User login
Clinical Guidelines: Hospital-acquired and ventilator-associated pneumonia
Hospital-acquired pneumonia (HAP) is pneumonia that presents at least 48 hours after admission to the hospital. In contrast, ventilator-associated pneumonia (VAP), is pneumonia that clinically presents 48 hours after endotracheal intubation. Together, these are some of the most common hospital-acquired infections in the United States and pose a considerable burden on hospitals nationwide.
The Infectious Diseases Society of America (IDSA) and the American Thoracic Society (ATS) recently updated their management guidelines for HAP and VAP with a goal of striking a balance between providing appropriate early antibiotic coverage and avoiding unnecessary treatment that can lead to adverse effects such as Clostridium difficile infections and development of antibiotic resistance.1 This update eliminated the concept of Healthcare Associated Pneumonia (HCAP), often used for patients in skilled care facilities, because newer evidence has shown that patients who had met these criteria did not have a higher incidence of multidrug resistant pathogens; rather, they have microbial etiologies and sensitivities that are similar to adults with community acquired pneumonia (CAP).
Hospital-acquired pneumonia
Reasons to cover for MRSA in HAP:
Risk factors:
• IV antibiotic treatment within 90 days
• Treatment in a unit where the prevalence of MRSA is greater than 20% or unknown
• Prior detection of MRSA by culture or nonculture screening (weaker risk factor)
High risk of mortality: • Septic shock
• Need for ventilator support
MRSA should be covered with use of either vancomycin or linezolid in these cases.
In addition, patients with HAP should be covered for Pseudomonas aeruginosa and other gram-negative bacilli. For patients with risk factors for pseudomonas or other gram-negative infection or a high risk for mortality, then two antipseudomonal antibiotics from different classes are recommended, such as piperacillin-tazobactam/tobramycin or cefepime/amikacin.
Use two antipseudomonal antibiotics in HAP if the patient has these risk factors:
Pseudomonas risk factors:
• IV antibiotic treatment within 90 days
• Structural lung disease increasing the risk of gram-negative infection (bronchiectasis, cystic fibrosis)
• High-quality gram stain from respiratory specimen showing predominant and numerous gram-negative bacilli
High risk of mortality:
• Septic shock
• Need for ventilator support
Ventilator-associated pneumonia
General management of VAP is similar to HAP in that empiric treatment should be tailored to the local distribution and susceptibilities of pathogens based on each hospital’s antibiogram. All regimens should cover for S. aureus, P. aeruginosa, and other gram-negative bacilli based on the risk of mortality associated with the need for ventilator support. MSSA should be covered for VAP unless the patient has methicillin-resistant risk factors (see below).
MRSA should be covered for VAP if:
• Patient has had IV antibiotic use within past 90 days
• Hospital unit has greater than 10%-20% of S. aureus isolates are MRSA or MRSA prevalence unknown
Only one antipseudomonal agent should be used unless there are one of the following characteristics present, as described below.
Use two antipseudomonal agents in VAP if:
• Prior IV antibiotic use within 90 days
• Septic shock at time of VAP
• Acute respiratory distress syndrome preceding VAP
• 5 or more days of hospitalization prior to the occurrence of VAP
• Acute renal replacement therapy prior to VAP onset
• Greater than 10% of gram-negative isolates are resistant to an agent being considered for monotherapy
• Local antibiotic susceptibility rates unknown
In both HAP and VAP, antibiotics should be de-escalated to those with a narrower spectrum after initial empiric therapy, ideally within 72 hours and based on sputum or blood culture results. The guidelines support obtaining noninvasive sputum cultures in patients with VAP (endotracheal aspirates) and HAP (spontaneous expectoration, induced sputum, or nasotracheal suctioning in a patient who is unable to cooperate to produce a sputum sample). Patients who are improving clinically may be switched to appropriate oral therapy based on the susceptibility of an identified organism. Another key change is that of the standard duration of therapy. Previously, patients were treated for up to 2-3 weeks with antibiotics. The new IDSA/ATS guidelines recommend that patients should be treated with 7 days of antibiotics rather than a longer course.
The bottom line
Empiric therapy for HAP and VAP should be tailored to each hospital’s local pathogen distribution and antimicrobial susceptibilities, as detailed in an antibiogram. In HAP and VAP, empiric antibiotics should cover for S. aureus, but it only needs to target MRSA if risk factors are present, prevalence is greater than 20% or unknown, and – if HAP – a high risk of mortality. P. aeruginosa and other gram-negative bacilli should also be covered in empiric regimens. Dual antipseudomonal antibiotics is only recommended to be used in HAP if there are specific pseudomonal risk factors or a high risk of mortality. They should be used in VAP if there are multidrug-resistant risk factors present or there is a high/unknown prevalence of resistant organisms. All antibiotic regimens should be deescalated rather than maintained, and both HAP and VAP patients ought to be treated for 7 days.
References
1. Kalil AC, Metersky ML, Klompas M, et al. Management of Adults With Hospital-acquired and Ventilator-associated Pneumonia: 2016 Clinical Practice Guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin Infect Dis. 2016 Sep 1;63(5):557-82.
2. Beardsley JR, Williamson JC, Johnson JW, Ohl CA, Karchmer TB, Bowton DL. Using local microbiologic data to develop institution-specific guidelines for the treatment of hospital-acquired pneumonia. Chest. 2006 Sep;130(3):787-93.
Dr. Botti is a second-year resident in the family medicine residency program department of family and community medicine at Jefferson Medical College, Philadelphia. Dr. Mills is assistant residency program director and assistant professor in the department of family and community medicine and department of physiology at Jefferson Medical College, Philadelphia. Dr. Skolnik is associate director of the family medicine residency program at Abington (Pa.) Memorial Hospital and professor of family and community medicine at Temple University, Philadelphia.
Hospital-acquired pneumonia (HAP) is pneumonia that presents at least 48 hours after admission to the hospital. In contrast, ventilator-associated pneumonia (VAP), is pneumonia that clinically presents 48 hours after endotracheal intubation. Together, these are some of the most common hospital-acquired infections in the United States and pose a considerable burden on hospitals nationwide.
The Infectious Diseases Society of America (IDSA) and the American Thoracic Society (ATS) recently updated their management guidelines for HAP and VAP with a goal of striking a balance between providing appropriate early antibiotic coverage and avoiding unnecessary treatment that can lead to adverse effects such as Clostridium difficile infections and development of antibiotic resistance.1 This update eliminated the concept of Healthcare Associated Pneumonia (HCAP), often used for patients in skilled care facilities, because newer evidence has shown that patients who had met these criteria did not have a higher incidence of multidrug resistant pathogens; rather, they have microbial etiologies and sensitivities that are similar to adults with community acquired pneumonia (CAP).
Hospital-acquired pneumonia
Reasons to cover for MRSA in HAP:
Risk factors:
• IV antibiotic treatment within 90 days
• Treatment in a unit where the prevalence of MRSA is greater than 20% or unknown
• Prior detection of MRSA by culture or nonculture screening (weaker risk factor)
High risk of mortality: • Septic shock
• Need for ventilator support
MRSA should be covered with use of either vancomycin or linezolid in these cases.
In addition, patients with HAP should be covered for Pseudomonas aeruginosa and other gram-negative bacilli. For patients with risk factors for pseudomonas or other gram-negative infection or a high risk for mortality, then two antipseudomonal antibiotics from different classes are recommended, such as piperacillin-tazobactam/tobramycin or cefepime/amikacin.
Use two antipseudomonal antibiotics in HAP if the patient has these risk factors:
Pseudomonas risk factors:
• IV antibiotic treatment within 90 days
• Structural lung disease increasing the risk of gram-negative infection (bronchiectasis, cystic fibrosis)
• High-quality gram stain from respiratory specimen showing predominant and numerous gram-negative bacilli
High risk of mortality:
• Septic shock
• Need for ventilator support
Ventilator-associated pneumonia
General management of VAP is similar to HAP in that empiric treatment should be tailored to the local distribution and susceptibilities of pathogens based on each hospital’s antibiogram. All regimens should cover for S. aureus, P. aeruginosa, and other gram-negative bacilli based on the risk of mortality associated with the need for ventilator support. MSSA should be covered for VAP unless the patient has methicillin-resistant risk factors (see below).
MRSA should be covered for VAP if:
• Patient has had IV antibiotic use within past 90 days
• Hospital unit has greater than 10%-20% of S. aureus isolates are MRSA or MRSA prevalence unknown
Only one antipseudomonal agent should be used unless there are one of the following characteristics present, as described below.
Use two antipseudomonal agents in VAP if:
• Prior IV antibiotic use within 90 days
• Septic shock at time of VAP
• Acute respiratory distress syndrome preceding VAP
• 5 or more days of hospitalization prior to the occurrence of VAP
• Acute renal replacement therapy prior to VAP onset
• Greater than 10% of gram-negative isolates are resistant to an agent being considered for monotherapy
• Local antibiotic susceptibility rates unknown
In both HAP and VAP, antibiotics should be de-escalated to those with a narrower spectrum after initial empiric therapy, ideally within 72 hours and based on sputum or blood culture results. The guidelines support obtaining noninvasive sputum cultures in patients with VAP (endotracheal aspirates) and HAP (spontaneous expectoration, induced sputum, or nasotracheal suctioning in a patient who is unable to cooperate to produce a sputum sample). Patients who are improving clinically may be switched to appropriate oral therapy based on the susceptibility of an identified organism. Another key change is that of the standard duration of therapy. Previously, patients were treated for up to 2-3 weeks with antibiotics. The new IDSA/ATS guidelines recommend that patients should be treated with 7 days of antibiotics rather than a longer course.
The bottom line
Empiric therapy for HAP and VAP should be tailored to each hospital’s local pathogen distribution and antimicrobial susceptibilities, as detailed in an antibiogram. In HAP and VAP, empiric antibiotics should cover for S. aureus, but it only needs to target MRSA if risk factors are present, prevalence is greater than 20% or unknown, and – if HAP – a high risk of mortality. P. aeruginosa and other gram-negative bacilli should also be covered in empiric regimens. Dual antipseudomonal antibiotics is only recommended to be used in HAP if there are specific pseudomonal risk factors or a high risk of mortality. They should be used in VAP if there are multidrug-resistant risk factors present or there is a high/unknown prevalence of resistant organisms. All antibiotic regimens should be deescalated rather than maintained, and both HAP and VAP patients ought to be treated for 7 days.
References
1. Kalil AC, Metersky ML, Klompas M, et al. Management of Adults With Hospital-acquired and Ventilator-associated Pneumonia: 2016 Clinical Practice Guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin Infect Dis. 2016 Sep 1;63(5):557-82.
2. Beardsley JR, Williamson JC, Johnson JW, Ohl CA, Karchmer TB, Bowton DL. Using local microbiologic data to develop institution-specific guidelines for the treatment of hospital-acquired pneumonia. Chest. 2006 Sep;130(3):787-93.
Dr. Botti is a second-year resident in the family medicine residency program department of family and community medicine at Jefferson Medical College, Philadelphia. Dr. Mills is assistant residency program director and assistant professor in the department of family and community medicine and department of physiology at Jefferson Medical College, Philadelphia. Dr. Skolnik is associate director of the family medicine residency program at Abington (Pa.) Memorial Hospital and professor of family and community medicine at Temple University, Philadelphia.
Hospital-acquired pneumonia (HAP) is pneumonia that presents at least 48 hours after admission to the hospital. In contrast, ventilator-associated pneumonia (VAP), is pneumonia that clinically presents 48 hours after endotracheal intubation. Together, these are some of the most common hospital-acquired infections in the United States and pose a considerable burden on hospitals nationwide.
The Infectious Diseases Society of America (IDSA) and the American Thoracic Society (ATS) recently updated their management guidelines for HAP and VAP with a goal of striking a balance between providing appropriate early antibiotic coverage and avoiding unnecessary treatment that can lead to adverse effects such as Clostridium difficile infections and development of antibiotic resistance.1 This update eliminated the concept of Healthcare Associated Pneumonia (HCAP), often used for patients in skilled care facilities, because newer evidence has shown that patients who had met these criteria did not have a higher incidence of multidrug resistant pathogens; rather, they have microbial etiologies and sensitivities that are similar to adults with community acquired pneumonia (CAP).
Hospital-acquired pneumonia
Reasons to cover for MRSA in HAP:
Risk factors:
• IV antibiotic treatment within 90 days
• Treatment in a unit where the prevalence of MRSA is greater than 20% or unknown
• Prior detection of MRSA by culture or nonculture screening (weaker risk factor)
High risk of mortality: • Septic shock
• Need for ventilator support
MRSA should be covered with use of either vancomycin or linezolid in these cases.
In addition, patients with HAP should be covered for Pseudomonas aeruginosa and other gram-negative bacilli. For patients with risk factors for pseudomonas or other gram-negative infection or a high risk for mortality, then two antipseudomonal antibiotics from different classes are recommended, such as piperacillin-tazobactam/tobramycin or cefepime/amikacin.
Use two antipseudomonal antibiotics in HAP if the patient has these risk factors:
Pseudomonas risk factors:
• IV antibiotic treatment within 90 days
• Structural lung disease increasing the risk of gram-negative infection (bronchiectasis, cystic fibrosis)
• High-quality gram stain from respiratory specimen showing predominant and numerous gram-negative bacilli
High risk of mortality:
• Septic shock
• Need for ventilator support
Ventilator-associated pneumonia
General management of VAP is similar to HAP in that empiric treatment should be tailored to the local distribution and susceptibilities of pathogens based on each hospital’s antibiogram. All regimens should cover for S. aureus, P. aeruginosa, and other gram-negative bacilli based on the risk of mortality associated with the need for ventilator support. MSSA should be covered for VAP unless the patient has methicillin-resistant risk factors (see below).
MRSA should be covered for VAP if:
• Patient has had IV antibiotic use within past 90 days
• Hospital unit has greater than 10%-20% of S. aureus isolates are MRSA or MRSA prevalence unknown
Only one antipseudomonal agent should be used unless there are one of the following characteristics present, as described below.
Use two antipseudomonal agents in VAP if:
• Prior IV antibiotic use within 90 days
• Septic shock at time of VAP
• Acute respiratory distress syndrome preceding VAP
• 5 or more days of hospitalization prior to the occurrence of VAP
• Acute renal replacement therapy prior to VAP onset
• Greater than 10% of gram-negative isolates are resistant to an agent being considered for monotherapy
• Local antibiotic susceptibility rates unknown
In both HAP and VAP, antibiotics should be de-escalated to those with a narrower spectrum after initial empiric therapy, ideally within 72 hours and based on sputum or blood culture results. The guidelines support obtaining noninvasive sputum cultures in patients with VAP (endotracheal aspirates) and HAP (spontaneous expectoration, induced sputum, or nasotracheal suctioning in a patient who is unable to cooperate to produce a sputum sample). Patients who are improving clinically may be switched to appropriate oral therapy based on the susceptibility of an identified organism. Another key change is that of the standard duration of therapy. Previously, patients were treated for up to 2-3 weeks with antibiotics. The new IDSA/ATS guidelines recommend that patients should be treated with 7 days of antibiotics rather than a longer course.
The bottom line
Empiric therapy for HAP and VAP should be tailored to each hospital’s local pathogen distribution and antimicrobial susceptibilities, as detailed in an antibiogram. In HAP and VAP, empiric antibiotics should cover for S. aureus, but it only needs to target MRSA if risk factors are present, prevalence is greater than 20% or unknown, and – if HAP – a high risk of mortality. P. aeruginosa and other gram-negative bacilli should also be covered in empiric regimens. Dual antipseudomonal antibiotics is only recommended to be used in HAP if there are specific pseudomonal risk factors or a high risk of mortality. They should be used in VAP if there are multidrug-resistant risk factors present or there is a high/unknown prevalence of resistant organisms. All antibiotic regimens should be deescalated rather than maintained, and both HAP and VAP patients ought to be treated for 7 days.
References
1. Kalil AC, Metersky ML, Klompas M, et al. Management of Adults With Hospital-acquired and Ventilator-associated Pneumonia: 2016 Clinical Practice Guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin Infect Dis. 2016 Sep 1;63(5):557-82.
2. Beardsley JR, Williamson JC, Johnson JW, Ohl CA, Karchmer TB, Bowton DL. Using local microbiologic data to develop institution-specific guidelines for the treatment of hospital-acquired pneumonia. Chest. 2006 Sep;130(3):787-93.
Dr. Botti is a second-year resident in the family medicine residency program department of family and community medicine at Jefferson Medical College, Philadelphia. Dr. Mills is assistant residency program director and assistant professor in the department of family and community medicine and department of physiology at Jefferson Medical College, Philadelphia. Dr. Skolnik is associate director of the family medicine residency program at Abington (Pa.) Memorial Hospital and professor of family and community medicine at Temple University, Philadelphia.
Update on the third international consensus definitions for sepsis and septic shock
Sepsis is the primary cause of death from infection. Early identification and treatment of sepsis is important in improving patient outcomes. The consensus conference sought to differentiate sepsis, which is defined as “life-threatening organ dysfunction caused by a dysregulated host response to infection” from uncomplicated infection.
Sepsis was last classified in a 2001 guideline that based its definition on the presence of two or more systemic inflammatory response syndrome (SIRS) criteria, which included an elevated temperature, heart rate higher than 90 bpm, respiratory rate higher than 20 breaths per minute, and a white blood cell count greater than greater than 12,000 mcL or less than 4,000 mcL or greater than 10% immature bands.
The problem with the SIRS definition of sepsis is that while it reflects a response to infection, it does not sufficiently distinguish between individuals with infections and those with a dysregulated response that leads to a poor prognosis, which is the definition of sepsis. The current consensus conference redefines sepsis with a more direct emphasis on organ dysfunction, as this is the aspect of sepsis that is most clearly linked to patient outcomes.
In the consensus conference document, sepsis is defined as a “life-threatening organ dysfunction caused by a dysregulated host response to infection.” The guidelines recommend using the quick version of the sequential (sepsis-related) organ failure assessment score (qSOFA) to identify patients with sepsis. In its long form, the SOFA used seven clinical and laboratory data points for completion, and is best suited to use in an intensive care setting where detailed data are available. The qSOFA score has only three criteria and by being easier to use can aid in rapid identification of sepsis and the patients most likely to deteriorate from sepsis.
The qSOFA criteria predict poor outcome in patients with infection who have two or more of the following: respiratory rate greater than or equal to 22 breaths/min, new or worsened altered mentation, or systolic blood pressure less than or equal to 100 mm Hg. Unlike the full SOFA score, the qSOFA does not require any laboratory testing and so can be performed in the office or bedside on a hospital floor. The qSOFA does not necessarily define sepsis, rather it identifies patients at a higher risk of hospital death or prolonged ICU stay. The consensus conference suggests that “qSOFA criteria be used to prompt clinicians to further investigate for organ dysfunction, initiate or escalate therapy as appropriate, and consider referral to critical care or increase the frequency of monitoring, if such actions have not already been undertaken.” The task force suggested that the qSOFA score may be a helpful adjunct to best clinical judgment for identifying patients who might benefit from a higher level of care.
Septic shock is defined as a subset of sepsis in which profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk for death than sepsis alone. Septic shock can be identified when, after adequate fluid resuscitation, the patient requires vasopressor therapy to maintain mean arterial pressure of at least 65 mm Hg and has a serum lactate level greater than 2 mmol/L.
Once sepsis is suspected, prompt therapy needs to be started as per the Surviving Sepsis Campaign Guidelines. The qSOFA criteria can be used to identify patients at high risk for morbidity and mortality. Within 3 hours, a lactate level should be obtained as well as blood cultures from two separate sites drawn prior to administration of antibiotics (but do not delay antibiotic administration). Empiric broad-spectrum antibiotics should be given within 45 minutes of the identification of sepsis. Antibiotic choice will vary per clinician/institution preference, but should likely include coverage for Pseudomonas and MRSA (piperacillin/tazobactam and vancomycin, for example). Antibiotics should be reassessed daily for de-escalation. Administer 30 mL/kg crystalloid for hypotension or lactate greater than or equal to 4 mmol/L. Within 6 hours, vasopressors should be given for hypotension that does not respond to initial fluid resuscitation to maintain a mean arterial pressure (MAP) of at least 65mm Hg. In the event of persistent hypotension after initial fluid administration (MAP under 65 mm Hg) or if initial lactate was greater than or equal to 4 mmol/L, volume status and tissue perfusion should be reassessed and lactate should be rechecked if it was initially elevated.
The bottom line
A 2016 international task force recommended that the definition of sepsis should be changed to emphasize organ dysfunction rather than a systemic inflammatory response. Use of the qSOFA score, which relies only on clinically observable data rather than laboratory evaluation, is recommended to identify patients at high risk for morbidity and mortality. Early recognition of sepsis and evaluation with qSOFT should facilitate early treatment and improve survival.
References
Singer M, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) FRCP; JAMA. 2016;315[8]:801-10. doi: 10.1001/jama.2016.0287.
Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med. 2003 Apr;31(4):1250-6.
Singer M, Deutschman CS, Seymour C, et al. The third international consensus definitions for sepsis and septic shock (sepsis-3). JAMA. 2016 Feb 23;315(8):801-10.
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 Mar;32(3):858-73.
Dr. Mills is assistant residency program director and assistant professor in the department of family and community medicine and department of physiology at Sidney Kimmel Medical College at Thomas Jefferson University. Dr. Botti is a second-year resident in the family medicine residency program department of family and community medicine at Sidney Kimmel Medical College at Thomas Jefferson University. Dr. Skolnik is associate director of the family medicine residency program at Abington (Pa.) Memorial Hospital and professor of family and community medicine at Temple University, Philadelphia.
Sepsis is the primary cause of death from infection. Early identification and treatment of sepsis is important in improving patient outcomes. The consensus conference sought to differentiate sepsis, which is defined as “life-threatening organ dysfunction caused by a dysregulated host response to infection” from uncomplicated infection.
Sepsis was last classified in a 2001 guideline that based its definition on the presence of two or more systemic inflammatory response syndrome (SIRS) criteria, which included an elevated temperature, heart rate higher than 90 bpm, respiratory rate higher than 20 breaths per minute, and a white blood cell count greater than greater than 12,000 mcL or less than 4,000 mcL or greater than 10% immature bands.
The problem with the SIRS definition of sepsis is that while it reflects a response to infection, it does not sufficiently distinguish between individuals with infections and those with a dysregulated response that leads to a poor prognosis, which is the definition of sepsis. The current consensus conference redefines sepsis with a more direct emphasis on organ dysfunction, as this is the aspect of sepsis that is most clearly linked to patient outcomes.
In the consensus conference document, sepsis is defined as a “life-threatening organ dysfunction caused by a dysregulated host response to infection.” The guidelines recommend using the quick version of the sequential (sepsis-related) organ failure assessment score (qSOFA) to identify patients with sepsis. In its long form, the SOFA used seven clinical and laboratory data points for completion, and is best suited to use in an intensive care setting where detailed data are available. The qSOFA score has only three criteria and by being easier to use can aid in rapid identification of sepsis and the patients most likely to deteriorate from sepsis.
The qSOFA criteria predict poor outcome in patients with infection who have two or more of the following: respiratory rate greater than or equal to 22 breaths/min, new or worsened altered mentation, or systolic blood pressure less than or equal to 100 mm Hg. Unlike the full SOFA score, the qSOFA does not require any laboratory testing and so can be performed in the office or bedside on a hospital floor. The qSOFA does not necessarily define sepsis, rather it identifies patients at a higher risk of hospital death or prolonged ICU stay. The consensus conference suggests that “qSOFA criteria be used to prompt clinicians to further investigate for organ dysfunction, initiate or escalate therapy as appropriate, and consider referral to critical care or increase the frequency of monitoring, if such actions have not already been undertaken.” The task force suggested that the qSOFA score may be a helpful adjunct to best clinical judgment for identifying patients who might benefit from a higher level of care.
Septic shock is defined as a subset of sepsis in which profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk for death than sepsis alone. Septic shock can be identified when, after adequate fluid resuscitation, the patient requires vasopressor therapy to maintain mean arterial pressure of at least 65 mm Hg and has a serum lactate level greater than 2 mmol/L.
Once sepsis is suspected, prompt therapy needs to be started as per the Surviving Sepsis Campaign Guidelines. The qSOFA criteria can be used to identify patients at high risk for morbidity and mortality. Within 3 hours, a lactate level should be obtained as well as blood cultures from two separate sites drawn prior to administration of antibiotics (but do not delay antibiotic administration). Empiric broad-spectrum antibiotics should be given within 45 minutes of the identification of sepsis. Antibiotic choice will vary per clinician/institution preference, but should likely include coverage for Pseudomonas and MRSA (piperacillin/tazobactam and vancomycin, for example). Antibiotics should be reassessed daily for de-escalation. Administer 30 mL/kg crystalloid for hypotension or lactate greater than or equal to 4 mmol/L. Within 6 hours, vasopressors should be given for hypotension that does not respond to initial fluid resuscitation to maintain a mean arterial pressure (MAP) of at least 65mm Hg. In the event of persistent hypotension after initial fluid administration (MAP under 65 mm Hg) or if initial lactate was greater than or equal to 4 mmol/L, volume status and tissue perfusion should be reassessed and lactate should be rechecked if it was initially elevated.
The bottom line
A 2016 international task force recommended that the definition of sepsis should be changed to emphasize organ dysfunction rather than a systemic inflammatory response. Use of the qSOFA score, which relies only on clinically observable data rather than laboratory evaluation, is recommended to identify patients at high risk for morbidity and mortality. Early recognition of sepsis and evaluation with qSOFT should facilitate early treatment and improve survival.
References
Singer M, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) FRCP; JAMA. 2016;315[8]:801-10. doi: 10.1001/jama.2016.0287.
Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med. 2003 Apr;31(4):1250-6.
Singer M, Deutschman CS, Seymour C, et al. The third international consensus definitions for sepsis and septic shock (sepsis-3). JAMA. 2016 Feb 23;315(8):801-10.
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 Mar;32(3):858-73.
Dr. Mills is assistant residency program director and assistant professor in the department of family and community medicine and department of physiology at Sidney Kimmel Medical College at Thomas Jefferson University. Dr. Botti is a second-year resident in the family medicine residency program department of family and community medicine at Sidney Kimmel Medical College at Thomas Jefferson University. Dr. Skolnik is associate director of the family medicine residency program at Abington (Pa.) Memorial Hospital and professor of family and community medicine at Temple University, Philadelphia.
Sepsis is the primary cause of death from infection. Early identification and treatment of sepsis is important in improving patient outcomes. The consensus conference sought to differentiate sepsis, which is defined as “life-threatening organ dysfunction caused by a dysregulated host response to infection” from uncomplicated infection.
Sepsis was last classified in a 2001 guideline that based its definition on the presence of two or more systemic inflammatory response syndrome (SIRS) criteria, which included an elevated temperature, heart rate higher than 90 bpm, respiratory rate higher than 20 breaths per minute, and a white blood cell count greater than greater than 12,000 mcL or less than 4,000 mcL or greater than 10% immature bands.
The problem with the SIRS definition of sepsis is that while it reflects a response to infection, it does not sufficiently distinguish between individuals with infections and those with a dysregulated response that leads to a poor prognosis, which is the definition of sepsis. The current consensus conference redefines sepsis with a more direct emphasis on organ dysfunction, as this is the aspect of sepsis that is most clearly linked to patient outcomes.
In the consensus conference document, sepsis is defined as a “life-threatening organ dysfunction caused by a dysregulated host response to infection.” The guidelines recommend using the quick version of the sequential (sepsis-related) organ failure assessment score (qSOFA) to identify patients with sepsis. In its long form, the SOFA used seven clinical and laboratory data points for completion, and is best suited to use in an intensive care setting where detailed data are available. The qSOFA score has only three criteria and by being easier to use can aid in rapid identification of sepsis and the patients most likely to deteriorate from sepsis.
The qSOFA criteria predict poor outcome in patients with infection who have two or more of the following: respiratory rate greater than or equal to 22 breaths/min, new or worsened altered mentation, or systolic blood pressure less than or equal to 100 mm Hg. Unlike the full SOFA score, the qSOFA does not require any laboratory testing and so can be performed in the office or bedside on a hospital floor. The qSOFA does not necessarily define sepsis, rather it identifies patients at a higher risk of hospital death or prolonged ICU stay. The consensus conference suggests that “qSOFA criteria be used to prompt clinicians to further investigate for organ dysfunction, initiate or escalate therapy as appropriate, and consider referral to critical care or increase the frequency of monitoring, if such actions have not already been undertaken.” The task force suggested that the qSOFA score may be a helpful adjunct to best clinical judgment for identifying patients who might benefit from a higher level of care.
Septic shock is defined as a subset of sepsis in which profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk for death than sepsis alone. Septic shock can be identified when, after adequate fluid resuscitation, the patient requires vasopressor therapy to maintain mean arterial pressure of at least 65 mm Hg and has a serum lactate level greater than 2 mmol/L.
Once sepsis is suspected, prompt therapy needs to be started as per the Surviving Sepsis Campaign Guidelines. The qSOFA criteria can be used to identify patients at high risk for morbidity and mortality. Within 3 hours, a lactate level should be obtained as well as blood cultures from two separate sites drawn prior to administration of antibiotics (but do not delay antibiotic administration). Empiric broad-spectrum antibiotics should be given within 45 minutes of the identification of sepsis. Antibiotic choice will vary per clinician/institution preference, but should likely include coverage for Pseudomonas and MRSA (piperacillin/tazobactam and vancomycin, for example). Antibiotics should be reassessed daily for de-escalation. Administer 30 mL/kg crystalloid for hypotension or lactate greater than or equal to 4 mmol/L. Within 6 hours, vasopressors should be given for hypotension that does not respond to initial fluid resuscitation to maintain a mean arterial pressure (MAP) of at least 65mm Hg. In the event of persistent hypotension after initial fluid administration (MAP under 65 mm Hg) or if initial lactate was greater than or equal to 4 mmol/L, volume status and tissue perfusion should be reassessed and lactate should be rechecked if it was initially elevated.
The bottom line
A 2016 international task force recommended that the definition of sepsis should be changed to emphasize organ dysfunction rather than a systemic inflammatory response. Use of the qSOFA score, which relies only on clinically observable data rather than laboratory evaluation, is recommended to identify patients at high risk for morbidity and mortality. Early recognition of sepsis and evaluation with qSOFT should facilitate early treatment and improve survival.
References
Singer M, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) FRCP; JAMA. 2016;315[8]:801-10. doi: 10.1001/jama.2016.0287.
Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med. 2003 Apr;31(4):1250-6.
Singer M, Deutschman CS, Seymour C, et al. The third international consensus definitions for sepsis and septic shock (sepsis-3). JAMA. 2016 Feb 23;315(8):801-10.
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 Mar;32(3):858-73.
Dr. Mills is assistant residency program director and assistant professor in the department of family and community medicine and department of physiology at Sidney Kimmel Medical College at Thomas Jefferson University. Dr. Botti is a second-year resident in the family medicine residency program department of family and community medicine at Sidney Kimmel Medical College at Thomas Jefferson University. Dr. Skolnik is associate director of the family medicine residency program at Abington (Pa.) Memorial Hospital and professor of family and community medicine at Temple University, Philadelphia.
