gender

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Robert G. Badgett, M.D.[2]

Synonyms and keywords: sepsis syndrome; septic shock; septicemia

Several entities have instituted mandatory reporting in their jurisdictions. These efforts are consistent with prior recommendations by the Academy of Medicine for mandatory reporting^[1].

Mandatory reporting of sepsis quality measures, “SEP-1” by Centers for Medicare and Medicaid Services was announced 08/2014 and implemented in 10/01/2015 as a value based purchase with the possibility of financial penalties^[8][9][2]. Variations in hospital mortality contributed to the rationale for SEP-1^[10]. As of 2017, 87% of eligible hospitals reported compliance measures with variation in rates of compliance^[11].

Concerns about the reporting is the complexity of determining compliance as the documentation for chart reviews if 120 pages and may require 2-3 hours per chart to review^[2]. The SEP-1 rule has been criticized for focusing on processes of care that are hard to measure rather than more easily measured rates and outcomes^[2]. As an example, abstractions of clinical charts usually disagree over determining “time zero”^[12].

Related is the voluntary Bundled Payments for Care Improvement (BPCI) initiative in 2013^[3]. After the first 9 months of the BPCI, 88 of 2918 eligible hospitals participated in BPCI for sepsis^[4]. No difference was found in the quality or costs of sepsis care^[4].

In 2013, the New York State Department of Health (NYSDOH) began mandatory state-wide reporting of quality measures (Rory’s Regulations)^[5][13][14]. This was in part due to the death in 2012 of Rory Staunton. Implementation was based on SEPSIS-2^[7]. Subsequent reduction in mortality was associated with increased compliance to process measures^[14]. The benefit may be specifically linked to speed of antibiotic administration; however, study of fluids examined when fluids were finished and not when fluids were started^[15].

In a controlled study, the improvement of care in New York exceeded the improvement in control states that were only under the influence of CMS pressure^[6].

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