Sepsis and low blood pressure

Why Sepsis Causes Low Blood Pressure

Sepsis, when severe, can lead to septic shock and death. One reason is bacterial infections which cause systemic reactions in the body also cause our immune system to release cytokines to fight the infection. In a typical infection, the cytokines will dilate the blood vessels at the site of the infection to allow more blood to pass through the area, carrying the cells and mediators needed to fight the bacteria. However, in sepsis, the response involves the entire body with inflammation essentially occurring everywhere.

With systemic response, all blood vessels dilate causing the blood pressure to drop. Instead of assisting in fighting the infection, the body’s response to sepsis actually slows down blood flow making our immune system less effective. The bacteria can damage vital organs and lack of blood flow can spark organ failure. Organ failure and low blood pressure are the two biggest dangers for severe sepsis and septic shock, making it a fatal condition for up to 40-50% of patients.

What Is Septic Shock? Everything to Know About the Complication of Sepsis

How Do Doctors Treat Septic Shock Exactly?

“When a person is in septic shock, treatment is designed not only to address the underlying infection and the body’s response to it, but also to correct the circulatory and metabolic abnormalities,” notes Dr. Roach.

Because of the severity of septic shock, this condition isn’t treatable at home. You will need to be admitted to the ICU. Here, you will continue to receive medication to fight the infection, which you’ll receive intravenously so it gets into your bloodstream quicker. (7)

When you’re diagnosed with sepsis, you’ll likely receive a broad-spectrum antibiotic that is effective against a variety of organisms. Once your doctor identifies the bacteria causing the infection, you’ll receive a more targeted antibiotic. (7)

Treatment differs when bacteria isn’t the cause of an infection. If your doctor determines that septic shock is the result of an underlying fungal or viral infection, you’ll receive an anti-fungal or antiviral medication, respectively.

Because septic shock causes extremely low blood pressure, treatment also focuses on increasing blood volume and blood pressure to avoid permanent organ damage. Therefore, septic shock treatment often involves receiving large amounts of intravenous fluids. Fluid not only helps increase blood pressure and blood flow, it can also prevent dehydration. (8)

Along with large amounts of fluid, your doctor may also give you a corticosteroid to lessen inflammation in your body. Sometimes, vasopressor medications are administered. This medication constricts blood vessels and helps raise blood pressure. (8)

Septic shock can also cause insulin resistance. You may receive insulin therapy while in the hospital to help your body maintain a healthy blood sugar level. (7)

Impaired breathing is also common with septic shock, but, Dr. Brown says, “patients in septic shock are often placed on mechanical ventilators to give their lungs and body rest and the ability to heal.”

You may require oxygen therapy through a face mask or a tube placed down your throat.

Even though medication and fluids are the standard treatments for severe sepsis and septic shock, surgery is sometimes necessary. (7)

Your doctor will conduct multiple tests to identify the source of the infection. This may include a urinalysis to check for urinary tract infections, a wound secretion test, and a mucus secretion test.

Similarly, you may have an X-ray, CT scan, ultrasound, or MRI to check for a perforation (hole) in your gastrointestinal tract or an abscess somewhere in the body. (7)

Surgery can remove an abscess if it’s the source of the infection, or repair a hole that forms in the gastrointestinal tract because of an ulcer, diverticulitis, or another inflammatory condition.

PMC

In the previous issue of Critical Care, Corrêa and colleagues reported on the effects of different target blood pressures during long-term, resuscitated porcine septic shock. Twelve hours after induction of peritonitis by inoculation of autologous feces into the abdominal cavity, animals were randomly assigned to a control group without resuscitation or to treatment groups with resuscitation with crystalloid and colloid fluids together with norepinephrine targeting a mean arterial pressure (MAP) of either 50 to 60 mm Hg (‘low-MAP’) or 75 to 85 mm Hg (‘high-MAP’). Whereas all control animals died within the first 30 hours, 7 out of 8 animals survived in each treatment group at 48 hours after induction of sepsis. The high-MAP group had higher requirements for fluid and, particularly, norepinephrine, whereas low-MAP animals presented with a higher incidence of acute kidney injury (AKI).

Although MAP is a cornerstone of the hemodynamic management of patients with septic shock, its optimal target value is still unknown. Clearly, prolonged phases of hypotension (MAP of less than 60 mm Hg) are associated with increased mortality , and early goal-directed therapy-related improved survival coincided with a higher MAP . Nevertheless, an upper threshold has not been identified: increasing MAP to greater than 70 mm Hg at the expense of a higher vasopressor load coincided with increased mortality in a retrospective analysis . However, in various prospective trials, no signs of excessive vasoconstriction were detected, although MAP values were frequently higher than recommended targets . Moreover, the prospective studies investigating the effects of MAP increments (from 60 to 90 mm Hg) on various outcomes, including renal function, studied only small numbers of already hemodynamically stabilized patients (10 and 28 patients) over short periods of time (105 minutes and 4 hours per MAP level) and reported no changes in kidney function .

What do we learn from the study by Corrêa and colleagues? First of all, the authors have to be commended for using an experimental design that nicely fulfills the criteria of a clinically relevant model, namely (a) lacking resuscitation led to 100% mortality, (b) treatment began 12 hours after the initial aggression, and (c) included antibiotics, protocol-guided mechanical ventilation, fluid resuscitation, and vasopressor treatment. Clearly, the higher incidence of AKI in the low-MAP group agrees well with observational data in patients: Dünser and colleagues observed a direct relation between plasma creatinine and the ‘hourly blood pressure time integral’, and Badin and colleagues reported decreased AKI at 72 hours with a MAP of at least 72 mm Hg, when septic shock patients already had AKI at 6 hours after inclusion in the study. Hence, although long-term renal effects of higher MAP remain unknown, the low MAP-related kidney dysfunction is an important finding, particularly given the strong association between AKI and poor outcome .

Nevertheless, the study cannot definitely answer the question of the optimal target MAP in septic shock. As in most experimental models, the pigs studied were young and ‘healthy’ before the experiment, which is not the case for adult patients admitted for septic shock in intensive care units. Consequently, the optimal MAP derived from such experiments may differ markedly from the level needed in old patients with comorbidities. Clinical settings require a more subtle balance, especially in patients with arterial hypertension or chronic kidney disease or both. It is well known that, in non-septic conditions, hypertension-related histological changes in the small arteries of the kidney alter renal autoregulation. The renal autoregulatory threshold (that is, the threshold MAP, below which renal blood flow becomes directly related to perfusion pressure) is higher in spontaneously hypertensive rats than in healthy controls . Moreover, during sepsis, little is known about the renal autoregulatory threshold, and, finally, we must keep in mind that autoregulatory thresholds may differ between organs . Any beneficial effect of high MAP on the kidney may coincide with harmful effects in other organs with lower autoregulatory threshold (for example, the brain and heart).

What is the ‘take home message’ on the relation between blood pressure and sepsis-induced kidney dysfunction? Clearly, Corrêa and colleagues demonstrated that low-MAP levels were associated with a higher incidence of AKI, even under conditions of a sustained increase in cardiac output. However, the link between MAP level and kidney function is probably more complex than usually considered. On the one hand, Di Giantomasso and colleagues reported that renal failure occurred in hypotensive ewes with sepsis despite increased kidney blood flow. On the other hand, Benes and colleagues elegantly showed that AKI developed in septic pigs despite well-maintained hyperdynamic and normotensive hemodynamics and that this was most likely because of systemic inflammation and oxidative stress. Of note, in that study, MAP was close to the values of the high-MAP group in the present study.

Furthermore, although this study was not designed to answer this question, Corrêa and colleagues raised the issue of the specific effect of norepinephrine. The consequences of the systemic effect of norepinephrine (that is, maintaining an elevated MAP level) cannot be distinguished from its specific intrarenal effect (that is, similar vasoconstrictive action on both afferent and efferent arterioles) . Moreover, this study does not address the question of whether higher MAP level (or higher norepinephrine doses) could also decrease histological injury severity or only improve renal function.

Finally, even in the low-MAP group, severity of shock was moderate (lactate levels did not increase in comparison with baseline, and the arterial base excess decreased to approximately 1 to 2 mmol/L), and only 1 out of 8 animals developed AKI stage 2 (increase in blood creatinine between 2 and 3 times). Unfortunately, as the authors do not report plasma protein or total hemoglobin content, any dilution effect of the higher amount of fluid resuscitation on creatinine concentrations could not be assessed in the high-MAP group. The lacking hemoglobin data leave the reader with another open question: according to the protocol, dobutamine was infused if the mixed venous oxygen saturation (SvO2) was less than 50%. Strikingly, baseline SvO2 values were only 48% and 50% in the two treatment arms, respectively, despite a stroke volume within the normal range. Thus, a contribution of pre-existing anemia cannot be excluded.

In conclusion, this elegant study adds an important brick in the wall. It nicely demonstrates that early hemodynamic intervention on MAP may attenuate the occurrence of AKI solely by increasing renal perfusion pressure. The direct translation to clinical practice is difficult because of the limitations acknowledged by the authors. In patients with septic shock, the SEPSISPAM trial (ClinicalTrial.gov NCT01149278), which has completed recruitment, will most likely answer some of the questions raised by the study by Corrêa and colleagues.

Sepsis

What is sepsis?

Sepsis is an extreme and overwhelming response to an infection anywhere in the body. The organisms that caused the serious infection stimulate the release of substances into the blood that cause widespread inflammation. This quickly leads to organ damage, organ failure, or even death.

There is often a lot of confusion about sepsis due to some related terms that people sometimes use interchangeably. However, they each mean something slightly different. Here is a look at these terms:

  • Sepsis is an extreme response to an infection somewhere in the body, which leads to organ problems. It is possible to have organ problems from sepsis and not know you have an infection. Doctors should consider sepsis as a potential cause for new organ problems.
  • Bacteremia: the presence of bacteria in the blood. This is mainly a lab finding. A healthy immune system normally clears the body of small amounts of bacteria introduced into the bloodstream. But under some circumstances, bacteria in the blood can begin an active infection that can spread throughout the body and organs. Bacteremia can also lead to sepsis.
  • Septicemia is a term some providers may still use to describe a widespread blood infection, blood poisoning, or a bloodstream infection. Bacteria are present, multiplying and spreading in the blood. In fact, septicemia is a narrow term that muddles the discussion and critical nature of sepsis. People incorrectly use the term septicemia in place of sepsis.

The truth is sepsis can occur without bacteria or other detectable microorganisms in the blood. Also, infection anywhere in the body can trigger sepsis.

Sepsis is one of the leading causes of hospital readmissions and hospital-related deaths. Every year, more than a million Americans suffer from sepsis. It can kill 10 to 30% of those affected. The most severe form—septic shock—kills up to 50% of people who develop it. Sepsis is especially dangerous for the elderly, the very young, and people with chronic medical conditions. People who survive it can also develop post-sepsis syndrome, which is characterized by chronic physical and psychological problems.

Anyone can develop sepsis from an infection. This can happen rapidly and unpredictably, so it’s important to know the signs and symptoms. When signs and symptoms develop, it is a medical emergency. Seek immediate medical attention (call 911) for any combination of fever, chills, rapid heart rate, shortness of breath, confusion, or disorientation. Without prompt treatment in a hospital, sepsis can swiftly lead to organ failure and death.

What are the symptoms of sepsis?

There is no single symptom that points to sepsis. Instead, sepsis consists of a combination of symptoms that appear with an infection. Recognizing sepsis symptoms early is vital to prevent organ damage and loss of life.

It’s important to know that most people who develop sepsis are already in the hospital. However, you can develop the condition outside the hospital, such as at home after surgery, after discharge from the hospital, or if you have other risk factors. Remember, you may not even realize you have an infection when sepsis symptoms develop.

How to spot sepsis

Symptoms can include any of the following:

  • Confusion or disorientation
  • Fever or chills
  • Pain or discomfort
  • Rapid heart rate
  • Rash
  • Shortness of breath or rapid breathing
  • Sweaty or clammy skin

Sepsis is progressive. The signs and symptoms can quickly become severe. Signs that the condition is progressing to serious organ problems can include:

  • Difficulty breathing
  • Liver enzyme problems, which is a laboratory finding
  • Low or no urine output
  • Mental status changes

Sepsis can also progress to septic shock, which is the most dangerous form of sepsis. Septic shock occurs when your blood pressure drops rapidly and dangerously low. This can lead to heart failure, other organ failure, and death.

Sepsis, even early sepsis, is a medical emergency. Seek immediate medical attention (call 911) if you suspect sepsis. Sepsis can be fatal in a short amount of time. It is better to be mistaken and call 911 than to delay potentially life-saving medical care.

What causes sepsis?

Sepsis occurs when your body overreacts to an infection. It pumps immune-related substances into your blood. These substances normally help your body fight infections. However, the extreme reaction triggers inflammation throughout your body. This leads to a cascade of events. The blood becomes more prone to clotting and blood vessels become leaky. Blood can’t flow to organs and tissues the way it should. Without adequate blood flow, tissues can’t get oxygen and nutrients. This leads to damage, tissue death, and eventually organ failure and death.

An infection anywhere in the body can lead to sepsis. But there are four types of infections that most commonly lead to sepsis:

  • Abdominal or gut infections
  • Lung infections
  • Skin infections
  • Urinary tract or kidney infections

A variety of microorganisms can cause these infections, including bacteria, fungi and viruses. However, bacteria are the most common culprits.

What are the risk factors for sepsis?

Sepsis can affect anyone. However, certain people have an increased risk of developing sepsis. People who get sepsis at a higher rate compared to the general population include:

  • Adults 65 year of age and older
  • Children younger than one year
  • People with chronic medical conditions, such as cancer, diabetes, or kidney, lung or liver disease
  • People with a compromised or weak immune system, such as those with HIV or AIDS
  • People with wounds including surgical wounds, injuries, or invasive devices such as catheters

Reducing your risk of sepsis

Sepsis can develop from any type of infection, even what appears to be a mild one. It is not always possible to prevent sepsis because you can’t prevent all infections, but you may be able to lower your risk of sepsis by:

  • Caring for wounds and keeping cuts clean
  • Keeping vaccinations up to date and getting adult vaccines as recommended by your doctor
  • Practicing good hygiene including frequent and proper hand washing
  • Treating chronic medical conditions

Ask your doctor about your personal risk of developing sepsis, especially when facing surgery or after hospitalization. Remember that sepsis is often hard to diagnose in the early stages because many things can cause the same symptoms. If you know you have risk factors, tell your doctor if you are concerned about sepsis. Make sure you are familiar with the warning signs if you are at risk or you care for someone at risk. Time is vital once the symptoms begin.

How is sepsis treated?

Sepsis is a medical emergency that requires treatment in a hospital. Sepsis treatment consists of intravenous (IV) antibiotics to halt the infection while supportive measures are administered to keep organs functioning, prevent further damage, and sustain blood pressure. Doctors maintain blood flow to organs and tissues with IV fluids. Supplemental oxygen is also important to make sure the blood flowing to the organs has enough oxygen. When sepsis becomes severe, other treatments may be necessary. This can include kidney dialysis, mechanical breathing machines, and surgery to remove the source of infection or damaged tissues.

Unfortunately, there is no treatment to directly target the extreme immune response that causes sepsis. Doctors use a variety of medicines to try to calm the immune system and support the organs. This can include corticosteroids, insulin for blood sugar control, pain medicines, and medicines to increase blood pressure.

What are the potential complications of sepsis?

It is possible to completely recover from sepsis, especially when it is mild. But blood clots and decreased blood flow can lead to permanent organ or tissue damage in some people. This can lead to amputation and the need for lifelong organ support, such as dialysis or breathing assistance. These problems are more likely to occur in people who already had chronic medical problems before developing sepsis.

People who have recovered from sepsis may also be at increased risk of future infections. Researchers believe sepsis disrupts a person’s normal immune function. This makes infections more likely.

Finally, people who survive sepsis can suffer from post-sepsis syndrome (PSS). Symptoms include:

  • Fatigue, poor concentration, and decreased mental function
  • Hallucinations
  • Low self-esteem
  • Muscle and joint pain
  • Panic attacks
  • Sleep problems, such as insomnia or nightmares

These chronic physical and psychological problems can affect up to 50% of survivors. PSS tends to strike older people and people who spent time in an intensive care unit. Researchers have linked sepsis to a similar disorder, PTSD (post-traumatic stress disorder). If you notice symptoms of PSS that persist, talk with your doctor. Mental health providers can assist you with counseling. Physical therapy and other forms of rehabilitation can also help you recover.

Cause of heart damage in sepsis patients identified

Sepsis is the most common cause of death in hospitalized critically ill people and affects up to 18 million people world-wide annually.

The electrical and mechanical malfunctions of the heart have been poorly understood in sepsis, with underdeveloped clinical management strategies, as a consequence. This new discovery, however, promises to benefit a high number of patients with heart failure or rhythm abnormalities that complicate sepsis.

The team discovered that nuclear proteins, called histones, induce damage to heart muscle cells when released into the blood circulation following extensive cell damage in sepsis.

Blood levels of histones, however, are robust biomarkers that can predict which patients are more likely to develop heart complications.

Dr Yasir Alhamdi, from the University’s Institute of Infection and Global Health, said: “This new discovery has important clinical implications. Firstly, we now provide a much-needed explanation for why cardiac injury markers are high in sepsis.

“Secondly, histone levels in the blood can potentially be used at an early stage to predict which septic patients are at highest risk of developing deadly heart complications. This can improve overall management of patients with sepsis worldwide.”

The research team has also developed and tested specific antibodies that can directly neutralise the toxic effects of histones in the blood circulation and found that their use can significantly prevent the development of heart complications in sepsis.

Professor Cheng-Hock Toh, from the University’s Institute of Infection and Global Health, said: “The translational impact to patients with sepsis can extend beyond biomarker prediction of heart complications, to novel targeted treatment for improved survival.

“This discovery could therefore enable us to better stratify patients for more precise and personalised treatment in sepsis.”

The study was funded by the British Heart Foundation (BHF) and the National Institute of Health Research (NIHR). The paper, ‘Circulating histones are major mediators of cardiac injury in patients with sepsis,’ is published in the journal Critical Care Medicine.

What are septic shock and sepsis? The facts behind these deadly conditions

Most Americans have never heard of it, but according to recent federal data, sepsis is the most expensive cause of hospitalization in the U.S., and is now the most common cause of ICU admission among older Americans.

Sepsis is a complication of infection that leads to organ failure. More than one million patients are hospitalized for sepsis each year. This is more than the number of hospitalizations for heart attack and stroke combined. People with chronic medical conditions, such as neurological disease, cancer, chronic lung disease and kidney disease, are at particular risk for developing sepsis.

And it is deadly. Between one in eight and one in four patients with sepsis will die during hospitalization – as most notably Muhammad Ali did in June 2016. In fact sepsis contributes to one-third to one-half of all in-hospital deaths. Despite these grave consequences, fewer than half of Americans know what the word sepsis means.

What is sepsis and why is it so dangerous?

Sepsis a severe health problem sparked by your body’s reaction to infection. When you get an infection, your body fights back, releasing chemicals into the bloodstream to kill the harmful bacteria or viruses. When this process works the way it is supposed to, your body takes care of the infection and you get better. With sepsis, the chemicals from your body’s own defenses trigger inflammatory responses, which can impair blood flow to organs, like the brain, heart or kidneys. This in turn can lead to organ failure and tissue damage.

At its most severe, the body’s response to infection can cause dangerously low blood pressure. This is called septic shock.

Sepsis can result from any type of infection. Most commonly, it starts as a pneumonia, urinary tract infection or intra-abdominal infection such as appendicitis. It is sometimes referred to as “blood poisoning,” but this is an outdated term. Blood poisoning is an infection present in the blood, while sepsis refers to the body’s response to any infection, wherever it is.

Once a person is diagnosed with sepsis, she will be treated with antibiotics, IV fluids and support for failing organs, such as dialysis or mechanical ventilation. This usually means a person needs to be hospitalized, often in an ICU. Sometimes the source of the infection must be removed, as with appendicitis or an infected medical device.

It can be difficult to distinguish sepsis from other diseases that can make one very sick, and there is no lab test that can confirm sepsis. Many conditions can mimic sepsis, including severe allergic reactions, bleeding, heart attacks, blood clots and medication overdoses. Sepsis requires particular prompt treatments, so getting the diagnosis right matters.

The revolving door of sepsis care

As recently as a decade ago, doctors believed that sepsis patients were out of the woods if they could just survive to hospital discharge. But that isn’t the case – 40 percent of sepsis patients go back into the hospital within just three months of heading home, creating a “revolving door” that gets costlier and riskier each time, as patients get weaker and weaker with each hospital stay. Sepsis survivors also have an increased risk of dying for months to years after the acute infection is cured.

If sepsis wasn’t bad enough, it can lead to another health problem: Post-Intensive Care Syndrome (PICS), a chronic health condition that arises from critical illness. Common symptoms include weakness, forgetfulness, anxiety and depression.

Post-Intensive Care Syndrome and frequent hospital readmissions mean that we have dramatically underestimated how much sepsis care costs. On top of the US$5.5 billion we now spend on initial hospitalization for sepsis, we must add untold billions in rehospitalizations, nursing home and professional in-home care, and unpaid care provided by devoted spouses and families at home.

Unfortunately, progress in improving sepsis care has lagged behind improvements in cancer and heart care, as attention has shifted to the treatment of chronic diseases. However, sepsis remains a common cause of death in patients with chronic diseases. One way to help reduce the death toll of these chronic diseases may be to improve our treatment of sepsis.

Rethinking sepsis identification

Raising public awareness increases the likelihood that patients will get to the hospital quickly when they are developing sepsis. This in turn allows prompt treatment, which lowers the risk of long-term problems.

Beyond increasing public awareness, doctors and policymakers are also working to improve the care of sepsis patients in the hospital.

For instance, a new sepsis definition was released by several physician groups in February 2016. The goal of this new definition is to better distinguish people with a healthy response to infection from those who are being harmed by their body’s response to infection.

As part of the sepsis redefinition process, the physician groups also developed a new prediction tool called qSOFA. This instrument identifies patients with infection who are at high risk of death or prolonged intensive care. The tools uses just three factors: thinking much less clearly than usual, quick breathing and low blood pressure. Patients with infection and two or more of these factors are at high risk of sepsis. In contrast to prior methods of screening patients at high risk of sepsis, the new qSOFA tool was developed through examining millions of patient records.

Life after sepsis

Even with great inpatient care, some survivors will still have problems after sepsis, such as memory loss and weakness.

Doctors are wrestling with how to best care for the growing number of sepsis survivors in the short and long term. This is no easy task, but there are several exciting developments in this area.

The Society of Critical Care Medicine’s THRIVE initiative is now building a network of support groups for patients and families after critical illness. THRIVE will forge new ways for survivors to work with each other, like how cancer patients provide each other advice and support.

As medical care is increasingly complex, many doctors contribute to a patient’s care for just a week or two. Electronic health records let doctors see how the sepsis hospitalization fits into the broader picture – which in turn helps doctors counsel patients and family members on what to expect going forward.

The high number of repeat hospitalizations after sepsis suggests another opportunity for improving care. We could analyze data about patients with sepsis to target the right interventions to each individual patient.

Better care through better policy

In 2012, New York state passed regulations to require every hospital to have a formal plan for identifying sepsis and providing prompt treatment. It is too early to tell if this is a strong enough intervention to make things better. However, it serves as a clarion call for hospitals to end the neglect of sepsis.

The Centers for Medicare & Medicaid Services (CMS) are also working to improve sepsis care. Starting in 2017, CMS will adjust hospital payments by quality of sepsis treatment. Hospitals with good report cards will be paid more, while hospitals with poor marks will be paid less.

To judge the quality of sepsis care, CMS will require hospitals to publicly report compliance with National Quality Forum’s “Sepsis Management Bundle.” This includes a handful of proven practices such as heavy-duty antibiotics and intravenous fluids.

While policy fixes are notorious for producing unintended consequences, the reporting mandate is certainly a step in the right direction. It would be even better if the mandate focused on helping hospitals work collaboratively to improve their detection and treatment of sepsis.

Right now, sepsis care varies greatly from hospital to hospital, and patient to patient. But as data, dollars and awareness converge, we may be at a tipping point that will help patients get the best care, while making the best use of our health care dollars.

This is an updated version of an article originally published on July 1, 2015. You can read the original version here.

Hallie Prescott, Assistant Professor in Internal Medicine, University of Michigan and Theodore Iwashyna, Associate Professor, University of Michigan

This article was originally published on The Conversation. Read the original article.

The impact of a multifaceted intervention including sepsis electronic alert system and sepsis response team on the outcomes of patients with sepsis and septic shock

  1. 1.

    Levy MM, Artigas A, Phillips GS, Rhodes A, Beale R, Osborn T, et al. Outcomes of the Surviving Sepsis Campaign in intensive care units in the USA and Europe: a prospective cohort study. Lancet Infect Dis. 2012;12(12):919–24.

    • Article
    • PubMed
    • Google Scholar
  2. 2.

    Phua J, Koh Y, Du B, Tang YQ, Divatia JV, Tan CC, et al. Management of severe sepsis in patients admitted to Asian intensive care units: prospective cohort study. BMJ. 2011;342:d3245.

    • Article
    • PubMed
    • PubMed Central
    • Google Scholar
  3. 3.

    Jones AE, Focht A, Horton JM, Kline JA. Prospective external validation of the clinical effectiveness of an emergency department-based early goal-directed therapy protocol for severe sepsis and septic shock. Chest. 2007;132(2):425–32.

    • Article
    • PubMed
    • PubMed Central
    • Google Scholar
  4. 4.

    Kortgen A, Niederprum P, Bauer M. Implementation of an evidence-based “standard operating procedure” and outcome in septic shock. Crit Care Med. 2006;34(4):943–9.

    • Article
    • PubMed
    • Google Scholar
  5. 5.

    Lin SM, Huang CD, Lin HC, Liu CY, Wang CH, Kuo HP. A modified goal-directed protocol improves clinical outcomes in intensive care unit patients with septic shock: a randomized controlled trial. Shock. 2006;26(6):551–7.

    • Article
    • PubMed
    • Google Scholar
  6. 6.

    Nguyen HB, Corbett SW, Steele R, Banta J, Clark RT, Hayes SR, et al. Implementation of a bundle of quality indicators for the early management of severe sepsis and septic shock is associated with decreased mortality. Crit Care Med. 2007;35(4):1105–12.

    • Article
    • PubMed
    • Google Scholar
  7. 7.

    Micek ST, Roubinian N, Heuring T, Bode M, Williams J, Harrison C, et al. Before-after study of a standardized hospital order set for the management of septic shock. Crit Care Med. 2006;34(11):2707–13.

    • Article
    • PubMed
    • Google Scholar
  8. 8.

    Sebat F, Musthafa AA, Johnson D, Kramer AA, Shoffner D, Eliason M, et al. Effect of a rapid response system for patients in shock on time to treatment and mortality during 5 years. Crit Care Med. 2007;35(11):2568–75.

    • Article
    • PubMed
    • Google Scholar
  9. 9.

    Shapiro NI, Howell MD, Talmor D, Lahey D, Ngo L, Buras J, et al. Implementation and outcomes of the Multiple Urgent Sepsis Therapies (MUST) protocol. Crit Care Med. 2006;34(4):1025–32.

    • Article
    • PubMed
    • Google Scholar
  10. 10.

    Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013;41(2):580–637.

    • Article
    • PubMed
    • Google Scholar
  11. 11.

    Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R, et al. Surviving Sepsis Campaign: international guidelines for management of sepsis and septic shock: 2016. Intensive Care Med. 2017;43:304–77.

    • Article
    • PubMed
    • Google Scholar
  12. 12.

    National Quality Forum: severe sepsis and septic shock: management bundle. http://www.qualityforum.org/Home.aspx.

  13. 13.

    World Sepsis Day. http://www.world-sepsis-day.org.

  14. 14.

    Sepsis UK Core Team. http://sepsistrust.org/meet-the-team/sepsis-uk-core-team/.

  15. 15.

    NSW Health System: Clinical Excellence Commission. http://www.cec.health.nsw.gov.au/programs/sepsis.

  16. 16.

    College of Emergency Medicine: standards for severe sepsis and septic shock in adults. http://www.collemergencymed.ac.uk/code/document.asp?id=4717.

  17. 17.

    Jones AE. Evidence-based therapies for sepsis care in the emergency department: striking a balance between feasibility and necessity. Acad Emerg Med. 2006;13(1):82–3.

    • Article
    • PubMed
    • Google Scholar
  18. 18.

    Carlbom DJ, Rubenfeld GD. Barriers to implementing protocol-based sepsis resuscitation in the emergency department–results of a national survey. Crit Care Med. 2007;35(11):2525–32.

    • Article
    • PubMed
    • Google Scholar
  19. 19.

    Jones AE, Shapiro NI, Roshon M. Implementing early goal-directed therapy in the emergency setting: the challenges and experiences of translating research innovations into clinical reality in academic and community settings. Acad Emerg Med. 2007;14(11):1072–8.

    • Article
    • PubMed
    • PubMed Central
    • Google Scholar
  20. 20.

    Wang Z, Xiong Y, Schorr C, Dellinger RP. Impact of sepsis bundle strategy on outcomes of patients suffering from severe sepsis and septic shock in china. J Emerg Med. 2013;44(4):735–41.

    • Article
    • PubMed
    • Google Scholar
  21. 21.

    Na S, Kuan WS, Mahadevan M, Li CH, Shrikhande P, Ray S, et al. Implementation of early goal-directed therapy and the surviving sepsis campaign resuscitation bundle in Asia. Int J Qual Health Care. 2012;24(5):452–62.

    • Article
    • PubMed
    • Google Scholar
  22. 22.

    Ferrer R, Artigas A, Levy MM, Blanco J, Gonzalez-Diaz G, Garnacho-Montero J, et al. Improvement in process of care and outcome after a multicenter severe sepsis educational program in Spain. JAMA. 2008;299(19):2294–303.

    • CAS
    • Article
    • PubMed
    • Google Scholar
  23. 23.

    Castellanos-Ortega A, Suberviola B, Garcia-Astudillo LA, Holanda MS, Ortiz F, Llorca J, et al. Impact of the Surviving Sepsis Campaign protocols on hospital length of stay and mortality in septic shock patients: results of a three-year follow-up quasi-experimental study. Crit Care Med. 2010;38(4):1036–43.

    • Article
    • PubMed
    • Google Scholar
  24. 24.

    Levy MM, Dellinger RP, Townsend SR, Linde-Zwirble WT, Marshall JC, Bion J, et al. The Surviving Sepsis Campaign: results of an international guideline-based performance improvement program targeting severe sepsis. Intensive Care Med. 2010;36(2):222–31.

    • Article
    • PubMed
    • PubMed Central
    • Google Scholar
  25. 25.

    Giuliano KK, Lecardo M, Staul L. Impact of protocol watch on compliance with the surviving sepsis campaign. Am J Crit Care. 2011;20(4):313–21.

    • Article
    • PubMed
    • Google Scholar
  26. 26.

    Schramm GE, Kashyap R, Mullon JJ, Gajic O, Afessa B. Septic shock: a multidisciplinary response team and weekly feedback to clinicians improve the process of care and mortality. Crit Care Med. 2011;39(2):252–8.

    • Article
    • PubMed
    • Google Scholar
  27. 27.

    Laguna-Perez A, Chilet-Rosell E, Delgado Lacosta M, Alvarez-Dardet C, Uris Selles J, Munoz-Mendoza CL. Clinical pathway intervention compliance and effectiveness when used in the treatment of patients with severe sepsis and septic shock at an Intensive Care Unit in Spain. Rev Lat Am Enfermagem. 2012;20(4):635–43.

    • Article
    • PubMed
    • Google Scholar
  28. 28.

    Shiramizo SC, Marra AR, Durao MS, Paes AT, Edmond MB, Pavao dos Santos OF. Decreasing mortality in severe sepsis and septic shock patients by implementing a sepsis bundle in a hospital setting. PLoS ONE. 2011;6(11):e26790.

    • CAS
    • Article
    • PubMed
    • PubMed Central
    • Google Scholar
  29. 29.

    Grimshaw JM, Thomas RE, MacLennan G, Fraser C, Ramsay CR, Vale L, et al. Effectiveness and efficiency of guideline dissemination and implementation strategies. Health Technol Assess. 2004;8(6):iii–iv, 1–72.

  30. 30.

    Cheung A, Weir M, Mayhew A, Kozloff N, Brown K, Grimshaw J. Overview of systematic reviews of the effectiveness of reminders in improving healthcare professional behavior. Syst Rev. 2012;1:36.

    • Article
    • PubMed
    • PubMed Central
    • Google Scholar
  31. 31.

    Davis DA, Taylor-Vaisey A. Translating guidelines into practice. A systematic review of theoretic concepts, practical experience and research evidence in the adoption of clinical practice guidelines. CMAJ. 1997;157(4):408–16.

    • CAS
    • PubMed
    • PubMed Central
    • Google Scholar
  32. 32.

    Sawyer AM, Deal EN, Labelle AJ, Witt C, Thiel SW, Heard K, et al. Implementation of a real-time computerized sepsis alert in nonintensive care unit patients. Crit Care Med. 2011;39(3):469–73.

    • Article
    • PubMed
    • Google Scholar
  33. 33.

    Meurer WJ, Smith BL, Losman ED, Sherman D, Yaksich JD, Jared JD, et al. Real-time identification of serious infection in geriatric patients using clinical information system surveillance. J Am Geriatr Soc. 2009;57(1):40–5.

    • Article
    • PubMed
    • Google Scholar
  34. 34.

    Nelson JL, Smith BL, Jared JD, Younger JG. Prospective trial of real-time electronic surveillance to expedite early care of severe sepsis. Ann Emerg Med. 2011;57(5):500–4.

    • Article
    • PubMed
    • Google Scholar
  35. 35.

    Arabi Y, Alshimemeri A, Taher S. Weekend and weeknight admissions have the same outcome of weekday admissions to an intensive care unit with onsite intensivist coverage. Crit Care Med. 2006;34(3):605–11.

    • Article
    • PubMed
    • Google Scholar
  36. 36.

    Al-Qahtani S, Al-Dorzi HM, Tamim HM, Hussain S, Fong L, Taher S, et al. Impact of an intensivist-led multidisciplinary extended rapid response team on hospital-wide cardiopulmonary arrests and mortality. Crit Care Med. 2013;41(2):506–17.

    • Article
    • PubMed
    • Google Scholar
  37. 37.

    Bullard MJ, Unger B, Spence J, Grafstein E. Revisions to the Canadian Emergency Department Triage and Acuity Scale (CTAS) adult guidelines. CJEM. 2008;10(2):136–51.

    • Article
    • PubMed
    • Google Scholar
  38. 38.

    Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al. The third international consensus definitions for sepsis and septic shock (sepsis-3). JAMA. 2016;315(8):801–10.

    • CAS
    • Article
    • PubMed
    • PubMed Central
    • Google Scholar
  39. 39.

    Dellinger RP, Levy MM, Carlet JM, Bion J, Parker MM, Jaeschke R, et al. Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med. 2008;36(1):296–327.

    • Article
    • PubMed
    • Google Scholar
  40. 40.

    Mouncey PR, Osborn TM, Power GS, Harrison DA, Sadique MZ, Grieve RD, et al. Trial of early, goal-directed resuscitation for septic shock. N Engl J Med. 2015;372(14):1301–11.

    • CAS
    • Article
    • PubMed
    • Google Scholar
  41. 41.

    ARISE Investigators; ANZICS Clinical Trials Group, Peake SL, Delaney A, Bailey M, Bellomo R, et al. Goal-directed resuscitation for patients with early septic shock. N Engl J Med. 2014;371(16):1496–506.

    • Article
    • Google Scholar
  42. 42.

    Pro CI, Yealy DM, Kellum JA, Huang DT, Barnato AE, Weissfeld LA, et al. A randomized trial of protocol-based care for early septic shock. N Engl J Med. 2014;370(18):1683–93.

    • Article
    • Google Scholar
  43. 43.

    Dellinger RP, Carlet JM, Masur H, Gerlach H, Calandra T, Cohen J, et al. Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Crit Care Med. 2004;32(3):858–73.

    • Article
    • PubMed
    • Google Scholar
  44. 44.

    Lecumberri R, Marques M, Diaz-Navarlaz MT, Panizo E, Toledo J, Garcia-Mouriz A, et al. Maintained effectiveness of an electronic alert system to prevent venous thromboembolism among hospitalized patients. Thromb Haemost. 2008;100(4):699–704.

    • CAS
    • PubMed
    • Google Scholar
  45. 45.

    Bradley EH, Curry LA, Webster TR, Mattera JA, Roumanis SA, Radford MJ, et al. Achieving rapid door-to-balloon times: how top hospitals improve complex clinical systems. Circulation. 2006;113(8):1079–85.

    • Article
    • PubMed
    • Google Scholar
  46. 46.

    Hamidon BB, Dewey HM. Impact of acute stroke team emergency calls on in-hospital delays in acute stroke care. J Clin Neurosci. 2007;14(9):831–4.

    • CAS
    • Article
    • PubMed
    • Google Scholar
  47. 47.

    Vernon DD, Furnival RA, Hansen KW, Diller EM, Bolte RG, Johnson DG, et al. Effect of a pediatric trauma response team on emergency department treatment time and mortality of pediatric trauma victims. Pediatrics. 1999;103(1):20–4.

    • CAS
    • Article
    • PubMed
    • Google Scholar
  48. 48.

    Lilly CM. The ProCESS trial—a new era of sepsis management. N Engl J Med. 2014;370:1750-1.

    • CAS
    • Article
    • PubMed
    • Google Scholar
  49. 49.

    Berg GM, Vasquez DG, Hale LS, Nyberg SM, Moran DA. Evaluation of process variations in noncompliance in the implementation of evidence-based sepsis care. J Healthc Qual. 2013;35(1):60–9.

    • Article
    • PubMed
    • Google Scholar
  50. 50.

    Maher L, Gustafson D, Evans A. NHS sustainability model and guide. NHS Institute for Innovation and Improvement. 2005.

Clinical Resources

  • Bundlesexternal icon (Surviving Sepsis Campaign)
  • Severe Sepsis Bundlesexternal icon (IHI – free registration required)

Education and Training

  • A Matter of Life and Death: How States Are Tackling Sepsis as Public Policyexternal icon (Association of State and Territorial Health Officials Public Health Review podcast)
  • Early Recognition and Treatmentexternal icon (American College of Emergency Physicians)
  • Surviving Sepsis Campaign, The Takeaways external icon (Medscape Expert Commentary)
  • Webcasts, Presentations, Podcasts, Videosexternal icon (Surviving Sepsis Campaign)
  • Harnessing the Home Care System for Early Sepsis Recognition & Interventionexternal icon (Quality Improvement Organizations)
  • Sepsis Standard Work: Improving Compliance with Early Recognition and Management of Perinatal Sepsis and Detailed Continuing Education Information pdf icon
  • Empowering Nurses for Early Sepsis Recognition
  • Advances in Sepsis: Protecting Patients Throughout the Lifespan
  • Think Sepsis and Act Fast external icon (Medscape Expert Commentary)

Sepsis Screening and Assessment Tools

About the author

Leave a Reply

Your email address will not be published. Required fields are marked *