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Prevention of Healthcare-Associated Infections and Antimicrobial Resistance. 2017 Hospital Medicine Revised Core Competencies
Healthcare-associated infections (HAIs) impose a significant burden on the healthcare system in the Unites States, both economically and in terms of patient outcomes. On any given day, approximately 1 in 25 patients in US acute care hospitals has at least 1 HAI, and more than 700,000 HAIs occur annually in hospitalized patients.1 More than half of HAIs occur outside the intensive care unit.1 HAIs are among the leading causes of preventable death. These infections often lead to increases in length of hospitalization and excess direct and indirect hospital costs. The overall annual direct medical cost of HAIs to US hospitals is $28 to $45 billon.2 The central aim of infection control is to prevent HAIs and the emergence of resistant organisms. Hospitalists work in concert with other members of the healthcare organization to reduce HAIs, develop institutional initiatives for prevention, and promote and implement evidence-based infection control measures.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
Describe acceptable methods of hand hygiene technique and timing in relationship to patient contact in various circumstances.
Describe the prophylactic measures required for all types of isolation precautions, which include standard, contact, droplet, and airborne precautions, and list the indications for implementing each type of precaution.
List common types of HAI and describe the risk factors associated with urinary tract infections, surgical site infections, hospital-acquired pneumonia, and blood stream infections.
Identify major resources for infection control information, including hospital infection control staff, hospital infection control policies and procedures, local and state public health departments, and Centers for Disease Control guidelines.
Describe the indicated prevention measures necessary to perform hospital-based procedures in a sterile fashion.
Appreciate that specific infection control practices and engineering controls are required to protect very high-risk patient populations, which may include hematopoietic stem cell transplant and solid organ transplant recipients, from HAIs.
SKILLS
Hospitalists should be able to:
Perform consistent and optimal hand hygiene techniques at all indicated points of care.
Identify and implement indicated isolation precautions for patients with high-risk transmissible diseases or highly resistant infections.
Identify and use local hospital resources, including antibiograms and infection control officers.
Perform indicated infection control and prevention technique during all procedures.
Implement precautions and infection control practices to protect patients from acquiring HAIs.
Implement antibiotic de-escalation when possible on the basis of microbiologic culture results.
Adopt the use of care bundles when shown to reduce the incidence of HAIs.
Avoid devices that are more likely to cause HAIs if alternatives are safe, effective, and available.
Encourage removal of invasive devices, especially central venous catheters and urinary catheters, early during the hospital stay and as soon as is clinically safe to do so.
Communicate effectively the rationale and importance of infection control practices to patients, families, visitors, other healthcare providers, and hospital staff.
Communicate appropriate patient information to infection control staff regarding potentially transmissible diseases.
Lead, coordinate, and/or participate in efforts to educate other healthcare personnel and hospital staff about necessary infection control prevention measures.
Lead, coordinate, and/or participate in multidisciplinary teams that organize, implement, and study infection control protocols, guidelines, or pathways using evidence-based systematic methods.
Lead, coordinate, and/or participate in multidisciplinary efforts to develop antibiotic stewardship programs.
ATTITUDES
Hospitalists should be able to:
Serve as a role model in adherence to recommended hand hygiene and infection control practices.
Engage collaboratively with multidisciplinary teams, which may include infection control, nursing service, and infectious disease consultants, to rapidly implement and maintain isolation precautions.
Engage collaboratively with multidisciplinary teams, which may include infection control, nursing service, care coordination, long-term care facilities, home healthcare staff, and public health personnel, to plan for hospital discharge of patients with transmissible infectious diseases.
1. Magill S, Edwards JR, Bamberg W, Beldavs ZG, Dumyati G, Kainer MA, et al; Emerging Infections Program Healthcare-Associated Infections and Antimicrobial Use Prevalence Survey Team. Multistate point-prevalence survey of health care-associated infections. N Engl J Med. 2014;370(13):1198-1208.
2. Scott DR. The Direct Medical Costs of Healthcare-Associated Infections in U.S. Hospitals and the Benefits of Prevention. Division of Healthcare Quality Promotion; National Center for Preparedness, Detection, and Control of Infectious Diseases; Coordinating Center for Infectious Diseases Centers; Centers for Disease Control and Prevention. March 2009.
Healthcare-associated infections (HAIs) impose a significant burden on the healthcare system in the Unites States, both economically and in terms of patient outcomes. On any given day, approximately 1 in 25 patients in US acute care hospitals has at least 1 HAI, and more than 700,000 HAIs occur annually in hospitalized patients.1 More than half of HAIs occur outside the intensive care unit.1 HAIs are among the leading causes of preventable death. These infections often lead to increases in length of hospitalization and excess direct and indirect hospital costs. The overall annual direct medical cost of HAIs to US hospitals is $28 to $45 billon.2 The central aim of infection control is to prevent HAIs and the emergence of resistant organisms. Hospitalists work in concert with other members of the healthcare organization to reduce HAIs, develop institutional initiatives for prevention, and promote and implement evidence-based infection control measures.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
Describe acceptable methods of hand hygiene technique and timing in relationship to patient contact in various circumstances.
Describe the prophylactic measures required for all types of isolation precautions, which include standard, contact, droplet, and airborne precautions, and list the indications for implementing each type of precaution.
List common types of HAI and describe the risk factors associated with urinary tract infections, surgical site infections, hospital-acquired pneumonia, and blood stream infections.
Identify major resources for infection control information, including hospital infection control staff, hospital infection control policies and procedures, local and state public health departments, and Centers for Disease Control guidelines.
Describe the indicated prevention measures necessary to perform hospital-based procedures in a sterile fashion.
Appreciate that specific infection control practices and engineering controls are required to protect very high-risk patient populations, which may include hematopoietic stem cell transplant and solid organ transplant recipients, from HAIs.
SKILLS
Hospitalists should be able to:
Perform consistent and optimal hand hygiene techniques at all indicated points of care.
Identify and implement indicated isolation precautions for patients with high-risk transmissible diseases or highly resistant infections.
Identify and use local hospital resources, including antibiograms and infection control officers.
Perform indicated infection control and prevention technique during all procedures.
Implement precautions and infection control practices to protect patients from acquiring HAIs.
Implement antibiotic de-escalation when possible on the basis of microbiologic culture results.
Adopt the use of care bundles when shown to reduce the incidence of HAIs.
Avoid devices that are more likely to cause HAIs if alternatives are safe, effective, and available.
Encourage removal of invasive devices, especially central venous catheters and urinary catheters, early during the hospital stay and as soon as is clinically safe to do so.
Communicate effectively the rationale and importance of infection control practices to patients, families, visitors, other healthcare providers, and hospital staff.
Communicate appropriate patient information to infection control staff regarding potentially transmissible diseases.
Lead, coordinate, and/or participate in efforts to educate other healthcare personnel and hospital staff about necessary infection control prevention measures.
Lead, coordinate, and/or participate in multidisciplinary teams that organize, implement, and study infection control protocols, guidelines, or pathways using evidence-based systematic methods.
Lead, coordinate, and/or participate in multidisciplinary efforts to develop antibiotic stewardship programs.
ATTITUDES
Hospitalists should be able to:
Serve as a role model in adherence to recommended hand hygiene and infection control practices.
Engage collaboratively with multidisciplinary teams, which may include infection control, nursing service, and infectious disease consultants, to rapidly implement and maintain isolation precautions.
Engage collaboratively with multidisciplinary teams, which may include infection control, nursing service, care coordination, long-term care facilities, home healthcare staff, and public health personnel, to plan for hospital discharge of patients with transmissible infectious diseases.
Healthcare-associated infections (HAIs) impose a significant burden on the healthcare system in the Unites States, both economically and in terms of patient outcomes. On any given day, approximately 1 in 25 patients in US acute care hospitals has at least 1 HAI, and more than 700,000 HAIs occur annually in hospitalized patients.1 More than half of HAIs occur outside the intensive care unit.1 HAIs are among the leading causes of preventable death. These infections often lead to increases in length of hospitalization and excess direct and indirect hospital costs. The overall annual direct medical cost of HAIs to US hospitals is $28 to $45 billon.2 The central aim of infection control is to prevent HAIs and the emergence of resistant organisms. Hospitalists work in concert with other members of the healthcare organization to reduce HAIs, develop institutional initiatives for prevention, and promote and implement evidence-based infection control measures.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
Describe acceptable methods of hand hygiene technique and timing in relationship to patient contact in various circumstances.
Describe the prophylactic measures required for all types of isolation precautions, which include standard, contact, droplet, and airborne precautions, and list the indications for implementing each type of precaution.
List common types of HAI and describe the risk factors associated with urinary tract infections, surgical site infections, hospital-acquired pneumonia, and blood stream infections.
Identify major resources for infection control information, including hospital infection control staff, hospital infection control policies and procedures, local and state public health departments, and Centers for Disease Control guidelines.
Describe the indicated prevention measures necessary to perform hospital-based procedures in a sterile fashion.
Appreciate that specific infection control practices and engineering controls are required to protect very high-risk patient populations, which may include hematopoietic stem cell transplant and solid organ transplant recipients, from HAIs.
SKILLS
Hospitalists should be able to:
Perform consistent and optimal hand hygiene techniques at all indicated points of care.
Identify and implement indicated isolation precautions for patients with high-risk transmissible diseases or highly resistant infections.
Identify and use local hospital resources, including antibiograms and infection control officers.
Perform indicated infection control and prevention technique during all procedures.
Implement precautions and infection control practices to protect patients from acquiring HAIs.
Implement antibiotic de-escalation when possible on the basis of microbiologic culture results.
Adopt the use of care bundles when shown to reduce the incidence of HAIs.
Avoid devices that are more likely to cause HAIs if alternatives are safe, effective, and available.
Encourage removal of invasive devices, especially central venous catheters and urinary catheters, early during the hospital stay and as soon as is clinically safe to do so.
Communicate effectively the rationale and importance of infection control practices to patients, families, visitors, other healthcare providers, and hospital staff.
Communicate appropriate patient information to infection control staff regarding potentially transmissible diseases.
Lead, coordinate, and/or participate in efforts to educate other healthcare personnel and hospital staff about necessary infection control prevention measures.
Lead, coordinate, and/or participate in multidisciplinary teams that organize, implement, and study infection control protocols, guidelines, or pathways using evidence-based systematic methods.
Lead, coordinate, and/or participate in multidisciplinary efforts to develop antibiotic stewardship programs.
ATTITUDES
Hospitalists should be able to:
Serve as a role model in adherence to recommended hand hygiene and infection control practices.
Engage collaboratively with multidisciplinary teams, which may include infection control, nursing service, and infectious disease consultants, to rapidly implement and maintain isolation precautions.
Engage collaboratively with multidisciplinary teams, which may include infection control, nursing service, care coordination, long-term care facilities, home healthcare staff, and public health personnel, to plan for hospital discharge of patients with transmissible infectious diseases.
1. Magill S, Edwards JR, Bamberg W, Beldavs ZG, Dumyati G, Kainer MA, et al; Emerging Infections Program Healthcare-Associated Infections and Antimicrobial Use Prevalence Survey Team. Multistate point-prevalence survey of health care-associated infections. N Engl J Med. 2014;370(13):1198-1208.
2. Scott DR. The Direct Medical Costs of Healthcare-Associated Infections in U.S. Hospitals and the Benefits of Prevention. Division of Healthcare Quality Promotion; National Center for Preparedness, Detection, and Control of Infectious Diseases; Coordinating Center for Infectious Diseases Centers; Centers for Disease Control and Prevention. March 2009.
1. Magill S, Edwards JR, Bamberg W, Beldavs ZG, Dumyati G, Kainer MA, et al; Emerging Infections Program Healthcare-Associated Infections and Antimicrobial Use Prevalence Survey Team. Multistate point-prevalence survey of health care-associated infections. N Engl J Med. 2014;370(13):1198-1208.
2. Scott DR. The Direct Medical Costs of Healthcare-Associated Infections in U.S. Hospitals and the Benefits of Prevention. Division of Healthcare Quality Promotion; National Center for Preparedness, Detection, and Control of Infectious Diseases; Coordinating Center for Infectious Diseases Centers; Centers for Disease Control and Prevention. March 2009.
© 2017 Society of Hospital Medicine
Professionalism and Medical Ethics. 2017 Hospital Medicine Revised Core Competencies
Professionalism refers to attitudes, behaviors, and skills for physicians to serve the interests of the patient above his or her self-interest. This denotes a commitment to the highest standards of excellence in the practice of medicine and to the generation and dissemination of knowledge to sustain the interests and welfare of patients. Within the practice of hospital medicine, professionalism also includes a commitment to be responsive to the health needs of society and a commitment to ethical principles.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
Define and differentiate ethical principles, which may include beneficence and nonmaleficence, justice, patient autonomy, truth-telling, informed consent, and confidentiality.
Describe the concept of double effect.
Define and distinguish competency and decision-making capacity.
Explain the utility of power of attorney and advance directives in medical care.
Describe the key elements of informed consent.
Explain determination of decision-making capacity and steps required for surrogate decision-making.
Describe local laws and regulations relevant to the practice of hospital medicine.
Explain medical futility.
Recognize when consultation from others who have expertise in psychiatry and ethics will promote optimal care for patients and help resolve ethical dilemmas.
Recognize the obligation to report fraud, professional misconduct, impairment, incompetence, or abandonment of patients.
Recognize potential conflicts of interest in accepting gifts and/or travel from commercial sources.
Recognize potential individual and institutional conflicts of interest with incentive-based contractual agreements with pharmaceutical companies and other funding agents.
SKILLS
Hospitalists should be able to:
Observe doctor-patient confidentiality and identify family members or surrogates to whom information can be released.
Communicate with patients and family members on a regular basis and develop a therapeutic relationship in both routine and challenging situations.
Recommend treatment options that prioritize patient preference, optimize patient care, include consideration of resource use, and are formulated without regard to financial incentives or other conflicts of interest.
Evaluate patients for medical decision-making capacity.
Obtain informed consent when indicated and ensure patient understanding.
Review power of attorney and advance directives with patients and family members.
Adhere to ethical principles and behaviors, including honesty, integrity, and professional responsibility.
Respect patient autonomy.
ATTITUDES
Hospitalists should be able to:
Commit to lifelong self-learning, maintenance of skills, and clinical excellence.
Promote access to medical care for the community, especially in underserved areas.
Demonstrate empathy for hospitalized patients.
Provide compassionate and relevant care for patients, including those whose beliefs diverge from those of the treating physician or from accepted medical advice.
Remain sensitive to differences in patients’ sex, age, race, culture, religion, and sexual orientation.
Appreciate that informed adults with decision-making capacity may refuse recommended medical treatment.
Appreciate that physicians are not required to provide care that is medically futile.
Endorse that physicians have an obligation not to discriminate against any patient or group of patients.
Recognize and observe appropriate boundaries of the physician-patient relationship.
Follow a systematic approach to risks, benefits, and conflicts of interest in human subject research.
Serve as a role model for professional and ethical conduct to house staff, medical students, and other members of the multidisciplinary team.
Professionalism refers to attitudes, behaviors, and skills for physicians to serve the interests of the patient above his or her self-interest. This denotes a commitment to the highest standards of excellence in the practice of medicine and to the generation and dissemination of knowledge to sustain the interests and welfare of patients. Within the practice of hospital medicine, professionalism also includes a commitment to be responsive to the health needs of society and a commitment to ethical principles.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
Define and differentiate ethical principles, which may include beneficence and nonmaleficence, justice, patient autonomy, truth-telling, informed consent, and confidentiality.
Describe the concept of double effect.
Define and distinguish competency and decision-making capacity.
Explain the utility of power of attorney and advance directives in medical care.
Describe the key elements of informed consent.
Explain determination of decision-making capacity and steps required for surrogate decision-making.
Describe local laws and regulations relevant to the practice of hospital medicine.
Explain medical futility.
Recognize when consultation from others who have expertise in psychiatry and ethics will promote optimal care for patients and help resolve ethical dilemmas.
Recognize the obligation to report fraud, professional misconduct, impairment, incompetence, or abandonment of patients.
Recognize potential conflicts of interest in accepting gifts and/or travel from commercial sources.
Recognize potential individual and institutional conflicts of interest with incentive-based contractual agreements with pharmaceutical companies and other funding agents.
SKILLS
Hospitalists should be able to:
Observe doctor-patient confidentiality and identify family members or surrogates to whom information can be released.
Communicate with patients and family members on a regular basis and develop a therapeutic relationship in both routine and challenging situations.
Recommend treatment options that prioritize patient preference, optimize patient care, include consideration of resource use, and are formulated without regard to financial incentives or other conflicts of interest.
Evaluate patients for medical decision-making capacity.
Obtain informed consent when indicated and ensure patient understanding.
Review power of attorney and advance directives with patients and family members.
Adhere to ethical principles and behaviors, including honesty, integrity, and professional responsibility.
Respect patient autonomy.
ATTITUDES
Hospitalists should be able to:
Commit to lifelong self-learning, maintenance of skills, and clinical excellence.
Promote access to medical care for the community, especially in underserved areas.
Demonstrate empathy for hospitalized patients.
Provide compassionate and relevant care for patients, including those whose beliefs diverge from those of the treating physician or from accepted medical advice.
Remain sensitive to differences in patients’ sex, age, race, culture, religion, and sexual orientation.
Appreciate that informed adults with decision-making capacity may refuse recommended medical treatment.
Appreciate that physicians are not required to provide care that is medically futile.
Endorse that physicians have an obligation not to discriminate against any patient or group of patients.
Recognize and observe appropriate boundaries of the physician-patient relationship.
Follow a systematic approach to risks, benefits, and conflicts of interest in human subject research.
Serve as a role model for professional and ethical conduct to house staff, medical students, and other members of the multidisciplinary team.
Professionalism refers to attitudes, behaviors, and skills for physicians to serve the interests of the patient above his or her self-interest. This denotes a commitment to the highest standards of excellence in the practice of medicine and to the generation and dissemination of knowledge to sustain the interests and welfare of patients. Within the practice of hospital medicine, professionalism also includes a commitment to be responsive to the health needs of society and a commitment to ethical principles.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
Define and differentiate ethical principles, which may include beneficence and nonmaleficence, justice, patient autonomy, truth-telling, informed consent, and confidentiality.
Describe the concept of double effect.
Define and distinguish competency and decision-making capacity.
Explain the utility of power of attorney and advance directives in medical care.
Describe the key elements of informed consent.
Explain determination of decision-making capacity and steps required for surrogate decision-making.
Describe local laws and regulations relevant to the practice of hospital medicine.
Explain medical futility.
Recognize when consultation from others who have expertise in psychiatry and ethics will promote optimal care for patients and help resolve ethical dilemmas.
Recognize the obligation to report fraud, professional misconduct, impairment, incompetence, or abandonment of patients.
Recognize potential conflicts of interest in accepting gifts and/or travel from commercial sources.
Recognize potential individual and institutional conflicts of interest with incentive-based contractual agreements with pharmaceutical companies and other funding agents.
SKILLS
Hospitalists should be able to:
Observe doctor-patient confidentiality and identify family members or surrogates to whom information can be released.
Communicate with patients and family members on a regular basis and develop a therapeutic relationship in both routine and challenging situations.
Recommend treatment options that prioritize patient preference, optimize patient care, include consideration of resource use, and are formulated without regard to financial incentives or other conflicts of interest.
Evaluate patients for medical decision-making capacity.
Obtain informed consent when indicated and ensure patient understanding.
Review power of attorney and advance directives with patients and family members.
Adhere to ethical principles and behaviors, including honesty, integrity, and professional responsibility.
Respect patient autonomy.
ATTITUDES
Hospitalists should be able to:
Commit to lifelong self-learning, maintenance of skills, and clinical excellence.
Promote access to medical care for the community, especially in underserved areas.
Demonstrate empathy for hospitalized patients.
Provide compassionate and relevant care for patients, including those whose beliefs diverge from those of the treating physician or from accepted medical advice.
Remain sensitive to differences in patients’ sex, age, race, culture, religion, and sexual orientation.
Appreciate that informed adults with decision-making capacity may refuse recommended medical treatment.
Appreciate that physicians are not required to provide care that is medically futile.
Endorse that physicians have an obligation not to discriminate against any patient or group of patients.
Recognize and observe appropriate boundaries of the physician-patient relationship.
Follow a systematic approach to risks, benefits, and conflicts of interest in human subject research.
Serve as a role model for professional and ethical conduct to house staff, medical students, and other members of the multidisciplinary team.
© 2017 Society of Hospital Medicine
Quality Improvement. 2017 Hospital Medicine Revised Core Competencies
Quality improvement (QI) is the process of continually evaluating existing processes of care and implementing/disseminating best practice. QI is influenced by objective data and focuses on systems change to optimize institutional performance and appropriate resource use. Since the Institute of Medicine released its report “To Err is Human” in 1999, the then fledgling field of hospital medicine and the QI movement have simultaneously evolved and worked synergistically. Hospitalists are uniquely positioned to improve the quality of inpatient care. Hospitalists should strive to lead or participate in QI efforts to optimize management of common inpatient conditions and improve clinical outcomes on the basis of standardized evidence-based practices.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
Describe the roles of quality and peer review committees in facilitating continuous QI processes.
Identify structure, process, and outcome measures appropriate for specific QI projects.
List the characteristics of high-reliability organizations and learning healthcare systems.
Describe the elements of effective teams and teamwork.
Describe the relationships among value, quality, and cost.
Explain different philosophies and techniques for thorough analysis of complex systems, such as root cause analysis, failure mode and effects analysis, Lean, Six-Sigma, Plan-Do-Study-Act, etc.
Identify and categorize adverse outcomes including sentinel events, medical errors, and near-misses.
Describe QI outcome measurements currently used by stakeholders and regulatory agencies.
Identify guidelines and protocols supported by outcomes data to shape and standardize clinical practice.
Identify the relative strengths and limitations of proposed interventions to address hospital-based QI concerns.
Identify appropriate institutional systems used to report medical errors, patient safety events, and near-misses.
SKILLS
Hospitalists should be able to:
Use quality data to inform hospitalist practice and improve patient care at the individual and system levels.
Distinguish outcome measurements from process measurements.
Interpret patient satisfaction metrics.
Incorporate patient preference and satisfaction into the optimization of healthcare quality.
Identify key stakeholders within individual institutions and work collaboratively in QI endeavors.
Use common methods to understand, describe, and analyze QI initiatives such as the fishbone diagram and the 5 why’s.
Apply the results of validated outcome studies to improve the quality of inpatient practice.
Structure QI initiatives that reflect evidence-based literature and high-quality outcomes data.
ATTITUDES
Hospitalists should be able to:
Practice patient-centered care and recognize its value in improving patient safety and satisfaction.
Promote the adoption of new practices, guidelines, and technology as supported by best available evidence.
Engage in a collaborative multidisciplinary team approach to lead, coordinate, and/or participate in the design and implementation of QI initiatives at individual, practice, and system levels.
Appreciate the importance and need to align quality goals with institutional and system goals.
Advocate for and foster a Just Culture around patient safety and QI.
Quality improvement (QI) is the process of continually evaluating existing processes of care and implementing/disseminating best practice. QI is influenced by objective data and focuses on systems change to optimize institutional performance and appropriate resource use. Since the Institute of Medicine released its report “To Err is Human” in 1999, the then fledgling field of hospital medicine and the QI movement have simultaneously evolved and worked synergistically. Hospitalists are uniquely positioned to improve the quality of inpatient care. Hospitalists should strive to lead or participate in QI efforts to optimize management of common inpatient conditions and improve clinical outcomes on the basis of standardized evidence-based practices.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
Describe the roles of quality and peer review committees in facilitating continuous QI processes.
Identify structure, process, and outcome measures appropriate for specific QI projects.
List the characteristics of high-reliability organizations and learning healthcare systems.
Describe the elements of effective teams and teamwork.
Describe the relationships among value, quality, and cost.
Explain different philosophies and techniques for thorough analysis of complex systems, such as root cause analysis, failure mode and effects analysis, Lean, Six-Sigma, Plan-Do-Study-Act, etc.
Identify and categorize adverse outcomes including sentinel events, medical errors, and near-misses.
Describe QI outcome measurements currently used by stakeholders and regulatory agencies.
Identify guidelines and protocols supported by outcomes data to shape and standardize clinical practice.
Identify the relative strengths and limitations of proposed interventions to address hospital-based QI concerns.
Identify appropriate institutional systems used to report medical errors, patient safety events, and near-misses.
SKILLS
Hospitalists should be able to:
Use quality data to inform hospitalist practice and improve patient care at the individual and system levels.
Distinguish outcome measurements from process measurements.
Interpret patient satisfaction metrics.
Incorporate patient preference and satisfaction into the optimization of healthcare quality.
Identify key stakeholders within individual institutions and work collaboratively in QI endeavors.
Use common methods to understand, describe, and analyze QI initiatives such as the fishbone diagram and the 5 why’s.
Apply the results of validated outcome studies to improve the quality of inpatient practice.
Structure QI initiatives that reflect evidence-based literature and high-quality outcomes data.
ATTITUDES
Hospitalists should be able to:
Practice patient-centered care and recognize its value in improving patient safety and satisfaction.
Promote the adoption of new practices, guidelines, and technology as supported by best available evidence.
Engage in a collaborative multidisciplinary team approach to lead, coordinate, and/or participate in the design and implementation of QI initiatives at individual, practice, and system levels.
Appreciate the importance and need to align quality goals with institutional and system goals.
Advocate for and foster a Just Culture around patient safety and QI.
Quality improvement (QI) is the process of continually evaluating existing processes of care and implementing/disseminating best practice. QI is influenced by objective data and focuses on systems change to optimize institutional performance and appropriate resource use. Since the Institute of Medicine released its report “To Err is Human” in 1999, the then fledgling field of hospital medicine and the QI movement have simultaneously evolved and worked synergistically. Hospitalists are uniquely positioned to improve the quality of inpatient care. Hospitalists should strive to lead or participate in QI efforts to optimize management of common inpatient conditions and improve clinical outcomes on the basis of standardized evidence-based practices.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
Describe the roles of quality and peer review committees in facilitating continuous QI processes.
Identify structure, process, and outcome measures appropriate for specific QI projects.
List the characteristics of high-reliability organizations and learning healthcare systems.
Describe the elements of effective teams and teamwork.
Describe the relationships among value, quality, and cost.
Explain different philosophies and techniques for thorough analysis of complex systems, such as root cause analysis, failure mode and effects analysis, Lean, Six-Sigma, Plan-Do-Study-Act, etc.
Identify and categorize adverse outcomes including sentinel events, medical errors, and near-misses.
Describe QI outcome measurements currently used by stakeholders and regulatory agencies.
Identify guidelines and protocols supported by outcomes data to shape and standardize clinical practice.
Identify the relative strengths and limitations of proposed interventions to address hospital-based QI concerns.
Identify appropriate institutional systems used to report medical errors, patient safety events, and near-misses.
SKILLS
Hospitalists should be able to:
Use quality data to inform hospitalist practice and improve patient care at the individual and system levels.
Distinguish outcome measurements from process measurements.
Interpret patient satisfaction metrics.
Incorporate patient preference and satisfaction into the optimization of healthcare quality.
Identify key stakeholders within individual institutions and work collaboratively in QI endeavors.
Use common methods to understand, describe, and analyze QI initiatives such as the fishbone diagram and the 5 why’s.
Apply the results of validated outcome studies to improve the quality of inpatient practice.
Structure QI initiatives that reflect evidence-based literature and high-quality outcomes data.
ATTITUDES
Hospitalists should be able to:
Practice patient-centered care and recognize its value in improving patient safety and satisfaction.
Promote the adoption of new practices, guidelines, and technology as supported by best available evidence.
Engage in a collaborative multidisciplinary team approach to lead, coordinate, and/or participate in the design and implementation of QI initiatives at individual, practice, and system levels.
Appreciate the importance and need to align quality goals with institutional and system goals.
Advocate for and foster a Just Culture around patient safety and QI.
© 2017 Society of Hospital Medicine
Risk Management. 2017 Hospital Medicine Revised Core Competencies
Risk management seeks to reduce hazards to patients through a process of identification, evaluation, and analysis of potential or actual adverse events. Hospitalists should strive to comply with applicable laws and regulations, avoid conflicts of interest, and conduct the practice of medicine with integrity and ethics. Hospitalists should also take a collaborative and proactive role in risk management to improve safety and satisfaction in the hospital setting.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
Explain the legal definition of negligence and the concept of standard of care.
Describe the components of informed consent.
Describe Health Insurance Portability and Accountability Act (HIPAA) regulations related to patient confidentiality.
Explain requirements for billing compliance.
Describe laws and regulations relevant to the practice of hospital medicine, including the Emergency Medical Treatment and Active Labor Act (EMTALA), the Patient Safety and Quality Improvement Act, and credentialing and licensing.
Explain how ethical principles can be applied to risk management.
SKILLS
Hospitalists should be able to:
Ensure patient confidentiality and comply with HIPAA regulations in day-to-day practice.
Conduct medical practice and complete chart documentation to meet patient care needs and billing compliance.
Reduce risks through effective communication with all involved parties on the healthcare team.
Elicit and appropriately document informed consent from patients or surrogates for treatment plans and procedures when indicated.
Provide adequate supervision of members of the patient care team, which may include physician assistants, fellows, residents, or medical students.
Apply guidelines of clinical ethics to patient care and risk management.
Compare and minimize hazards of diagnostic and treatment management strategies for the individual patient.
Use appropriate systems to identify and report potential areas of risk to patients, families, or healthcare providers.
ATTITUDES
Hospitalists should be able to:
Apply ethical principles, which may include autonomy, beneficence, nonmaleficence, and justice, to promote patient-centered care.
Recognize the importance of prompt, honest, and open discussions with patients and families regarding medical errors or harm.
Respect patient wishes for treatment decisions and plans, including those that may not resonate with personal beliefs.
Respect patient confidentiality.
Collaborate with risk management specialists to review and/or address adverse events.
Risk management seeks to reduce hazards to patients through a process of identification, evaluation, and analysis of potential or actual adverse events. Hospitalists should strive to comply with applicable laws and regulations, avoid conflicts of interest, and conduct the practice of medicine with integrity and ethics. Hospitalists should also take a collaborative and proactive role in risk management to improve safety and satisfaction in the hospital setting.
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KNOWLEDGE
Hospitalists should be able to:
Explain the legal definition of negligence and the concept of standard of care.
Describe the components of informed consent.
Describe Health Insurance Portability and Accountability Act (HIPAA) regulations related to patient confidentiality.
Explain requirements for billing compliance.
Describe laws and regulations relevant to the practice of hospital medicine, including the Emergency Medical Treatment and Active Labor Act (EMTALA), the Patient Safety and Quality Improvement Act, and credentialing and licensing.
Explain how ethical principles can be applied to risk management.
SKILLS
Hospitalists should be able to:
Ensure patient confidentiality and comply with HIPAA regulations in day-to-day practice.
Conduct medical practice and complete chart documentation to meet patient care needs and billing compliance.
Reduce risks through effective communication with all involved parties on the healthcare team.
Elicit and appropriately document informed consent from patients or surrogates for treatment plans and procedures when indicated.
Provide adequate supervision of members of the patient care team, which may include physician assistants, fellows, residents, or medical students.
Apply guidelines of clinical ethics to patient care and risk management.
Compare and minimize hazards of diagnostic and treatment management strategies for the individual patient.
Use appropriate systems to identify and report potential areas of risk to patients, families, or healthcare providers.
ATTITUDES
Hospitalists should be able to:
Apply ethical principles, which may include autonomy, beneficence, nonmaleficence, and justice, to promote patient-centered care.
Recognize the importance of prompt, honest, and open discussions with patients and families regarding medical errors or harm.
Respect patient wishes for treatment decisions and plans, including those that may not resonate with personal beliefs.
Respect patient confidentiality.
Collaborate with risk management specialists to review and/or address adverse events.
Risk management seeks to reduce hazards to patients through a process of identification, evaluation, and analysis of potential or actual adverse events. Hospitalists should strive to comply with applicable laws and regulations, avoid conflicts of interest, and conduct the practice of medicine with integrity and ethics. Hospitalists should also take a collaborative and proactive role in risk management to improve safety and satisfaction in the hospital setting.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
Explain the legal definition of negligence and the concept of standard of care.
Describe the components of informed consent.
Describe Health Insurance Portability and Accountability Act (HIPAA) regulations related to patient confidentiality.
Explain requirements for billing compliance.
Describe laws and regulations relevant to the practice of hospital medicine, including the Emergency Medical Treatment and Active Labor Act (EMTALA), the Patient Safety and Quality Improvement Act, and credentialing and licensing.
Explain how ethical principles can be applied to risk management.
SKILLS
Hospitalists should be able to:
Ensure patient confidentiality and comply with HIPAA regulations in day-to-day practice.
Conduct medical practice and complete chart documentation to meet patient care needs and billing compliance.
Reduce risks through effective communication with all involved parties on the healthcare team.
Elicit and appropriately document informed consent from patients or surrogates for treatment plans and procedures when indicated.
Provide adequate supervision of members of the patient care team, which may include physician assistants, fellows, residents, or medical students.
Apply guidelines of clinical ethics to patient care and risk management.
Compare and minimize hazards of diagnostic and treatment management strategies for the individual patient.
Use appropriate systems to identify and report potential areas of risk to patients, families, or healthcare providers.
ATTITUDES
Hospitalists should be able to:
Apply ethical principles, which may include autonomy, beneficence, nonmaleficence, and justice, to promote patient-centered care.
Recognize the importance of prompt, honest, and open discussions with patients and families regarding medical errors or harm.
Respect patient wishes for treatment decisions and plans, including those that may not resonate with personal beliefs.
Respect patient confidentiality.
Collaborate with risk management specialists to review and/or address adverse events.
© 2017 Society of Hospital Medicine
Team Approach and Multidisciplinary Care. 2017 Hospital Medicine Revised Core Competencies
Multidisciplinary care refers to active collaboration among various members of the healthcare team to develop and deliver optimal care plans for hospitalized patients. In an era of healthcare delivery reform, team-based care delivery is an integral strategy for enhancing care quality, improving patient safety, decreasing length of stay, lowering costs, and improving health outcomes.1,2 It is well documented that communication and teamwork failures are the root cause of many preventable adverse events.3-5 In addition, patients’ rating of nurse-physician coordination correlates with their perception of the quality of care they have received.6,7 Hospitalists often lead multidisciplinary teams to coordinate complex inpatient medical care to address these and other issues and to improve care processes.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
- Describe the important elements of teamwork including mutual respect, effective communication techniques, establishing common goals and plans, and individual and team accountability.
- List behaviors and skills that contribute to effective and ineffective interactions, which may also influence team performance.
- Describe factors within an institution, including its local organizational culture, that may influence the structure and function of multidisciplinary teams.
- Recognize the complexity of healthcare systems and the myriad factors involved in patient care.
SKILLS
Hospitalists should be able to:
- Determine an effective team composition and work collaboratively to designate individual responsibilities within the group.
- Demonstrate skills necessary to lead a team, including effective communication, negotiation, conflict resolution, delegation, and time management.
- Assess individual team member abilities to identify areas of strength and improvement such that each member is incorporated effectively and productively into the team.
- Assess and reassess group dynamics as needed and make necessary changes to optimize team function.
- Use active listening techniques during interactions with team members and engage team participation.
- Communicate effectively with all members of the multidisciplinary team.
- Conduct effective multidisciplinary team rounds, which may include patients and their families.
- Appropriately integrate and balance the assessments and recommendations from all contributing team members into a cohesive care plan.
- Assess performance of all team members, including self-assessment, and identify opportunities for improvement.
- Provide meaningful, behavior-based feedback to improve individual performance.
ATTITUDES
Hospitalists should be able to:
- Emphasize the importance of mutual respect among team members.
- Role model in professional conflict resolution and discussion of disagreements.
- Within appropriate scopes of practice, share decision-making responsibilities with care team members.
- Create an environment of shared responsibility with patients and caregivers and provide opportunities for patients and/or caregivers to participate in medical decision-making.
- Encourage interactive education among team members.
- Encourage team members to educate patients and families using effective techniques.
1. American Hospital Association’s Physician Leadership Forum. Team-Based Health Care Delivery: Lessons from the Field. American Hospital Association; 2012.
2. O’Leary KJ, Sehgal NL, Terrell G, Williams MW; High Performance Teams and the Hospital of the Future Project Team. Interdisciplinary teamwork in hospitals: a review and practical recommendations for improvement. J Hosp Med. 2012;7(1):48-54.
3. Neale G, Woloshynowych M, Vincent C. Exploring the causes of adverse events in NHS hospital practice. J R Soc Med. 2001;94(7):322-330.
4. Sutcliffe KM, Lewton E, Rosenthal MM. Communication failures: an insidious contributor to medical mishaps. Acad Med. 2004;79(2):186-194.
5. Wilson RM, Runciman WB, Gibberd RW, Harrison BT, Newby L, Hamilton JD. The Quality in Australian Health Care Study. Med J Aust. 1995;163(9):458-471.
6. Beaudin CL, Lammers JC, Pedroja AT. Patient perceptions of coordinated care: the importance of organized communication in hospitals. J Healthc Qual. 1999;21(5):18-23.
7. Wolosin RJ, Vercler L, Matthews JL. Am I safe here? Improving patients’ perceptions of safety in hospitals. J Nurs Care Qual. 2006;21(1):30-40.
Multidisciplinary care refers to active collaboration among various members of the healthcare team to develop and deliver optimal care plans for hospitalized patients. In an era of healthcare delivery reform, team-based care delivery is an integral strategy for enhancing care quality, improving patient safety, decreasing length of stay, lowering costs, and improving health outcomes.1,2 It is well documented that communication and teamwork failures are the root cause of many preventable adverse events.3-5 In addition, patients’ rating of nurse-physician coordination correlates with their perception of the quality of care they have received.6,7 Hospitalists often lead multidisciplinary teams to coordinate complex inpatient medical care to address these and other issues and to improve care processes.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
- Describe the important elements of teamwork including mutual respect, effective communication techniques, establishing common goals and plans, and individual and team accountability.
- List behaviors and skills that contribute to effective and ineffective interactions, which may also influence team performance.
- Describe factors within an institution, including its local organizational culture, that may influence the structure and function of multidisciplinary teams.
- Recognize the complexity of healthcare systems and the myriad factors involved in patient care.
SKILLS
Hospitalists should be able to:
- Determine an effective team composition and work collaboratively to designate individual responsibilities within the group.
- Demonstrate skills necessary to lead a team, including effective communication, negotiation, conflict resolution, delegation, and time management.
- Assess individual team member abilities to identify areas of strength and improvement such that each member is incorporated effectively and productively into the team.
- Assess and reassess group dynamics as needed and make necessary changes to optimize team function.
- Use active listening techniques during interactions with team members and engage team participation.
- Communicate effectively with all members of the multidisciplinary team.
- Conduct effective multidisciplinary team rounds, which may include patients and their families.
- Appropriately integrate and balance the assessments and recommendations from all contributing team members into a cohesive care plan.
- Assess performance of all team members, including self-assessment, and identify opportunities for improvement.
- Provide meaningful, behavior-based feedback to improve individual performance.
ATTITUDES
Hospitalists should be able to:
- Emphasize the importance of mutual respect among team members.
- Role model in professional conflict resolution and discussion of disagreements.
- Within appropriate scopes of practice, share decision-making responsibilities with care team members.
- Create an environment of shared responsibility with patients and caregivers and provide opportunities for patients and/or caregivers to participate in medical decision-making.
- Encourage interactive education among team members.
- Encourage team members to educate patients and families using effective techniques.
Multidisciplinary care refers to active collaboration among various members of the healthcare team to develop and deliver optimal care plans for hospitalized patients. In an era of healthcare delivery reform, team-based care delivery is an integral strategy for enhancing care quality, improving patient safety, decreasing length of stay, lowering costs, and improving health outcomes.1,2 It is well documented that communication and teamwork failures are the root cause of many preventable adverse events.3-5 In addition, patients’ rating of nurse-physician coordination correlates with their perception of the quality of care they have received.6,7 Hospitalists often lead multidisciplinary teams to coordinate complex inpatient medical care to address these and other issues and to improve care processes.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
- Describe the important elements of teamwork including mutual respect, effective communication techniques, establishing common goals and plans, and individual and team accountability.
- List behaviors and skills that contribute to effective and ineffective interactions, which may also influence team performance.
- Describe factors within an institution, including its local organizational culture, that may influence the structure and function of multidisciplinary teams.
- Recognize the complexity of healthcare systems and the myriad factors involved in patient care.
SKILLS
Hospitalists should be able to:
- Determine an effective team composition and work collaboratively to designate individual responsibilities within the group.
- Demonstrate skills necessary to lead a team, including effective communication, negotiation, conflict resolution, delegation, and time management.
- Assess individual team member abilities to identify areas of strength and improvement such that each member is incorporated effectively and productively into the team.
- Assess and reassess group dynamics as needed and make necessary changes to optimize team function.
- Use active listening techniques during interactions with team members and engage team participation.
- Communicate effectively with all members of the multidisciplinary team.
- Conduct effective multidisciplinary team rounds, which may include patients and their families.
- Appropriately integrate and balance the assessments and recommendations from all contributing team members into a cohesive care plan.
- Assess performance of all team members, including self-assessment, and identify opportunities for improvement.
- Provide meaningful, behavior-based feedback to improve individual performance.
ATTITUDES
Hospitalists should be able to:
- Emphasize the importance of mutual respect among team members.
- Role model in professional conflict resolution and discussion of disagreements.
- Within appropriate scopes of practice, share decision-making responsibilities with care team members.
- Create an environment of shared responsibility with patients and caregivers and provide opportunities for patients and/or caregivers to participate in medical decision-making.
- Encourage interactive education among team members.
- Encourage team members to educate patients and families using effective techniques.
1. American Hospital Association’s Physician Leadership Forum. Team-Based Health Care Delivery: Lessons from the Field. American Hospital Association; 2012.
2. O’Leary KJ, Sehgal NL, Terrell G, Williams MW; High Performance Teams and the Hospital of the Future Project Team. Interdisciplinary teamwork in hospitals: a review and practical recommendations for improvement. J Hosp Med. 2012;7(1):48-54.
3. Neale G, Woloshynowych M, Vincent C. Exploring the causes of adverse events in NHS hospital practice. J R Soc Med. 2001;94(7):322-330.
4. Sutcliffe KM, Lewton E, Rosenthal MM. Communication failures: an insidious contributor to medical mishaps. Acad Med. 2004;79(2):186-194.
5. Wilson RM, Runciman WB, Gibberd RW, Harrison BT, Newby L, Hamilton JD. The Quality in Australian Health Care Study. Med J Aust. 1995;163(9):458-471.
6. Beaudin CL, Lammers JC, Pedroja AT. Patient perceptions of coordinated care: the importance of organized communication in hospitals. J Healthc Qual. 1999;21(5):18-23.
7. Wolosin RJ, Vercler L, Matthews JL. Am I safe here? Improving patients’ perceptions of safety in hospitals. J Nurs Care Qual. 2006;21(1):30-40.
1. American Hospital Association’s Physician Leadership Forum. Team-Based Health Care Delivery: Lessons from the Field. American Hospital Association; 2012.
2. O’Leary KJ, Sehgal NL, Terrell G, Williams MW; High Performance Teams and the Hospital of the Future Project Team. Interdisciplinary teamwork in hospitals: a review and practical recommendations for improvement. J Hosp Med. 2012;7(1):48-54.
3. Neale G, Woloshynowych M, Vincent C. Exploring the causes of adverse events in NHS hospital practice. J R Soc Med. 2001;94(7):322-330.
4. Sutcliffe KM, Lewton E, Rosenthal MM. Communication failures: an insidious contributor to medical mishaps. Acad Med. 2004;79(2):186-194.
5. Wilson RM, Runciman WB, Gibberd RW, Harrison BT, Newby L, Hamilton JD. The Quality in Australian Health Care Study. Med J Aust. 1995;163(9):458-471.
6. Beaudin CL, Lammers JC, Pedroja AT. Patient perceptions of coordinated care: the importance of organized communication in hospitals. J Healthc Qual. 1999;21(5):18-23.
7. Wolosin RJ, Vercler L, Matthews JL. Am I safe here? Improving patients’ perceptions of safety in hospitals. J Nurs Care Qual. 2006;21(1):30-40.
© 2017 Society of Hospital Medicine
Transitions of Care. 2017 Hospital Medicine Revised Core Competencies
The term “transitions of care” refers to specific interactions, communication, and planning required for patients to safely move from one care setting to another. These transitions apply not only to transfers of care between the inpatient and outpatient settings but also to handoffs that occur within facilities (eg, service to service) and communities (eg, inpatient to subacute rehabilitation). Ineffective transitions of care are associated with adverse events, and nearly 20% of patients experience adverse events (many of which are preventable) within 3 weeks of hospital discharge.1,2 Hospitalists should promote efficient, safe transitions of care to ensure patient safety, reduce loss of information, and maintain the continuum of high-quality care.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
- Describe the relevant parts of the medical record that should be retrieved and communicated during each care transition to ensure patient safety and maintain the continuum of care.
- Describe the importance and limitations of patient transition processes.
- Describe ancillary services that are available to facilitate patient transitions.
- Compare postacute care options for patients.
- Explain the strengths and limitations of different communication modalities and their role in patient transitions.
- Explain elements of a high-quality patient handoff.
- Recognize the value of real-time interactive dialogue among clinicians during care transitions.
- Describe the characteristics of a high-quality discharge summary document.
- Recognize the impact of care transitions on patient outcomes and satisfaction.
SKILLS
Hospitalists should be able to:
- Use the most efficient, effective, reliable, and expeditious communication modalities appropriate for a patient’s care transition.
- Communicate and synthesize relevant medical information to and from referring healthcare providers into a cohesive care plan.
- Develop a care plan early during hospitalization that anticipates care needs beyond the inpatient care setting.
- Prepare patients and families early in the hospitalization for anticipated care transitions.
- Access available ancillary services that can facilitate patient transitions.
- Expeditiously inform the primary care provider about significant changes in patient clinical status.
- Inform receiving healthcare providers of pending tests and determine responsibility for the follow-up of pending results.
- Select an appropriate level of postacute care that is best suited to the patient’s needs.
- Incorporate patient preferences and use shared decision-making in the selection of postacute care.
- Anticipate and address language and/or literacy barriers to patient education.
- Communicate with patients and families to explain the patient’s condition, ongoing medical regimens and therapies, follow-up care, and available support services.
- Communicate with patients and families to explain clinical symptomatology that may require medical attention before scheduled follow-up.
- Coordinate multidisciplinary teams early during hospitalization to facilitate patient education, optimize patient function, and improve discharge planning.
- Lead, coordinate, and/or participate in initiatives to develop and implement new protocols to improve or optimize transitions of care.
- Lead, coordinate, and/or participate in the evaluation of new strategies or information systems designed to improve care transitions.
ATTITUDES
Hospitalists should be able to:
- Engage in a multidisciplinary approach to care transitions, including nursing, rehabilitation, nutrition, pharmaceutical, and social services.
- Engage stakeholders in hospital initiatives to continuously assess the quality of care transitions.
- Maintain availability to discharged patients for questions during discharge and between discharge and the follow-up visit with the receiving physician.
1. Forster AJ, Murff HJ, Peterson JF, Gandhi TK, Bates DW. Adverse drug events occurring following hospital discharge. J Gen Intern Med. 2005;20(4):317-323.
2. Forster AJ, Murff HJ, Peterson JF, Gandhi TK, Bates DW. The incidence and severity of adverse events affecting patients after discharge from the hospital. Ann Intern Med. 2003;138(3):161-167.
The term “transitions of care” refers to specific interactions, communication, and planning required for patients to safely move from one care setting to another. These transitions apply not only to transfers of care between the inpatient and outpatient settings but also to handoffs that occur within facilities (eg, service to service) and communities (eg, inpatient to subacute rehabilitation). Ineffective transitions of care are associated with adverse events, and nearly 20% of patients experience adverse events (many of which are preventable) within 3 weeks of hospital discharge.1,2 Hospitalists should promote efficient, safe transitions of care to ensure patient safety, reduce loss of information, and maintain the continuum of high-quality care.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
- Describe the relevant parts of the medical record that should be retrieved and communicated during each care transition to ensure patient safety and maintain the continuum of care.
- Describe the importance and limitations of patient transition processes.
- Describe ancillary services that are available to facilitate patient transitions.
- Compare postacute care options for patients.
- Explain the strengths and limitations of different communication modalities and their role in patient transitions.
- Explain elements of a high-quality patient handoff.
- Recognize the value of real-time interactive dialogue among clinicians during care transitions.
- Describe the characteristics of a high-quality discharge summary document.
- Recognize the impact of care transitions on patient outcomes and satisfaction.
SKILLS
Hospitalists should be able to:
- Use the most efficient, effective, reliable, and expeditious communication modalities appropriate for a patient’s care transition.
- Communicate and synthesize relevant medical information to and from referring healthcare providers into a cohesive care plan.
- Develop a care plan early during hospitalization that anticipates care needs beyond the inpatient care setting.
- Prepare patients and families early in the hospitalization for anticipated care transitions.
- Access available ancillary services that can facilitate patient transitions.
- Expeditiously inform the primary care provider about significant changes in patient clinical status.
- Inform receiving healthcare providers of pending tests and determine responsibility for the follow-up of pending results.
- Select an appropriate level of postacute care that is best suited to the patient’s needs.
- Incorporate patient preferences and use shared decision-making in the selection of postacute care.
- Anticipate and address language and/or literacy barriers to patient education.
- Communicate with patients and families to explain the patient’s condition, ongoing medical regimens and therapies, follow-up care, and available support services.
- Communicate with patients and families to explain clinical symptomatology that may require medical attention before scheduled follow-up.
- Coordinate multidisciplinary teams early during hospitalization to facilitate patient education, optimize patient function, and improve discharge planning.
- Lead, coordinate, and/or participate in initiatives to develop and implement new protocols to improve or optimize transitions of care.
- Lead, coordinate, and/or participate in the evaluation of new strategies or information systems designed to improve care transitions.
ATTITUDES
Hospitalists should be able to:
- Engage in a multidisciplinary approach to care transitions, including nursing, rehabilitation, nutrition, pharmaceutical, and social services.
- Engage stakeholders in hospital initiatives to continuously assess the quality of care transitions.
- Maintain availability to discharged patients for questions during discharge and between discharge and the follow-up visit with the receiving physician.
The term “transitions of care” refers to specific interactions, communication, and planning required for patients to safely move from one care setting to another. These transitions apply not only to transfers of care between the inpatient and outpatient settings but also to handoffs that occur within facilities (eg, service to service) and communities (eg, inpatient to subacute rehabilitation). Ineffective transitions of care are associated with adverse events, and nearly 20% of patients experience adverse events (many of which are preventable) within 3 weeks of hospital discharge.1,2 Hospitalists should promote efficient, safe transitions of care to ensure patient safety, reduce loss of information, and maintain the continuum of high-quality care.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
- Describe the relevant parts of the medical record that should be retrieved and communicated during each care transition to ensure patient safety and maintain the continuum of care.
- Describe the importance and limitations of patient transition processes.
- Describe ancillary services that are available to facilitate patient transitions.
- Compare postacute care options for patients.
- Explain the strengths and limitations of different communication modalities and their role in patient transitions.
- Explain elements of a high-quality patient handoff.
- Recognize the value of real-time interactive dialogue among clinicians during care transitions.
- Describe the characteristics of a high-quality discharge summary document.
- Recognize the impact of care transitions on patient outcomes and satisfaction.
SKILLS
Hospitalists should be able to:
- Use the most efficient, effective, reliable, and expeditious communication modalities appropriate for a patient’s care transition.
- Communicate and synthesize relevant medical information to and from referring healthcare providers into a cohesive care plan.
- Develop a care plan early during hospitalization that anticipates care needs beyond the inpatient care setting.
- Prepare patients and families early in the hospitalization for anticipated care transitions.
- Access available ancillary services that can facilitate patient transitions.
- Expeditiously inform the primary care provider about significant changes in patient clinical status.
- Inform receiving healthcare providers of pending tests and determine responsibility for the follow-up of pending results.
- Select an appropriate level of postacute care that is best suited to the patient’s needs.
- Incorporate patient preferences and use shared decision-making in the selection of postacute care.
- Anticipate and address language and/or literacy barriers to patient education.
- Communicate with patients and families to explain the patient’s condition, ongoing medical regimens and therapies, follow-up care, and available support services.
- Communicate with patients and families to explain clinical symptomatology that may require medical attention before scheduled follow-up.
- Coordinate multidisciplinary teams early during hospitalization to facilitate patient education, optimize patient function, and improve discharge planning.
- Lead, coordinate, and/or participate in initiatives to develop and implement new protocols to improve or optimize transitions of care.
- Lead, coordinate, and/or participate in the evaluation of new strategies or information systems designed to improve care transitions.
ATTITUDES
Hospitalists should be able to:
- Engage in a multidisciplinary approach to care transitions, including nursing, rehabilitation, nutrition, pharmaceutical, and social services.
- Engage stakeholders in hospital initiatives to continuously assess the quality of care transitions.
- Maintain availability to discharged patients for questions during discharge and between discharge and the follow-up visit with the receiving physician.
1. Forster AJ, Murff HJ, Peterson JF, Gandhi TK, Bates DW. Adverse drug events occurring following hospital discharge. J Gen Intern Med. 2005;20(4):317-323.
2. Forster AJ, Murff HJ, Peterson JF, Gandhi TK, Bates DW. The incidence and severity of adverse events affecting patients after discharge from the hospital. Ann Intern Med. 2003;138(3):161-167.
1. Forster AJ, Murff HJ, Peterson JF, Gandhi TK, Bates DW. Adverse drug events occurring following hospital discharge. J Gen Intern Med. 2005;20(4):317-323.
2. Forster AJ, Murff HJ, Peterson JF, Gandhi TK, Bates DW. The incidence and severity of adverse events affecting patients after discharge from the hospital. Ann Intern Med. 2003;138(3):161-167.
© 2017 Society of Hospital Medicine
Acute Coronary Syndrome. 2017 Hospital Medicine Revised Core Competency
Acute coronary syndrome (ACS) encompasses a spectrum of ischemic heart disease that may include unstable angina (UA), non–ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). Coronary artery disease (CAD) is the leading cause of mortality in the United States and accounts for 1 in 6 deaths annually. Each year, approximately 635,000 Americans have ACS and 300,000 have a recurrent event.1 Of persons who experience a coronary event or myocardial infarction, approximately 34% and 15%, respectively, will die.1 More than 45% of patients with symptoms of acute myocardial infarction arrive at the hospital 4 or more hours after symptom onset, and the mortality rate increases for every 30 minutes that elapse before a patient with ACS is diagnosed and treated.2,3 A shorter time to intervention leads to improved outcomes.4,5 If the acute stage of a myocardial infarction is survived, patients have a risk of illness and mortality that is 1.5 to 15 times higher than that of the general population.1,6 Annually in the United States, the number of hospital discharges with a primary or secondary diagnosis of ACS approaches 1.2 million.1 Hospitalists diagnose, risk stratify, and initiate early management of patients with ACS. Hospitalists provide leadership for multidisciplinary teams that optimize the quality of inpatient care, maximize opportunities for patient education, and efficiently use resources. In addition, hospitalists initiate secondary preventive measures and facilitate adherence to outpatient medical regimens.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
- Define and differentiate UA, NSTEMI, and STEMI.
- Describe the pathophysiologic processes and variable clinical presentations of patients with ACS.
- Distinguish ACS from other cardiac and noncardiac conditions that may mimic this disease process.
- Describe the use of cardiac biomarkers in the diagnosis of ACS, including timing of testing and the effects of renal disease and other conditions (such as pulmonary embolism or sepsis) on cardiac biomarker levels.
- Describe the role of noninvasive cardiac tests in the diagnosis and management of ACS.
- Explain indications for and risks associated with cardiac catheterization.
- Recognize indications for early specialty consultation, which may include cardiology and cardiothoracic surgery.
- List the major and minor risk factors predisposing patients to CAD.
- Explain the value and use of validated risk stratification tools.
- Explain indications for hospitalization of patients with chest pain.
- Explain indications and contraindications for fibrinolytic therapy.
- Explain indications, contraindications, and mechanisms of action of pharmacologic agents that are used both upstream and downstream to treat ACS.
- Describe factors that indicate the need for early invasive interventions, including angiography, percutaneous coronary intervention, and/or coronary artery bypass grafting.
- Describe the optimal timeframe for coronary reperfusion when indicated.
- Identify clinical, laboratory, and imaging studies that indicate severity of disease.
- Recognize appropriate timing and thresholds for hospital discharge, including specific measures of clinical stability for safe transition of care.
SKILLS
Hospitalists should be able to:
- Elicit a thorough and relevant medical history with emphasis on presenting symptoms and patient risk factors for CAD.
- Perform a physical examination with emphasis on the cardiovascular and pulmonary systems and recognize clinical signs of ACS and disease severity.
- Diagnose ACS through interpretation of expedited testing, including history, physical examination, electrocardiogram, chest radiograph, and biomarkers.
- Perform early risk stratification using validated risk stratification tools.
- Synthesize results of history, physical examination, electrocardiography, laboratory and imaging studies, and risk stratification tools to determine therapeutic options, formulate an evidence-based treatment plan, and determine level of care required.
- Identify patients who may benefit from fibrinolytic therapy and/or early revascularization in a timely manner, and activate appropriate teams accordingly.
- Treat patients’ symptoms of chest pain, anxiety, and other discomfort associated with ACS.
- Initiate immediate indicated therapies when patients display symptoms and signs of decompensation.
- Anticipate and address factors that may complicate ACS or its management, which may include inadequate response to therapies, hemodynamic and cardiopulmonary compromise, life-threatening cardiac arrhythmias, or bleeding.
- Assess patients with suspected ACS in a timely manner, identify the level of care required, and manage or comanage the patient with the primary requesting service.
- Communicate with patients and families to explain the history and prognosis of their cardiac disease.
- Communicate with patients and families to explain tests and procedures and their indications and to obtain informed consent.
- Communicate with patients and families to explain the use and potential adverse effects of pharmacologic agents.
- Facilitate discharge planning early during hospitalization.
- Communicate with patients and families to explain the goals of care, discharge instructions, and management after hospital discharge to ensure safe follow-up and transition of care.
- Initiate secondary preventive measures before discharge, which may include smoking cessation, dietary modification, and evidence-based medical therapies.
- Communicate to outpatient providers the notable events of the hospitalization and postdischarge needs including outpatient cardiac rehabilitation.
- Provide and coordinate resources to ensure safe transition from the hospital to arranged follow-up care.
ATTITUDES
Hospitalists should be able to:
- Employ a multidisciplinary approach, which may include nursing, nutrition, rehabilitation, and social services, in the care of patients with ACS that begins at admission and continues through all care transitions.
- Follow evidence-based recommendations, protocols, and risk-stratification tools for the treatment of ACS.
SYSTEM ORGANIZATION AND IMPROVEMENT
To improve efficiency and quality within their organizations, hospitalists should:
- Lead, coordinate, and/or participate in efforts to develop protocols to rapidly identify patients with ACS and minimize time to intervention.
- Lead, coordinate, and/or participate in efforts among institutions to develop protocols for the rapid identification and transfer of patients with ACS to appropriate facilities.
- Implement systems to ensure hospital-wide adherence to national standards and document those measures as specified by recognized organizations (eg, The Joint Commission, American Heart Association, American College of Cardiology, Agency for Healthcare Research and Quality).
- Lead, coordinate, and/or participate in multidisciplinary initiatives to promote patient safety and optimize resource use, which may include order sets for ACS and chest pain.
- Lead, coordinate, and/or participate in efforts to educate staff on the importance of smoking cessation counseling and other preventive measures.
- Integrate outcomes research, institution-specific laboratory policies, and hospital formulary to create indicated and cost-effective diagnostic and management strategies for patients with ACS.
1. Mozaffarian D, Benjamin EJ, Go AS, Arnett DK, Blaha MJ, Cushman M, et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2015 update: a report from the American Heart Association. Circulation. 2015;131(4):e29-e322.
2. McGinn AP, Rosamond WD, Goff DC Jr, Taylor HA, Miles JS, Chambless L. Trends in prehospital delay time and use of emergency medical services for acute myocardial infarction: experience in 4 US communities from 1987-2000. Am Heart J. 2005;150(3):392-400.
3. Rogers WJ, Canto JG, Lambrew CT, Tiefenbrunn AJ, Kinkaid B, Shoultz DA, et al. Temporal trends in the treatment of over 1.5 million patients with myocardial infarction in the US from 1990 through 1999: the National Registry of Myocardial Infarction 1, 2 and 3. J Am Coll Cardiol. 2000;36(7):2056-2063.
4. McNamara RL, Wang Y, Herrin J, Curtis JP, Bradley EH, Magid DJ, et al; NRMI Investigators. Effect of door-to-balloon time on mortality in patients with ST-segment elevation myocardial infarction. J Am Coll Cardiol. 2006;47(11):2180-2186.
5. Saczynski JS, Yarzebski J, Lessard D, Spencer FA, Gurwitz JH, Gore JM, et al. Trends in prehospital delay in patients with acute myocardial infarction (from the Worcester Heart Attack Study). Am J Cardiol. 2008;102(12):1589-1594.
6. Thom TJ, Kannel WB, Silbershatz H, D’Agostino RB Sr. Cardiovascular diseases in the United States and prevention approaches. In: Fuster V, Alexander RW, O’Rourke RA, Roberts R, King SB 3rd, Wellens HJJ, eds. Hurst’s the Heart. 10th ed. New York, NY: McGraw-Hill; 2001:3-7.
Acute coronary syndrome (ACS) encompasses a spectrum of ischemic heart disease that may include unstable angina (UA), non–ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). Coronary artery disease (CAD) is the leading cause of mortality in the United States and accounts for 1 in 6 deaths annually. Each year, approximately 635,000 Americans have ACS and 300,000 have a recurrent event.1 Of persons who experience a coronary event or myocardial infarction, approximately 34% and 15%, respectively, will die.1 More than 45% of patients with symptoms of acute myocardial infarction arrive at the hospital 4 or more hours after symptom onset, and the mortality rate increases for every 30 minutes that elapse before a patient with ACS is diagnosed and treated.2,3 A shorter time to intervention leads to improved outcomes.4,5 If the acute stage of a myocardial infarction is survived, patients have a risk of illness and mortality that is 1.5 to 15 times higher than that of the general population.1,6 Annually in the United States, the number of hospital discharges with a primary or secondary diagnosis of ACS approaches 1.2 million.1 Hospitalists diagnose, risk stratify, and initiate early management of patients with ACS. Hospitalists provide leadership for multidisciplinary teams that optimize the quality of inpatient care, maximize opportunities for patient education, and efficiently use resources. In addition, hospitalists initiate secondary preventive measures and facilitate adherence to outpatient medical regimens.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
- Define and differentiate UA, NSTEMI, and STEMI.
- Describe the pathophysiologic processes and variable clinical presentations of patients with ACS.
- Distinguish ACS from other cardiac and noncardiac conditions that may mimic this disease process.
- Describe the use of cardiac biomarkers in the diagnosis of ACS, including timing of testing and the effects of renal disease and other conditions (such as pulmonary embolism or sepsis) on cardiac biomarker levels.
- Describe the role of noninvasive cardiac tests in the diagnosis and management of ACS.
- Explain indications for and risks associated with cardiac catheterization.
- Recognize indications for early specialty consultation, which may include cardiology and cardiothoracic surgery.
- List the major and minor risk factors predisposing patients to CAD.
- Explain the value and use of validated risk stratification tools.
- Explain indications for hospitalization of patients with chest pain.
- Explain indications and contraindications for fibrinolytic therapy.
- Explain indications, contraindications, and mechanisms of action of pharmacologic agents that are used both upstream and downstream to treat ACS.
- Describe factors that indicate the need for early invasive interventions, including angiography, percutaneous coronary intervention, and/or coronary artery bypass grafting.
- Describe the optimal timeframe for coronary reperfusion when indicated.
- Identify clinical, laboratory, and imaging studies that indicate severity of disease.
- Recognize appropriate timing and thresholds for hospital discharge, including specific measures of clinical stability for safe transition of care.
SKILLS
Hospitalists should be able to:
- Elicit a thorough and relevant medical history with emphasis on presenting symptoms and patient risk factors for CAD.
- Perform a physical examination with emphasis on the cardiovascular and pulmonary systems and recognize clinical signs of ACS and disease severity.
- Diagnose ACS through interpretation of expedited testing, including history, physical examination, electrocardiogram, chest radiograph, and biomarkers.
- Perform early risk stratification using validated risk stratification tools.
- Synthesize results of history, physical examination, electrocardiography, laboratory and imaging studies, and risk stratification tools to determine therapeutic options, formulate an evidence-based treatment plan, and determine level of care required.
- Identify patients who may benefit from fibrinolytic therapy and/or early revascularization in a timely manner, and activate appropriate teams accordingly.
- Treat patients’ symptoms of chest pain, anxiety, and other discomfort associated with ACS.
- Initiate immediate indicated therapies when patients display symptoms and signs of decompensation.
- Anticipate and address factors that may complicate ACS or its management, which may include inadequate response to therapies, hemodynamic and cardiopulmonary compromise, life-threatening cardiac arrhythmias, or bleeding.
- Assess patients with suspected ACS in a timely manner, identify the level of care required, and manage or comanage the patient with the primary requesting service.
- Communicate with patients and families to explain the history and prognosis of their cardiac disease.
- Communicate with patients and families to explain tests and procedures and their indications and to obtain informed consent.
- Communicate with patients and families to explain the use and potential adverse effects of pharmacologic agents.
- Facilitate discharge planning early during hospitalization.
- Communicate with patients and families to explain the goals of care, discharge instructions, and management after hospital discharge to ensure safe follow-up and transition of care.
- Initiate secondary preventive measures before discharge, which may include smoking cessation, dietary modification, and evidence-based medical therapies.
- Communicate to outpatient providers the notable events of the hospitalization and postdischarge needs including outpatient cardiac rehabilitation.
- Provide and coordinate resources to ensure safe transition from the hospital to arranged follow-up care.
ATTITUDES
Hospitalists should be able to:
- Employ a multidisciplinary approach, which may include nursing, nutrition, rehabilitation, and social services, in the care of patients with ACS that begins at admission and continues through all care transitions.
- Follow evidence-based recommendations, protocols, and risk-stratification tools for the treatment of ACS.
SYSTEM ORGANIZATION AND IMPROVEMENT
To improve efficiency and quality within their organizations, hospitalists should:
- Lead, coordinate, and/or participate in efforts to develop protocols to rapidly identify patients with ACS and minimize time to intervention.
- Lead, coordinate, and/or participate in efforts among institutions to develop protocols for the rapid identification and transfer of patients with ACS to appropriate facilities.
- Implement systems to ensure hospital-wide adherence to national standards and document those measures as specified by recognized organizations (eg, The Joint Commission, American Heart Association, American College of Cardiology, Agency for Healthcare Research and Quality).
- Lead, coordinate, and/or participate in multidisciplinary initiatives to promote patient safety and optimize resource use, which may include order sets for ACS and chest pain.
- Lead, coordinate, and/or participate in efforts to educate staff on the importance of smoking cessation counseling and other preventive measures.
- Integrate outcomes research, institution-specific laboratory policies, and hospital formulary to create indicated and cost-effective diagnostic and management strategies for patients with ACS.
Acute coronary syndrome (ACS) encompasses a spectrum of ischemic heart disease that may include unstable angina (UA), non–ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). Coronary artery disease (CAD) is the leading cause of mortality in the United States and accounts for 1 in 6 deaths annually. Each year, approximately 635,000 Americans have ACS and 300,000 have a recurrent event.1 Of persons who experience a coronary event or myocardial infarction, approximately 34% and 15%, respectively, will die.1 More than 45% of patients with symptoms of acute myocardial infarction arrive at the hospital 4 or more hours after symptom onset, and the mortality rate increases for every 30 minutes that elapse before a patient with ACS is diagnosed and treated.2,3 A shorter time to intervention leads to improved outcomes.4,5 If the acute stage of a myocardial infarction is survived, patients have a risk of illness and mortality that is 1.5 to 15 times higher than that of the general population.1,6 Annually in the United States, the number of hospital discharges with a primary or secondary diagnosis of ACS approaches 1.2 million.1 Hospitalists diagnose, risk stratify, and initiate early management of patients with ACS. Hospitalists provide leadership for multidisciplinary teams that optimize the quality of inpatient care, maximize opportunities for patient education, and efficiently use resources. In addition, hospitalists initiate secondary preventive measures and facilitate adherence to outpatient medical regimens.
Want all 52 JHM Core Competency articles in an easy-to-read compendium? Order your copy now from Amazon.com.
KNOWLEDGE
Hospitalists should be able to:
- Define and differentiate UA, NSTEMI, and STEMI.
- Describe the pathophysiologic processes and variable clinical presentations of patients with ACS.
- Distinguish ACS from other cardiac and noncardiac conditions that may mimic this disease process.
- Describe the use of cardiac biomarkers in the diagnosis of ACS, including timing of testing and the effects of renal disease and other conditions (such as pulmonary embolism or sepsis) on cardiac biomarker levels.
- Describe the role of noninvasive cardiac tests in the diagnosis and management of ACS.
- Explain indications for and risks associated with cardiac catheterization.
- Recognize indications for early specialty consultation, which may include cardiology and cardiothoracic surgery.
- List the major and minor risk factors predisposing patients to CAD.
- Explain the value and use of validated risk stratification tools.
- Explain indications for hospitalization of patients with chest pain.
- Explain indications and contraindications for fibrinolytic therapy.
- Explain indications, contraindications, and mechanisms of action of pharmacologic agents that are used both upstream and downstream to treat ACS.
- Describe factors that indicate the need for early invasive interventions, including angiography, percutaneous coronary intervention, and/or coronary artery bypass grafting.
- Describe the optimal timeframe for coronary reperfusion when indicated.
- Identify clinical, laboratory, and imaging studies that indicate severity of disease.
- Recognize appropriate timing and thresholds for hospital discharge, including specific measures of clinical stability for safe transition of care.
SKILLS
Hospitalists should be able to:
- Elicit a thorough and relevant medical history with emphasis on presenting symptoms and patient risk factors for CAD.
- Perform a physical examination with emphasis on the cardiovascular and pulmonary systems and recognize clinical signs of ACS and disease severity.
- Diagnose ACS through interpretation of expedited testing, including history, physical examination, electrocardiogram, chest radiograph, and biomarkers.
- Perform early risk stratification using validated risk stratification tools.
- Synthesize results of history, physical examination, electrocardiography, laboratory and imaging studies, and risk stratification tools to determine therapeutic options, formulate an evidence-based treatment plan, and determine level of care required.
- Identify patients who may benefit from fibrinolytic therapy and/or early revascularization in a timely manner, and activate appropriate teams accordingly.
- Treat patients’ symptoms of chest pain, anxiety, and other discomfort associated with ACS.
- Initiate immediate indicated therapies when patients display symptoms and signs of decompensation.
- Anticipate and address factors that may complicate ACS or its management, which may include inadequate response to therapies, hemodynamic and cardiopulmonary compromise, life-threatening cardiac arrhythmias, or bleeding.
- Assess patients with suspected ACS in a timely manner, identify the level of care required, and manage or comanage the patient with the primary requesting service.
- Communicate with patients and families to explain the history and prognosis of their cardiac disease.
- Communicate with patients and families to explain tests and procedures and their indications and to obtain informed consent.
- Communicate with patients and families to explain the use and potential adverse effects of pharmacologic agents.
- Facilitate discharge planning early during hospitalization.
- Communicate with patients and families to explain the goals of care, discharge instructions, and management after hospital discharge to ensure safe follow-up and transition of care.
- Initiate secondary preventive measures before discharge, which may include smoking cessation, dietary modification, and evidence-based medical therapies.
- Communicate to outpatient providers the notable events of the hospitalization and postdischarge needs including outpatient cardiac rehabilitation.
- Provide and coordinate resources to ensure safe transition from the hospital to arranged follow-up care.
ATTITUDES
Hospitalists should be able to:
- Employ a multidisciplinary approach, which may include nursing, nutrition, rehabilitation, and social services, in the care of patients with ACS that begins at admission and continues through all care transitions.
- Follow evidence-based recommendations, protocols, and risk-stratification tools for the treatment of ACS.
SYSTEM ORGANIZATION AND IMPROVEMENT
To improve efficiency and quality within their organizations, hospitalists should:
- Lead, coordinate, and/or participate in efforts to develop protocols to rapidly identify patients with ACS and minimize time to intervention.
- Lead, coordinate, and/or participate in efforts among institutions to develop protocols for the rapid identification and transfer of patients with ACS to appropriate facilities.
- Implement systems to ensure hospital-wide adherence to national standards and document those measures as specified by recognized organizations (eg, The Joint Commission, American Heart Association, American College of Cardiology, Agency for Healthcare Research and Quality).
- Lead, coordinate, and/or participate in multidisciplinary initiatives to promote patient safety and optimize resource use, which may include order sets for ACS and chest pain.
- Lead, coordinate, and/or participate in efforts to educate staff on the importance of smoking cessation counseling and other preventive measures.
- Integrate outcomes research, institution-specific laboratory policies, and hospital formulary to create indicated and cost-effective diagnostic and management strategies for patients with ACS.
1. Mozaffarian D, Benjamin EJ, Go AS, Arnett DK, Blaha MJ, Cushman M, et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2015 update: a report from the American Heart Association. Circulation. 2015;131(4):e29-e322.
2. McGinn AP, Rosamond WD, Goff DC Jr, Taylor HA, Miles JS, Chambless L. Trends in prehospital delay time and use of emergency medical services for acute myocardial infarction: experience in 4 US communities from 1987-2000. Am Heart J. 2005;150(3):392-400.
3. Rogers WJ, Canto JG, Lambrew CT, Tiefenbrunn AJ, Kinkaid B, Shoultz DA, et al. Temporal trends in the treatment of over 1.5 million patients with myocardial infarction in the US from 1990 through 1999: the National Registry of Myocardial Infarction 1, 2 and 3. J Am Coll Cardiol. 2000;36(7):2056-2063.
4. McNamara RL, Wang Y, Herrin J, Curtis JP, Bradley EH, Magid DJ, et al; NRMI Investigators. Effect of door-to-balloon time on mortality in patients with ST-segment elevation myocardial infarction. J Am Coll Cardiol. 2006;47(11):2180-2186.
5. Saczynski JS, Yarzebski J, Lessard D, Spencer FA, Gurwitz JH, Gore JM, et al. Trends in prehospital delay in patients with acute myocardial infarction (from the Worcester Heart Attack Study). Am J Cardiol. 2008;102(12):1589-1594.
6. Thom TJ, Kannel WB, Silbershatz H, D’Agostino RB Sr. Cardiovascular diseases in the United States and prevention approaches. In: Fuster V, Alexander RW, O’Rourke RA, Roberts R, King SB 3rd, Wellens HJJ, eds. Hurst’s the Heart. 10th ed. New York, NY: McGraw-Hill; 2001:3-7.
1. Mozaffarian D, Benjamin EJ, Go AS, Arnett DK, Blaha MJ, Cushman M, et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2015 update: a report from the American Heart Association. Circulation. 2015;131(4):e29-e322.
2. McGinn AP, Rosamond WD, Goff DC Jr, Taylor HA, Miles JS, Chambless L. Trends in prehospital delay time and use of emergency medical services for acute myocardial infarction: experience in 4 US communities from 1987-2000. Am Heart J. 2005;150(3):392-400.
3. Rogers WJ, Canto JG, Lambrew CT, Tiefenbrunn AJ, Kinkaid B, Shoultz DA, et al. Temporal trends in the treatment of over 1.5 million patients with myocardial infarction in the US from 1990 through 1999: the National Registry of Myocardial Infarction 1, 2 and 3. J Am Coll Cardiol. 2000;36(7):2056-2063.
4. McNamara RL, Wang Y, Herrin J, Curtis JP, Bradley EH, Magid DJ, et al; NRMI Investigators. Effect of door-to-balloon time on mortality in patients with ST-segment elevation myocardial infarction. J Am Coll Cardiol. 2006;47(11):2180-2186.
5. Saczynski JS, Yarzebski J, Lessard D, Spencer FA, Gurwitz JH, Gore JM, et al. Trends in prehospital delay in patients with acute myocardial infarction (from the Worcester Heart Attack Study). Am J Cardiol. 2008;102(12):1589-1594.
6. Thom TJ, Kannel WB, Silbershatz H, D’Agostino RB Sr. Cardiovascular diseases in the United States and prevention approaches. In: Fuster V, Alexander RW, O’Rourke RA, Roberts R, King SB 3rd, Wellens HJJ, eds. Hurst’s the Heart. 10th ed. New York, NY: McGraw-Hill; 2001:3-7.
© 2017 Society of Hospital Medicine
Reverse T3 or perverse T3? Still puzzling after 40 years
Four decades after reverse T3 (3,3´5´-triiodothyronine) was discovered, its physiologic and clinical relevance remains unclear and is still being studied. But scientific uncertainty has not stopped writers in the consumer press and on the Internet from making unsubstantiated claims about this hormone. Many patients believe their hypothyroid symptoms are due to high levels of reverse T3 and want to be tested for it, and some even bring in test results from independent laboratories.
HOW THYROID HORMONES WERE DISCOVERED
In 1970, Braverman et al9 showed that T4 is converted to T3 in athyreotic humans, and Sterling et al10 demonstrated the same in healthy humans. During that decade, techniques for measuring T4 were refined,11 and a specific radioimmunoassay for reverse T3 allowed a glimpse of its physiologic role.12 In 1975, Chopra et al13 noted reciprocal changes in the levels of T3 and reverse T3 in systemic illnesses—ie, when people are sick, their T3 levels go down and their reverse T3 levels go up.
The end of the 70s was marked by a surge of interest in T4 metabolites, including the development of a radioimmunoassay for 3,3´-diiodothyronine (3-3´ T2).18
The observed reciprocal changes in serum levels of T3 and reverse T3 suggested that T4 degradation is regulated into activating (T3) or inactivating (reverse T3) pathways, and that these changes are a presumed homeostatic process of energy conservation.19
HOW THYROID HORMONES ARE METABOLIZED
In the thyroid gland, for thyroid hormones to be synthesized, iodide must be oxidized and incorporated into the precursors 3-monoiodotyrosine (MIT) and 3,5-diiodotyrosine (DIT). This process is mediated by the enzyme thyroid peroxidase in the presence of hydrogen peroxide.20
The thyroid can make T4 and some T3
T4 is the main iodothyronine produced by the thyroid gland, at a rate of 80 to 100 µg per day.21 It is synthesized from the fusion of 2 DIT molecules.
The thyroid can also make T3 by fusing 1 DIT and 1 MIT molecule, but this process accounts for no more than 20% of the circulating T3 in humans. The rest of T3, and 95% to 98% of all reverse T3, is derived from peripheral conversion of T4 through deiodination.
T4 is converted to T3 or reverse T3
The metabolic transformation of thyroid hormones in peripheral tissues determines their biologic potency and regulates their biologic effects.
The number 4 in T4 means it has 4 iodine atoms. It can lose 1 of them, yielding either T3 or reverse T3, depending on which iodine atom it loses (Figure 3). Loss of iodine from the five-prime (5´) position on its outer ring yields T3, the most potent thyroid hormone, produced at a rate of 30 to 40 µg per day.21 On the other hand, when T4 loses an iodine atom from the five (5) position on its inner ring it yields reverse T3, produced at a rate slightly less than that of T3, 28 to 40 µg per day.21 Reverse T3 is inactive.
Both T3 and reverse T3 can shed more iodine atoms, forming in turn various isomers of T2, T1, and ultimately T0. Other pathways for thyroid hormone metabolism include glucuronidation, sulfation, oxidative deamination, and ether bond cleavage.20–22
D1 and D2 catalyze T3, D3 catalyzes reverse T3
Three types of enzymes that mediate deiodination have been identified and designated D1, D2, and D3. In humans they are expressed in variable amounts throughout the body:
- D1 mainly in the liver, kidneys, thyroid, and pituitary, but notably absent in the central nervous system
- D2 in the central nervous system, pituitary, brown adipose tissue, thyroid, placenta, skeletal muscle, and heart
- D3 in the central nervous system, skin, hemangiomas, fetal liver, placenta, and fetal tissues.23
D1 and D2 are responsible for converting T4 to T3, and D3 is responsible for converting T4 to reverse T3.
Plasma concentrations of free T4 and free T3 are relatively constant; however, tissue concentrations of free T3 vary in different tissues according to the amount of hormone transported and the activity of local deiodinases.23 Most thyroid hormone actions are initiated after T3 binds to its nuclear receptor. In this setting, deiodinases play a critical role in maintaining tissue and cellular thyroid hormone levels, so that thyroid hormone signaling can change irrespective of serum hormonal concentrations.22–24 For example, in the central nervous system, production of T3 by local D2 is significantly relevant for T3 homeostasis.22,23
Deiodinases also modulate the tissue-specific concentrations of T3 in response to iodine deficiency and to changes in thyroid state.23 During iodine deficiency and hypothyroidism, tissues that express D2, especially brain tissues, increase the activity of this enzyme in order to increase local conversion of T4 to T3. In hyperthyroidism, D1 overexpression contributes to the relative excess of T3 production, while D3 up-regulation in the brain protects the central nervous system from excessive amounts of thyroid hormone.23
REVERSE T3 AND SYSTEMIC ILLNESS
D3 is the main physiologic inactivator of thyroid hormones. This enzyme plays a central role in protecting tissues from an excess of thyroid hormone.23,24 This mechanism is crucial for fetal development and explains the high expression of D3 in the human placenta and fetal tissues.
In adult tissues, the importance of D3 in the regulation of thyroid hormone homeostasis becomes apparent under certain pathophysiologic conditions, such as nonthyroidal illness and malnutrition.
Whenever a reduction in metabolism is homeostatically desirable, such as in critically ill patients or during starvation, conversion to T3 is reduced and, alternatively, conversion to reverse T3 is increased. This pathway represents a metabolic adaptation that may protect the tissues from the catabolic effects of thyroid hormone that could otherwise worsen the patient’s basic clinical condition.
Euthyroid sick syndrome or hypothyroid?
In a variety of systemic illnesses, some patients with low T3, low or normal T4, and normal thyroid-stimulating hormone (TSH) levels could in fact be “sick euthyroid” rather than hypothyroid. The first reports of the euthyroid sick syndrome or low T3 syndrome date back to about 1976, and even though assays for reverse T3 were not widely available, some authors linked the syndrome to high levels of reverse T3.15,16 The syndrome is also known as nonthyroidal illness syndrome.
Advances in techniques for measuring T3, reverse T3, and other iodothyronines filled a gap in the understanding of the alterations that occur in thyroid hormone economy during severe nonthyroidal diseases. In 1982, Wartofsky and Burman25 reviewed the alterations in thyroid function in patients with systemic illness and discussed other factors that may alter thyroid economy, such as age, stress, and diverse drugs.
More recently, the low-T3 syndrome was revisited with a generalized concept regarding the role of D3 in the syndrome.26 D3, normally undetectable in mature tissues, is reactivated in diverse cell types in response to injury and is responsible for a fall in serum T3 levels. Hypoxia induces D3 activity and mRNA in vitro and in vivo.27 Recent studies have focused on the role of cytokines in the low T3 syndrome. For instance, interleukin 6 reduces D1 and D2 activity and increases D3 activity in vitro.28
In the outpatient setting, diverse conditions may affect thyroid hormone homeostasis, compatible with mild or atypical forms of low-T3 syndrome, including caloric deprivation, heart failure, and human immunodeficiency virus infection.29
POSSIBLE CLINICAL UTILITY OF MEASURING REVERSE T3
In inpatients
Unfortunately, measuring serum reverse T3 levels has not, in general, proven clinically useful for the diagnosis of hypothyroidism in systemically ill patients. Burmeister30 demonstrated, in a retrospective study, that when illness complicates the interpretation of thyroid function tests, serum reverse T3 measurements do not reliably distinguish the hypothyroid sick patient from the euthyroid sick patient. The best way to make the diagnosis, Burmeister suggested, is by clinical assessment, combined use of free T4 and TSH measurements, and patient follow-up.
In the outpatient setting, the utility of reverse T3 measurements is controversial. In intensive care units, the differential diagnosis between hypothyroidism and nonthyroidal illness syndrome can sometimes be difficult. Reverse T3 levels can be low, normal, or high regardless of the thyroidal state of the patient.30 Moreover, endogenous changes in the hypothalamic-pituitary-thyroid axis may be further complicated by medications commonly used in intensive care units, such as dopamine and glucocorticoids. Changes in thyroid function should be evaluated in the context of the patient’s clinical condition (Table 1).20 But regardless of the T3 level, treatment with T3 or T4 should not be started without taking into consideration the patient’s general clinical context; controlled trials have not shown such therapy to be beneficial.20
In outpatients
In noncritical conditions that may be associated with mild forms of low T3 syndrome, patients generally present with low T3 concentrations concurrently with low or normal TSH. Not infrequently, however, patients present with a serum reverse T3 measurement and impute their symptoms of hypothyroidism to “abnormal” reverse T3 levels, in spite of normal TSH levels.
There is no rationale for measuring reverse T3 to initiate or to adjust levothyroxine therapy—the single test relevant for these purposes is the TSH measurement. The risks of basing treatment decisions on reverse T3 levels include the use of excessive doses of levothyroxine that may lead to a state of subclinical or even clinical hyperthyroidism.
TAKE-HOME MESSAGE
The existence of an inactivating pathway of thyroid hormones represents a homeostatic mechanism, and in selected circumstances measuring serum reverse T3 may be useful, such as in euthyroid sick patients. The discovery of the molecular mechanisms that lead to the reactivation of D3 in illness is an important field of research.
- Kendall EC. Landmark article, June 19, 1915. The isolation in crystalline form of the compound containing iodin, which occurs in the thyroid. Its chemical nature and physiologic activity. By E.C. Kendall. JAMA 1983; 250(15):2045–2046. doi:10.1001/jama.1983.03340150087037
- Harington CR. Chemistry of thyroxine: isolation of thyroxine from the thyroid gland. Biochem J 1926; 20(2):293–299. pmid: 16743658
- Harington CR, Barger G. Chemistry of thyroxine: constitution and synthesis of thyroxine. Biochem J 1927; 21(1):169–183. pmid:16743801
- Gross J, Pitt-Rivers R. The identification of 3,5,3’L-triiodothyronine in human plasma. Lancet 1952; 1(6705):439–441. doi:10.1016/S0140-6736(52)91952-1
- Gross J, Pitt-Rivers R. 3:5:3’-triiodothyronine. 1. Isolation from thyroid gland and synthesis. Biochem J 1953; 53(4):645–650. pmid:13032123
- Pitt-Rivers R, Stanbury JB, Rapp B. Conversion of thyroxine to 3-5-3´-triiodothyronine in vivo. J Clin Endocrinol Metab 1955; 15(5):616–620. doi:10.1210/jcem-15-5-616
- Maclagan NF, Bowden CH, Wilkinson JH. The metabolism of thyroid hormones. 2. Detection of thyroxine and tri-iodothyronine in human plasma. Biochem J. 1957; 67(1):5–11. pmid:13471502
- Galton VA, Pitt-Rivers R. The identification of the acetic acid analogues of thyroxine and tri-iodothyronine in mammalian tissues. Biochem J 1959; 72(2):319–321. pmid: 13662303
- Braverman LE, Ingbar SH, Sterling K. Conversion of thyroxine (T4) to triiodothyronine (T3) in athyreotic human subjects. J Clin Invest 1970; 49(5):855–864. doi:10.1172/JCI106304
- Sterling K, Brenner MA, Newman ES. Conversion of thyroxine to triiodothyronine in normal human subjects. Science 1970; 169(3950):1099–1100. doi:10.1126/science.169.3950.1099
- Chopra IJ. A radioimmunoassay for measurement of thyroxine in unextracted serum. J Clin Endocrinol Metab 1972; 34:938–947. doi:10.1210/jcem-34-6-938
- Chopra IJ. A radioimmunoassay for measurement of 3,3´,5´-triiodothyronine (reverse T3). J Clin Invest 1974; 54(3):583–592. doi:10.1172/JCI107795
- Chopra IJ, Chopra U, Smith SR, Reza M, Solomon DH. Reciprocal changes in serum concentrations of 3,3´,5-triiodothyronine (T3) in systemic illnesses. J Clin Endocrinol Metab 1975; 41(6):1043–1049. doi:10.1210/jcem-41-6-1043
- Burman KD, Read J, Dimond RC, Strum D, et al. Measurement of 3,3’,5’-triiodothyroinine (reverse T3), 3,3’-L-diiodothyronine, T3 and T4 in human amniotic fluid and in cord and maternal serum. J Clin Endocrinol Metab 1976; 43(6):1351–1359. doi:10.1210/jcem-43-6-1351
- Rubenfeld S. Euthyroid sick syndrome. N Engl J Med 1978; 299(25):1414. doi:10.1056/NEJM197812212992514
- Burger A, Nicod P, Suter P, Vallotton MB, Vagenakis P, Braverman L. Reduced active thyroid hormone levels in acute illness. Lancet 1976; 1(7961):653–655. doi:10.1016/S0140-6736(76)92774-4
- Burman KD, Dimond RC, Wright FD, Earll JM, Bruton J, Wartofsky L. A radioimmunoassay for 3,3´,5´-L-triiodothyronine (reverse T3): assessment of thyroid gland content and serum measurements in conditions of normal and altered thyroidal economy and following administration of thyrotropin releasing hormone (TRH) and thyrotropin (TSH). J Clin Endocrinol Metab 1977; 44(4):660–672. doi:10.1210/jcem-44-4-660
- Burman KD, Strum D, Dimond RC, et al. A radioimmunoassay for 3,3´-L-diiodothyronine (3,3´T2). J Clin Endocrinol Metab 1977; 45(2):339–352. doi:10.1210/jcem-45-2-339
- Burman KD. Recent developments in thyroid hormone metabolism: interpretation and significance of measurements of reverse T3, 3,3´T2, and thyroglobulin. Metabolism 1978; 27(5):615–630. doi:10.1016/0026-0495(78)90028-8.
- Salvatore D, Davies TF, Schlumberger M, Hay ID, Larsen PR. Thyroid physiology and diagnostic evaluation of patients with thyroid disorders. In: Melmed S, Polonsky KS, Larsen PR, Kronenberg HM, eds. Williams Textbook of Endocrinology. 13th ed. Philadelphia, PA; Elsevier; 2016:334–368.
- Engler D, Burger AG. The deiodination of the iodothyronines and of their derivatives in man. Endocr Rev 1984; 5(2):151–184. doi:10.1210/edrv-5-2-151
- Peeters RP, Visser TJ, Peeters RP. Metabolism of thyroid hormone. Thyroid Disease Manager. www.thyroidmanager.org/chapter/metabolism-of-thyroid-hormone. Accessed March 14, 2018.
- Bianco AC, Salvatore D, Gereben B, Berry MJ, Larsen PR. Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases. Endocr Rev 2002; 23(1):38–89. doi:10.1210/edrv.23.1.0455
- Dentice M, Salvatore D. Deiodinases: the balance of thyroid hormone: local impact of thyroid hormone inactivation. J Endocrinol 2011; 209(3):273–282. doi:10.1530/JOE-11-0002
- Wartofsky L, Burman KD. Alterations in thyroid function in patients with systemic illness: the “euthyroid sick syndrome.” Endocr Rev 1982; 3(2):164–217. doi:10.1210/edrv-3-2-164
- Huang SA, Bianco AC. Reawakened interest in type III iodothyronine deiodinase in critical illness and injury. Nat Clin Pract Endocrinol Metab 2008; 4(3):148–155. doi:10.1038/ncpendmet0727
- Simonides WS, Mulcahey MA, Redout EM, et al. Hypoxia-inducible factor induces local thyroid hormone inactivation during hypoxic-ischemic disease in rats. J Clin Invest 2008; 118(3):975–983. doi:10.1172/JCI32824
- Wajner SM, Goemann IM, Bueno AL, Larsen PR, Maia AL. IL-6 promotes nonthyroidal illness syndrome by blocking thyroxine activation while promoting thyroid hormone inactivation in human cells. J Clin Invest 2011; 121(5):1834–1845. doi:10.1172/JCI44678
- Moura Neto A, Zantut-Wittmann DE. Abnormalities of thyroid hormone metabolism during systemic illness: the low T3 syndrome in different clinical settings. Int J Endocrinol 2016; 2016:2157583. doi:10.1155/2016/2157583
- Burmeister LA. Reverse T3 does not reliably differentiate hypothyroid sick syndrome from euthyroid sick syndrome. Thyroid 1995; 5(6):435–441. doi:10.1089/thy.1995.5.435
- Huang SA, Tu HM, Harney JW, et al. Severe hypothyroidism caused by type 3 iodothyronine deiodinase in infantile hemangiomas. N Engl J Med 2000; 343(3):185–189. doi:10.1056/NEJM200007203430305
Four decades after reverse T3 (3,3´5´-triiodothyronine) was discovered, its physiologic and clinical relevance remains unclear and is still being studied. But scientific uncertainty has not stopped writers in the consumer press and on the Internet from making unsubstantiated claims about this hormone. Many patients believe their hypothyroid symptoms are due to high levels of reverse T3 and want to be tested for it, and some even bring in test results from independent laboratories.
HOW THYROID HORMONES WERE DISCOVERED
In 1970, Braverman et al9 showed that T4 is converted to T3 in athyreotic humans, and Sterling et al10 demonstrated the same in healthy humans. During that decade, techniques for measuring T4 were refined,11 and a specific radioimmunoassay for reverse T3 allowed a glimpse of its physiologic role.12 In 1975, Chopra et al13 noted reciprocal changes in the levels of T3 and reverse T3 in systemic illnesses—ie, when people are sick, their T3 levels go down and their reverse T3 levels go up.
The end of the 70s was marked by a surge of interest in T4 metabolites, including the development of a radioimmunoassay for 3,3´-diiodothyronine (3-3´ T2).18
The observed reciprocal changes in serum levels of T3 and reverse T3 suggested that T4 degradation is regulated into activating (T3) or inactivating (reverse T3) pathways, and that these changes are a presumed homeostatic process of energy conservation.19
HOW THYROID HORMONES ARE METABOLIZED
In the thyroid gland, for thyroid hormones to be synthesized, iodide must be oxidized and incorporated into the precursors 3-monoiodotyrosine (MIT) and 3,5-diiodotyrosine (DIT). This process is mediated by the enzyme thyroid peroxidase in the presence of hydrogen peroxide.20
The thyroid can make T4 and some T3
T4 is the main iodothyronine produced by the thyroid gland, at a rate of 80 to 100 µg per day.21 It is synthesized from the fusion of 2 DIT molecules.
The thyroid can also make T3 by fusing 1 DIT and 1 MIT molecule, but this process accounts for no more than 20% of the circulating T3 in humans. The rest of T3, and 95% to 98% of all reverse T3, is derived from peripheral conversion of T4 through deiodination.
T4 is converted to T3 or reverse T3
The metabolic transformation of thyroid hormones in peripheral tissues determines their biologic potency and regulates their biologic effects.
The number 4 in T4 means it has 4 iodine atoms. It can lose 1 of them, yielding either T3 or reverse T3, depending on which iodine atom it loses (Figure 3). Loss of iodine from the five-prime (5´) position on its outer ring yields T3, the most potent thyroid hormone, produced at a rate of 30 to 40 µg per day.21 On the other hand, when T4 loses an iodine atom from the five (5) position on its inner ring it yields reverse T3, produced at a rate slightly less than that of T3, 28 to 40 µg per day.21 Reverse T3 is inactive.
Both T3 and reverse T3 can shed more iodine atoms, forming in turn various isomers of T2, T1, and ultimately T0. Other pathways for thyroid hormone metabolism include glucuronidation, sulfation, oxidative deamination, and ether bond cleavage.20–22
D1 and D2 catalyze T3, D3 catalyzes reverse T3
Three types of enzymes that mediate deiodination have been identified and designated D1, D2, and D3. In humans they are expressed in variable amounts throughout the body:
- D1 mainly in the liver, kidneys, thyroid, and pituitary, but notably absent in the central nervous system
- D2 in the central nervous system, pituitary, brown adipose tissue, thyroid, placenta, skeletal muscle, and heart
- D3 in the central nervous system, skin, hemangiomas, fetal liver, placenta, and fetal tissues.23
D1 and D2 are responsible for converting T4 to T3, and D3 is responsible for converting T4 to reverse T3.
Plasma concentrations of free T4 and free T3 are relatively constant; however, tissue concentrations of free T3 vary in different tissues according to the amount of hormone transported and the activity of local deiodinases.23 Most thyroid hormone actions are initiated after T3 binds to its nuclear receptor. In this setting, deiodinases play a critical role in maintaining tissue and cellular thyroid hormone levels, so that thyroid hormone signaling can change irrespective of serum hormonal concentrations.22–24 For example, in the central nervous system, production of T3 by local D2 is significantly relevant for T3 homeostasis.22,23
Deiodinases also modulate the tissue-specific concentrations of T3 in response to iodine deficiency and to changes in thyroid state.23 During iodine deficiency and hypothyroidism, tissues that express D2, especially brain tissues, increase the activity of this enzyme in order to increase local conversion of T4 to T3. In hyperthyroidism, D1 overexpression contributes to the relative excess of T3 production, while D3 up-regulation in the brain protects the central nervous system from excessive amounts of thyroid hormone.23
REVERSE T3 AND SYSTEMIC ILLNESS
D3 is the main physiologic inactivator of thyroid hormones. This enzyme plays a central role in protecting tissues from an excess of thyroid hormone.23,24 This mechanism is crucial for fetal development and explains the high expression of D3 in the human placenta and fetal tissues.
In adult tissues, the importance of D3 in the regulation of thyroid hormone homeostasis becomes apparent under certain pathophysiologic conditions, such as nonthyroidal illness and malnutrition.
Whenever a reduction in metabolism is homeostatically desirable, such as in critically ill patients or during starvation, conversion to T3 is reduced and, alternatively, conversion to reverse T3 is increased. This pathway represents a metabolic adaptation that may protect the tissues from the catabolic effects of thyroid hormone that could otherwise worsen the patient’s basic clinical condition.
Euthyroid sick syndrome or hypothyroid?
In a variety of systemic illnesses, some patients with low T3, low or normal T4, and normal thyroid-stimulating hormone (TSH) levels could in fact be “sick euthyroid” rather than hypothyroid. The first reports of the euthyroid sick syndrome or low T3 syndrome date back to about 1976, and even though assays for reverse T3 were not widely available, some authors linked the syndrome to high levels of reverse T3.15,16 The syndrome is also known as nonthyroidal illness syndrome.
Advances in techniques for measuring T3, reverse T3, and other iodothyronines filled a gap in the understanding of the alterations that occur in thyroid hormone economy during severe nonthyroidal diseases. In 1982, Wartofsky and Burman25 reviewed the alterations in thyroid function in patients with systemic illness and discussed other factors that may alter thyroid economy, such as age, stress, and diverse drugs.
More recently, the low-T3 syndrome was revisited with a generalized concept regarding the role of D3 in the syndrome.26 D3, normally undetectable in mature tissues, is reactivated in diverse cell types in response to injury and is responsible for a fall in serum T3 levels. Hypoxia induces D3 activity and mRNA in vitro and in vivo.27 Recent studies have focused on the role of cytokines in the low T3 syndrome. For instance, interleukin 6 reduces D1 and D2 activity and increases D3 activity in vitro.28
In the outpatient setting, diverse conditions may affect thyroid hormone homeostasis, compatible with mild or atypical forms of low-T3 syndrome, including caloric deprivation, heart failure, and human immunodeficiency virus infection.29
POSSIBLE CLINICAL UTILITY OF MEASURING REVERSE T3
In inpatients
Unfortunately, measuring serum reverse T3 levels has not, in general, proven clinically useful for the diagnosis of hypothyroidism in systemically ill patients. Burmeister30 demonstrated, in a retrospective study, that when illness complicates the interpretation of thyroid function tests, serum reverse T3 measurements do not reliably distinguish the hypothyroid sick patient from the euthyroid sick patient. The best way to make the diagnosis, Burmeister suggested, is by clinical assessment, combined use of free T4 and TSH measurements, and patient follow-up.
In the outpatient setting, the utility of reverse T3 measurements is controversial. In intensive care units, the differential diagnosis between hypothyroidism and nonthyroidal illness syndrome can sometimes be difficult. Reverse T3 levels can be low, normal, or high regardless of the thyroidal state of the patient.30 Moreover, endogenous changes in the hypothalamic-pituitary-thyroid axis may be further complicated by medications commonly used in intensive care units, such as dopamine and glucocorticoids. Changes in thyroid function should be evaluated in the context of the patient’s clinical condition (Table 1).20 But regardless of the T3 level, treatment with T3 or T4 should not be started without taking into consideration the patient’s general clinical context; controlled trials have not shown such therapy to be beneficial.20
In outpatients
In noncritical conditions that may be associated with mild forms of low T3 syndrome, patients generally present with low T3 concentrations concurrently with low or normal TSH. Not infrequently, however, patients present with a serum reverse T3 measurement and impute their symptoms of hypothyroidism to “abnormal” reverse T3 levels, in spite of normal TSH levels.
There is no rationale for measuring reverse T3 to initiate or to adjust levothyroxine therapy—the single test relevant for these purposes is the TSH measurement. The risks of basing treatment decisions on reverse T3 levels include the use of excessive doses of levothyroxine that may lead to a state of subclinical or even clinical hyperthyroidism.
TAKE-HOME MESSAGE
The existence of an inactivating pathway of thyroid hormones represents a homeostatic mechanism, and in selected circumstances measuring serum reverse T3 may be useful, such as in euthyroid sick patients. The discovery of the molecular mechanisms that lead to the reactivation of D3 in illness is an important field of research.
Four decades after reverse T3 (3,3´5´-triiodothyronine) was discovered, its physiologic and clinical relevance remains unclear and is still being studied. But scientific uncertainty has not stopped writers in the consumer press and on the Internet from making unsubstantiated claims about this hormone. Many patients believe their hypothyroid symptoms are due to high levels of reverse T3 and want to be tested for it, and some even bring in test results from independent laboratories.
HOW THYROID HORMONES WERE DISCOVERED
In 1970, Braverman et al9 showed that T4 is converted to T3 in athyreotic humans, and Sterling et al10 demonstrated the same in healthy humans. During that decade, techniques for measuring T4 were refined,11 and a specific radioimmunoassay for reverse T3 allowed a glimpse of its physiologic role.12 In 1975, Chopra et al13 noted reciprocal changes in the levels of T3 and reverse T3 in systemic illnesses—ie, when people are sick, their T3 levels go down and their reverse T3 levels go up.
The end of the 70s was marked by a surge of interest in T4 metabolites, including the development of a radioimmunoassay for 3,3´-diiodothyronine (3-3´ T2).18
The observed reciprocal changes in serum levels of T3 and reverse T3 suggested that T4 degradation is regulated into activating (T3) or inactivating (reverse T3) pathways, and that these changes are a presumed homeostatic process of energy conservation.19
HOW THYROID HORMONES ARE METABOLIZED
In the thyroid gland, for thyroid hormones to be synthesized, iodide must be oxidized and incorporated into the precursors 3-monoiodotyrosine (MIT) and 3,5-diiodotyrosine (DIT). This process is mediated by the enzyme thyroid peroxidase in the presence of hydrogen peroxide.20
The thyroid can make T4 and some T3
T4 is the main iodothyronine produced by the thyroid gland, at a rate of 80 to 100 µg per day.21 It is synthesized from the fusion of 2 DIT molecules.
The thyroid can also make T3 by fusing 1 DIT and 1 MIT molecule, but this process accounts for no more than 20% of the circulating T3 in humans. The rest of T3, and 95% to 98% of all reverse T3, is derived from peripheral conversion of T4 through deiodination.
T4 is converted to T3 or reverse T3
The metabolic transformation of thyroid hormones in peripheral tissues determines their biologic potency and regulates their biologic effects.
The number 4 in T4 means it has 4 iodine atoms. It can lose 1 of them, yielding either T3 or reverse T3, depending on which iodine atom it loses (Figure 3). Loss of iodine from the five-prime (5´) position on its outer ring yields T3, the most potent thyroid hormone, produced at a rate of 30 to 40 µg per day.21 On the other hand, when T4 loses an iodine atom from the five (5) position on its inner ring it yields reverse T3, produced at a rate slightly less than that of T3, 28 to 40 µg per day.21 Reverse T3 is inactive.
Both T3 and reverse T3 can shed more iodine atoms, forming in turn various isomers of T2, T1, and ultimately T0. Other pathways for thyroid hormone metabolism include glucuronidation, sulfation, oxidative deamination, and ether bond cleavage.20–22
D1 and D2 catalyze T3, D3 catalyzes reverse T3
Three types of enzymes that mediate deiodination have been identified and designated D1, D2, and D3. In humans they are expressed in variable amounts throughout the body:
- D1 mainly in the liver, kidneys, thyroid, and pituitary, but notably absent in the central nervous system
- D2 in the central nervous system, pituitary, brown adipose tissue, thyroid, placenta, skeletal muscle, and heart
- D3 in the central nervous system, skin, hemangiomas, fetal liver, placenta, and fetal tissues.23
D1 and D2 are responsible for converting T4 to T3, and D3 is responsible for converting T4 to reverse T3.
Plasma concentrations of free T4 and free T3 are relatively constant; however, tissue concentrations of free T3 vary in different tissues according to the amount of hormone transported and the activity of local deiodinases.23 Most thyroid hormone actions are initiated after T3 binds to its nuclear receptor. In this setting, deiodinases play a critical role in maintaining tissue and cellular thyroid hormone levels, so that thyroid hormone signaling can change irrespective of serum hormonal concentrations.22–24 For example, in the central nervous system, production of T3 by local D2 is significantly relevant for T3 homeostasis.22,23
Deiodinases also modulate the tissue-specific concentrations of T3 in response to iodine deficiency and to changes in thyroid state.23 During iodine deficiency and hypothyroidism, tissues that express D2, especially brain tissues, increase the activity of this enzyme in order to increase local conversion of T4 to T3. In hyperthyroidism, D1 overexpression contributes to the relative excess of T3 production, while D3 up-regulation in the brain protects the central nervous system from excessive amounts of thyroid hormone.23
REVERSE T3 AND SYSTEMIC ILLNESS
D3 is the main physiologic inactivator of thyroid hormones. This enzyme plays a central role in protecting tissues from an excess of thyroid hormone.23,24 This mechanism is crucial for fetal development and explains the high expression of D3 in the human placenta and fetal tissues.
In adult tissues, the importance of D3 in the regulation of thyroid hormone homeostasis becomes apparent under certain pathophysiologic conditions, such as nonthyroidal illness and malnutrition.
Whenever a reduction in metabolism is homeostatically desirable, such as in critically ill patients or during starvation, conversion to T3 is reduced and, alternatively, conversion to reverse T3 is increased. This pathway represents a metabolic adaptation that may protect the tissues from the catabolic effects of thyroid hormone that could otherwise worsen the patient’s basic clinical condition.
Euthyroid sick syndrome or hypothyroid?
In a variety of systemic illnesses, some patients with low T3, low or normal T4, and normal thyroid-stimulating hormone (TSH) levels could in fact be “sick euthyroid” rather than hypothyroid. The first reports of the euthyroid sick syndrome or low T3 syndrome date back to about 1976, and even though assays for reverse T3 were not widely available, some authors linked the syndrome to high levels of reverse T3.15,16 The syndrome is also known as nonthyroidal illness syndrome.
Advances in techniques for measuring T3, reverse T3, and other iodothyronines filled a gap in the understanding of the alterations that occur in thyroid hormone economy during severe nonthyroidal diseases. In 1982, Wartofsky and Burman25 reviewed the alterations in thyroid function in patients with systemic illness and discussed other factors that may alter thyroid economy, such as age, stress, and diverse drugs.
More recently, the low-T3 syndrome was revisited with a generalized concept regarding the role of D3 in the syndrome.26 D3, normally undetectable in mature tissues, is reactivated in diverse cell types in response to injury and is responsible for a fall in serum T3 levels. Hypoxia induces D3 activity and mRNA in vitro and in vivo.27 Recent studies have focused on the role of cytokines in the low T3 syndrome. For instance, interleukin 6 reduces D1 and D2 activity and increases D3 activity in vitro.28
In the outpatient setting, diverse conditions may affect thyroid hormone homeostasis, compatible with mild or atypical forms of low-T3 syndrome, including caloric deprivation, heart failure, and human immunodeficiency virus infection.29
POSSIBLE CLINICAL UTILITY OF MEASURING REVERSE T3
In inpatients
Unfortunately, measuring serum reverse T3 levels has not, in general, proven clinically useful for the diagnosis of hypothyroidism in systemically ill patients. Burmeister30 demonstrated, in a retrospective study, that when illness complicates the interpretation of thyroid function tests, serum reverse T3 measurements do not reliably distinguish the hypothyroid sick patient from the euthyroid sick patient. The best way to make the diagnosis, Burmeister suggested, is by clinical assessment, combined use of free T4 and TSH measurements, and patient follow-up.
In the outpatient setting, the utility of reverse T3 measurements is controversial. In intensive care units, the differential diagnosis between hypothyroidism and nonthyroidal illness syndrome can sometimes be difficult. Reverse T3 levels can be low, normal, or high regardless of the thyroidal state of the patient.30 Moreover, endogenous changes in the hypothalamic-pituitary-thyroid axis may be further complicated by medications commonly used in intensive care units, such as dopamine and glucocorticoids. Changes in thyroid function should be evaluated in the context of the patient’s clinical condition (Table 1).20 But regardless of the T3 level, treatment with T3 or T4 should not be started without taking into consideration the patient’s general clinical context; controlled trials have not shown such therapy to be beneficial.20
In outpatients
In noncritical conditions that may be associated with mild forms of low T3 syndrome, patients generally present with low T3 concentrations concurrently with low or normal TSH. Not infrequently, however, patients present with a serum reverse T3 measurement and impute their symptoms of hypothyroidism to “abnormal” reverse T3 levels, in spite of normal TSH levels.
There is no rationale for measuring reverse T3 to initiate or to adjust levothyroxine therapy—the single test relevant for these purposes is the TSH measurement. The risks of basing treatment decisions on reverse T3 levels include the use of excessive doses of levothyroxine that may lead to a state of subclinical or even clinical hyperthyroidism.
TAKE-HOME MESSAGE
The existence of an inactivating pathway of thyroid hormones represents a homeostatic mechanism, and in selected circumstances measuring serum reverse T3 may be useful, such as in euthyroid sick patients. The discovery of the molecular mechanisms that lead to the reactivation of D3 in illness is an important field of research.
- Kendall EC. Landmark article, June 19, 1915. The isolation in crystalline form of the compound containing iodin, which occurs in the thyroid. Its chemical nature and physiologic activity. By E.C. Kendall. JAMA 1983; 250(15):2045–2046. doi:10.1001/jama.1983.03340150087037
- Harington CR. Chemistry of thyroxine: isolation of thyroxine from the thyroid gland. Biochem J 1926; 20(2):293–299. pmid: 16743658
- Harington CR, Barger G. Chemistry of thyroxine: constitution and synthesis of thyroxine. Biochem J 1927; 21(1):169–183. pmid:16743801
- Gross J, Pitt-Rivers R. The identification of 3,5,3’L-triiodothyronine in human plasma. Lancet 1952; 1(6705):439–441. doi:10.1016/S0140-6736(52)91952-1
- Gross J, Pitt-Rivers R. 3:5:3’-triiodothyronine. 1. Isolation from thyroid gland and synthesis. Biochem J 1953; 53(4):645–650. pmid:13032123
- Pitt-Rivers R, Stanbury JB, Rapp B. Conversion of thyroxine to 3-5-3´-triiodothyronine in vivo. J Clin Endocrinol Metab 1955; 15(5):616–620. doi:10.1210/jcem-15-5-616
- Maclagan NF, Bowden CH, Wilkinson JH. The metabolism of thyroid hormones. 2. Detection of thyroxine and tri-iodothyronine in human plasma. Biochem J. 1957; 67(1):5–11. pmid:13471502
- Galton VA, Pitt-Rivers R. The identification of the acetic acid analogues of thyroxine and tri-iodothyronine in mammalian tissues. Biochem J 1959; 72(2):319–321. pmid: 13662303
- Braverman LE, Ingbar SH, Sterling K. Conversion of thyroxine (T4) to triiodothyronine (T3) in athyreotic human subjects. J Clin Invest 1970; 49(5):855–864. doi:10.1172/JCI106304
- Sterling K, Brenner MA, Newman ES. Conversion of thyroxine to triiodothyronine in normal human subjects. Science 1970; 169(3950):1099–1100. doi:10.1126/science.169.3950.1099
- Chopra IJ. A radioimmunoassay for measurement of thyroxine in unextracted serum. J Clin Endocrinol Metab 1972; 34:938–947. doi:10.1210/jcem-34-6-938
- Chopra IJ. A radioimmunoassay for measurement of 3,3´,5´-triiodothyronine (reverse T3). J Clin Invest 1974; 54(3):583–592. doi:10.1172/JCI107795
- Chopra IJ, Chopra U, Smith SR, Reza M, Solomon DH. Reciprocal changes in serum concentrations of 3,3´,5-triiodothyronine (T3) in systemic illnesses. J Clin Endocrinol Metab 1975; 41(6):1043–1049. doi:10.1210/jcem-41-6-1043
- Burman KD, Read J, Dimond RC, Strum D, et al. Measurement of 3,3’,5’-triiodothyroinine (reverse T3), 3,3’-L-diiodothyronine, T3 and T4 in human amniotic fluid and in cord and maternal serum. J Clin Endocrinol Metab 1976; 43(6):1351–1359. doi:10.1210/jcem-43-6-1351
- Rubenfeld S. Euthyroid sick syndrome. N Engl J Med 1978; 299(25):1414. doi:10.1056/NEJM197812212992514
- Burger A, Nicod P, Suter P, Vallotton MB, Vagenakis P, Braverman L. Reduced active thyroid hormone levels in acute illness. Lancet 1976; 1(7961):653–655. doi:10.1016/S0140-6736(76)92774-4
- Burman KD, Dimond RC, Wright FD, Earll JM, Bruton J, Wartofsky L. A radioimmunoassay for 3,3´,5´-L-triiodothyronine (reverse T3): assessment of thyroid gland content and serum measurements in conditions of normal and altered thyroidal economy and following administration of thyrotropin releasing hormone (TRH) and thyrotropin (TSH). J Clin Endocrinol Metab 1977; 44(4):660–672. doi:10.1210/jcem-44-4-660
- Burman KD, Strum D, Dimond RC, et al. A radioimmunoassay for 3,3´-L-diiodothyronine (3,3´T2). J Clin Endocrinol Metab 1977; 45(2):339–352. doi:10.1210/jcem-45-2-339
- Burman KD. Recent developments in thyroid hormone metabolism: interpretation and significance of measurements of reverse T3, 3,3´T2, and thyroglobulin. Metabolism 1978; 27(5):615–630. doi:10.1016/0026-0495(78)90028-8.
- Salvatore D, Davies TF, Schlumberger M, Hay ID, Larsen PR. Thyroid physiology and diagnostic evaluation of patients with thyroid disorders. In: Melmed S, Polonsky KS, Larsen PR, Kronenberg HM, eds. Williams Textbook of Endocrinology. 13th ed. Philadelphia, PA; Elsevier; 2016:334–368.
- Engler D, Burger AG. The deiodination of the iodothyronines and of their derivatives in man. Endocr Rev 1984; 5(2):151–184. doi:10.1210/edrv-5-2-151
- Peeters RP, Visser TJ, Peeters RP. Metabolism of thyroid hormone. Thyroid Disease Manager. www.thyroidmanager.org/chapter/metabolism-of-thyroid-hormone. Accessed March 14, 2018.
- Bianco AC, Salvatore D, Gereben B, Berry MJ, Larsen PR. Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases. Endocr Rev 2002; 23(1):38–89. doi:10.1210/edrv.23.1.0455
- Dentice M, Salvatore D. Deiodinases: the balance of thyroid hormone: local impact of thyroid hormone inactivation. J Endocrinol 2011; 209(3):273–282. doi:10.1530/JOE-11-0002
- Wartofsky L, Burman KD. Alterations in thyroid function in patients with systemic illness: the “euthyroid sick syndrome.” Endocr Rev 1982; 3(2):164–217. doi:10.1210/edrv-3-2-164
- Huang SA, Bianco AC. Reawakened interest in type III iodothyronine deiodinase in critical illness and injury. Nat Clin Pract Endocrinol Metab 2008; 4(3):148–155. doi:10.1038/ncpendmet0727
- Simonides WS, Mulcahey MA, Redout EM, et al. Hypoxia-inducible factor induces local thyroid hormone inactivation during hypoxic-ischemic disease in rats. J Clin Invest 2008; 118(3):975–983. doi:10.1172/JCI32824
- Wajner SM, Goemann IM, Bueno AL, Larsen PR, Maia AL. IL-6 promotes nonthyroidal illness syndrome by blocking thyroxine activation while promoting thyroid hormone inactivation in human cells. J Clin Invest 2011; 121(5):1834–1845. doi:10.1172/JCI44678
- Moura Neto A, Zantut-Wittmann DE. Abnormalities of thyroid hormone metabolism during systemic illness: the low T3 syndrome in different clinical settings. Int J Endocrinol 2016; 2016:2157583. doi:10.1155/2016/2157583
- Burmeister LA. Reverse T3 does not reliably differentiate hypothyroid sick syndrome from euthyroid sick syndrome. Thyroid 1995; 5(6):435–441. doi:10.1089/thy.1995.5.435
- Huang SA, Tu HM, Harney JW, et al. Severe hypothyroidism caused by type 3 iodothyronine deiodinase in infantile hemangiomas. N Engl J Med 2000; 343(3):185–189. doi:10.1056/NEJM200007203430305
- Kendall EC. Landmark article, June 19, 1915. The isolation in crystalline form of the compound containing iodin, which occurs in the thyroid. Its chemical nature and physiologic activity. By E.C. Kendall. JAMA 1983; 250(15):2045–2046. doi:10.1001/jama.1983.03340150087037
- Harington CR. Chemistry of thyroxine: isolation of thyroxine from the thyroid gland. Biochem J 1926; 20(2):293–299. pmid: 16743658
- Harington CR, Barger G. Chemistry of thyroxine: constitution and synthesis of thyroxine. Biochem J 1927; 21(1):169–183. pmid:16743801
- Gross J, Pitt-Rivers R. The identification of 3,5,3’L-triiodothyronine in human plasma. Lancet 1952; 1(6705):439–441. doi:10.1016/S0140-6736(52)91952-1
- Gross J, Pitt-Rivers R. 3:5:3’-triiodothyronine. 1. Isolation from thyroid gland and synthesis. Biochem J 1953; 53(4):645–650. pmid:13032123
- Pitt-Rivers R, Stanbury JB, Rapp B. Conversion of thyroxine to 3-5-3´-triiodothyronine in vivo. J Clin Endocrinol Metab 1955; 15(5):616–620. doi:10.1210/jcem-15-5-616
- Maclagan NF, Bowden CH, Wilkinson JH. The metabolism of thyroid hormones. 2. Detection of thyroxine and tri-iodothyronine in human plasma. Biochem J. 1957; 67(1):5–11. pmid:13471502
- Galton VA, Pitt-Rivers R. The identification of the acetic acid analogues of thyroxine and tri-iodothyronine in mammalian tissues. Biochem J 1959; 72(2):319–321. pmid: 13662303
- Braverman LE, Ingbar SH, Sterling K. Conversion of thyroxine (T4) to triiodothyronine (T3) in athyreotic human subjects. J Clin Invest 1970; 49(5):855–864. doi:10.1172/JCI106304
- Sterling K, Brenner MA, Newman ES. Conversion of thyroxine to triiodothyronine in normal human subjects. Science 1970; 169(3950):1099–1100. doi:10.1126/science.169.3950.1099
- Chopra IJ. A radioimmunoassay for measurement of thyroxine in unextracted serum. J Clin Endocrinol Metab 1972; 34:938–947. doi:10.1210/jcem-34-6-938
- Chopra IJ. A radioimmunoassay for measurement of 3,3´,5´-triiodothyronine (reverse T3). J Clin Invest 1974; 54(3):583–592. doi:10.1172/JCI107795
- Chopra IJ, Chopra U, Smith SR, Reza M, Solomon DH. Reciprocal changes in serum concentrations of 3,3´,5-triiodothyronine (T3) in systemic illnesses. J Clin Endocrinol Metab 1975; 41(6):1043–1049. doi:10.1210/jcem-41-6-1043
- Burman KD, Read J, Dimond RC, Strum D, et al. Measurement of 3,3’,5’-triiodothyroinine (reverse T3), 3,3’-L-diiodothyronine, T3 and T4 in human amniotic fluid and in cord and maternal serum. J Clin Endocrinol Metab 1976; 43(6):1351–1359. doi:10.1210/jcem-43-6-1351
- Rubenfeld S. Euthyroid sick syndrome. N Engl J Med 1978; 299(25):1414. doi:10.1056/NEJM197812212992514
- Burger A, Nicod P, Suter P, Vallotton MB, Vagenakis P, Braverman L. Reduced active thyroid hormone levels in acute illness. Lancet 1976; 1(7961):653–655. doi:10.1016/S0140-6736(76)92774-4
- Burman KD, Dimond RC, Wright FD, Earll JM, Bruton J, Wartofsky L. A radioimmunoassay for 3,3´,5´-L-triiodothyronine (reverse T3): assessment of thyroid gland content and serum measurements in conditions of normal and altered thyroidal economy and following administration of thyrotropin releasing hormone (TRH) and thyrotropin (TSH). J Clin Endocrinol Metab 1977; 44(4):660–672. doi:10.1210/jcem-44-4-660
- Burman KD, Strum D, Dimond RC, et al. A radioimmunoassay for 3,3´-L-diiodothyronine (3,3´T2). J Clin Endocrinol Metab 1977; 45(2):339–352. doi:10.1210/jcem-45-2-339
- Burman KD. Recent developments in thyroid hormone metabolism: interpretation and significance of measurements of reverse T3, 3,3´T2, and thyroglobulin. Metabolism 1978; 27(5):615–630. doi:10.1016/0026-0495(78)90028-8.
- Salvatore D, Davies TF, Schlumberger M, Hay ID, Larsen PR. Thyroid physiology and diagnostic evaluation of patients with thyroid disorders. In: Melmed S, Polonsky KS, Larsen PR, Kronenberg HM, eds. Williams Textbook of Endocrinology. 13th ed. Philadelphia, PA; Elsevier; 2016:334–368.
- Engler D, Burger AG. The deiodination of the iodothyronines and of their derivatives in man. Endocr Rev 1984; 5(2):151–184. doi:10.1210/edrv-5-2-151
- Peeters RP, Visser TJ, Peeters RP. Metabolism of thyroid hormone. Thyroid Disease Manager. www.thyroidmanager.org/chapter/metabolism-of-thyroid-hormone. Accessed March 14, 2018.
- Bianco AC, Salvatore D, Gereben B, Berry MJ, Larsen PR. Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases. Endocr Rev 2002; 23(1):38–89. doi:10.1210/edrv.23.1.0455
- Dentice M, Salvatore D. Deiodinases: the balance of thyroid hormone: local impact of thyroid hormone inactivation. J Endocrinol 2011; 209(3):273–282. doi:10.1530/JOE-11-0002
- Wartofsky L, Burman KD. Alterations in thyroid function in patients with systemic illness: the “euthyroid sick syndrome.” Endocr Rev 1982; 3(2):164–217. doi:10.1210/edrv-3-2-164
- Huang SA, Bianco AC. Reawakened interest in type III iodothyronine deiodinase in critical illness and injury. Nat Clin Pract Endocrinol Metab 2008; 4(3):148–155. doi:10.1038/ncpendmet0727
- Simonides WS, Mulcahey MA, Redout EM, et al. Hypoxia-inducible factor induces local thyroid hormone inactivation during hypoxic-ischemic disease in rats. J Clin Invest 2008; 118(3):975–983. doi:10.1172/JCI32824
- Wajner SM, Goemann IM, Bueno AL, Larsen PR, Maia AL. IL-6 promotes nonthyroidal illness syndrome by blocking thyroxine activation while promoting thyroid hormone inactivation in human cells. J Clin Invest 2011; 121(5):1834–1845. doi:10.1172/JCI44678
- Moura Neto A, Zantut-Wittmann DE. Abnormalities of thyroid hormone metabolism during systemic illness: the low T3 syndrome in different clinical settings. Int J Endocrinol 2016; 2016:2157583. doi:10.1155/2016/2157583
- Burmeister LA. Reverse T3 does not reliably differentiate hypothyroid sick syndrome from euthyroid sick syndrome. Thyroid 1995; 5(6):435–441. doi:10.1089/thy.1995.5.435
- Huang SA, Tu HM, Harney JW, et al. Severe hypothyroidism caused by type 3 iodothyronine deiodinase in infantile hemangiomas. N Engl J Med 2000; 343(3):185–189. doi:10.1056/NEJM200007203430305
Training physician leaders to save the health system…and us
Lerman and Jameson1 recently called for expanding formal leadership development of physicians and increasing the reach of effective physician leaders. From the perspective of physicians, these are certainly good goals. We should have leaders in white coats who understand the joy of practicing medicine and can rally for our missions, challenges, and passions as doctors, clinical educators, and researchers.
But the rationale for most of their argument seems to stem from the perceived need to train physician leaders to promote the survival of increasingly complex health systems and strategically guide individual institutions. This seems also to be the focus of many health systems as they search for and hire physicians for various system leadership positions. But only in the final sentence of their thoughtful essay do Lerman and Jameson mention “patient and physician satisfaction and improved clinical outcomes,” and then only as a byproduct of achieving “organizational efficiency.”1
The financial success (ie, survival) of a health system and the emotional well-being and clinical skills of its physicians are clearly interrelated and cannot be completely dichotomized, and I am not implying that Lerman and Jameson have done so. But trying to promote both can create potential for mission malalignment. Achieving an appropriate balance between these two goals, which at a tactical level are not always congruent, is critical. Training leaders in the skills to achieve alignment with the organization’s culture and priorities may make it easier to administer and guide the course of a medical system with apparent physician leadership, but it still may not well represent the human constituents. The recent trend for health systems to establish new committees charged with improving physician wellness is a statement of problem recognition, but whether their existence can accomplish “mission alignment” remains to be seen.
Swensen et al2 from the Mayo Clinic have highlighted the need to focus on the needs of the physician, and not primarily on those of the institution, to reduce the epidemic of physician burnout. A physician leader who is wonderfully trained in organizational psychology, communication skills, and performance metrics analysis, but who lacks a deep and authentic understanding of the joys of practicing medicine and delivering care to the sick, of the need to stoke the individual physician’s intellectual curiosity and provide time for reflection to clinicians working in their institutions, is a unidirectional institutional leader, and thus a leader in name alone. We need to be careful about grooming young physician leaders at too early a stage. Having the book knowledge of a physician is not the same as having the heart of one.
We have appropriately morphed away from the academic curriculum vitae as the only ticket to titled organizational leadership. But we need to look closely at our choice of physician leaders and be careful that the physician component of that terminology is not defined by degree alone. Just as the number of first-authored publications and surgical procedures performed should not suffice for selection to leadership positions, nor should participation in leadership courses or the ability to respond as desired in a behavioral interview be viewed as adequate for selection as a leader of physicians. Administrators with a tailored MBA degree, extensive and real job experience in a clinical center, and participation in a seminar on physician behavior can also be successful supervisors and (maybe) leaders in a medical center.
But if we really care about our clinical staff, organizational leadership must include physicians in positions of influence who are true advocates for clinicians and patients, and not primarily caretakers of the health system and enforcers of performance metrics. Although (some of) the latter are absolutely necessary, we need more than that from our physician leaders. We need them to reflect and support our perspective as well as the institution’s needs. We need them to understand and defend the need to maintain the joy of practicing medicine. How can we as physicians really take care of others if there is no one to take care of us?3
Note: this discussion is not new. We had a dialogue on this topic in the Journal almost 10 years ago!4
- Lerman C, Jameson JL. Leadership development in medicine. N Engl J Med 2018; 378(20):1862–1863. doi:10.1056/NEJMp1801610
- Swensen S, Kabcenell A, Shanafelt T. Physician-organization collaboration reduces physician burnout and promotes engagement: the Mayo Clinic experience. J Healthcare Manag 2016; 61(2):105–127. pmid:27111930
- Shem S. The House of God: A Novel. New York: R. Marek Publishers, 1978.
- Longworth D. A medical center is not a hospital: reflections of a department chair still in the game. Cleve Clin J Med 2008; 75(12):832–834. doi:10.3949/ccjm.75a.08094
Lerman and Jameson1 recently called for expanding formal leadership development of physicians and increasing the reach of effective physician leaders. From the perspective of physicians, these are certainly good goals. We should have leaders in white coats who understand the joy of practicing medicine and can rally for our missions, challenges, and passions as doctors, clinical educators, and researchers.
But the rationale for most of their argument seems to stem from the perceived need to train physician leaders to promote the survival of increasingly complex health systems and strategically guide individual institutions. This seems also to be the focus of many health systems as they search for and hire physicians for various system leadership positions. But only in the final sentence of their thoughtful essay do Lerman and Jameson mention “patient and physician satisfaction and improved clinical outcomes,” and then only as a byproduct of achieving “organizational efficiency.”1
The financial success (ie, survival) of a health system and the emotional well-being and clinical skills of its physicians are clearly interrelated and cannot be completely dichotomized, and I am not implying that Lerman and Jameson have done so. But trying to promote both can create potential for mission malalignment. Achieving an appropriate balance between these two goals, which at a tactical level are not always congruent, is critical. Training leaders in the skills to achieve alignment with the organization’s culture and priorities may make it easier to administer and guide the course of a medical system with apparent physician leadership, but it still may not well represent the human constituents. The recent trend for health systems to establish new committees charged with improving physician wellness is a statement of problem recognition, but whether their existence can accomplish “mission alignment” remains to be seen.
Swensen et al2 from the Mayo Clinic have highlighted the need to focus on the needs of the physician, and not primarily on those of the institution, to reduce the epidemic of physician burnout. A physician leader who is wonderfully trained in organizational psychology, communication skills, and performance metrics analysis, but who lacks a deep and authentic understanding of the joys of practicing medicine and delivering care to the sick, of the need to stoke the individual physician’s intellectual curiosity and provide time for reflection to clinicians working in their institutions, is a unidirectional institutional leader, and thus a leader in name alone. We need to be careful about grooming young physician leaders at too early a stage. Having the book knowledge of a physician is not the same as having the heart of one.
We have appropriately morphed away from the academic curriculum vitae as the only ticket to titled organizational leadership. But we need to look closely at our choice of physician leaders and be careful that the physician component of that terminology is not defined by degree alone. Just as the number of first-authored publications and surgical procedures performed should not suffice for selection to leadership positions, nor should participation in leadership courses or the ability to respond as desired in a behavioral interview be viewed as adequate for selection as a leader of physicians. Administrators with a tailored MBA degree, extensive and real job experience in a clinical center, and participation in a seminar on physician behavior can also be successful supervisors and (maybe) leaders in a medical center.
But if we really care about our clinical staff, organizational leadership must include physicians in positions of influence who are true advocates for clinicians and patients, and not primarily caretakers of the health system and enforcers of performance metrics. Although (some of) the latter are absolutely necessary, we need more than that from our physician leaders. We need them to reflect and support our perspective as well as the institution’s needs. We need them to understand and defend the need to maintain the joy of practicing medicine. How can we as physicians really take care of others if there is no one to take care of us?3
Note: this discussion is not new. We had a dialogue on this topic in the Journal almost 10 years ago!4
Lerman and Jameson1 recently called for expanding formal leadership development of physicians and increasing the reach of effective physician leaders. From the perspective of physicians, these are certainly good goals. We should have leaders in white coats who understand the joy of practicing medicine and can rally for our missions, challenges, and passions as doctors, clinical educators, and researchers.
But the rationale for most of their argument seems to stem from the perceived need to train physician leaders to promote the survival of increasingly complex health systems and strategically guide individual institutions. This seems also to be the focus of many health systems as they search for and hire physicians for various system leadership positions. But only in the final sentence of their thoughtful essay do Lerman and Jameson mention “patient and physician satisfaction and improved clinical outcomes,” and then only as a byproduct of achieving “organizational efficiency.”1
The financial success (ie, survival) of a health system and the emotional well-being and clinical skills of its physicians are clearly interrelated and cannot be completely dichotomized, and I am not implying that Lerman and Jameson have done so. But trying to promote both can create potential for mission malalignment. Achieving an appropriate balance between these two goals, which at a tactical level are not always congruent, is critical. Training leaders in the skills to achieve alignment with the organization’s culture and priorities may make it easier to administer and guide the course of a medical system with apparent physician leadership, but it still may not well represent the human constituents. The recent trend for health systems to establish new committees charged with improving physician wellness is a statement of problem recognition, but whether their existence can accomplish “mission alignment” remains to be seen.
Swensen et al2 from the Mayo Clinic have highlighted the need to focus on the needs of the physician, and not primarily on those of the institution, to reduce the epidemic of physician burnout. A physician leader who is wonderfully trained in organizational psychology, communication skills, and performance metrics analysis, but who lacks a deep and authentic understanding of the joys of practicing medicine and delivering care to the sick, of the need to stoke the individual physician’s intellectual curiosity and provide time for reflection to clinicians working in their institutions, is a unidirectional institutional leader, and thus a leader in name alone. We need to be careful about grooming young physician leaders at too early a stage. Having the book knowledge of a physician is not the same as having the heart of one.
We have appropriately morphed away from the academic curriculum vitae as the only ticket to titled organizational leadership. But we need to look closely at our choice of physician leaders and be careful that the physician component of that terminology is not defined by degree alone. Just as the number of first-authored publications and surgical procedures performed should not suffice for selection to leadership positions, nor should participation in leadership courses or the ability to respond as desired in a behavioral interview be viewed as adequate for selection as a leader of physicians. Administrators with a tailored MBA degree, extensive and real job experience in a clinical center, and participation in a seminar on physician behavior can also be successful supervisors and (maybe) leaders in a medical center.
But if we really care about our clinical staff, organizational leadership must include physicians in positions of influence who are true advocates for clinicians and patients, and not primarily caretakers of the health system and enforcers of performance metrics. Although (some of) the latter are absolutely necessary, we need more than that from our physician leaders. We need them to reflect and support our perspective as well as the institution’s needs. We need them to understand and defend the need to maintain the joy of practicing medicine. How can we as physicians really take care of others if there is no one to take care of us?3
Note: this discussion is not new. We had a dialogue on this topic in the Journal almost 10 years ago!4
- Lerman C, Jameson JL. Leadership development in medicine. N Engl J Med 2018; 378(20):1862–1863. doi:10.1056/NEJMp1801610
- Swensen S, Kabcenell A, Shanafelt T. Physician-organization collaboration reduces physician burnout and promotes engagement: the Mayo Clinic experience. J Healthcare Manag 2016; 61(2):105–127. pmid:27111930
- Shem S. The House of God: A Novel. New York: R. Marek Publishers, 1978.
- Longworth D. A medical center is not a hospital: reflections of a department chair still in the game. Cleve Clin J Med 2008; 75(12):832–834. doi:10.3949/ccjm.75a.08094
- Lerman C, Jameson JL. Leadership development in medicine. N Engl J Med 2018; 378(20):1862–1863. doi:10.1056/NEJMp1801610
- Swensen S, Kabcenell A, Shanafelt T. Physician-organization collaboration reduces physician burnout and promotes engagement: the Mayo Clinic experience. J Healthcare Manag 2016; 61(2):105–127. pmid:27111930
- Shem S. The House of God: A Novel. New York: R. Marek Publishers, 1978.
- Longworth D. A medical center is not a hospital: reflections of a department chair still in the game. Cleve Clin J Med 2008; 75(12):832–834. doi:10.3949/ccjm.75a.08094
Use of Short Peripheral Intravenous Catheters: Characteristics, Management, and Outcomes Worldwide
The majority of hospitalized patients worldwide have at least one peripheral intravenous catheter (PIVC),1 making PIVC insertion one of the most common clinical procedures. In the United States, physicians, advanced practitioners, and nurses insert over 300 million of these devices in hospitalized patients annually.2 Despite their prevalence, PIVCs are associated with high rates of complications, including insertion difficulty, phlebitis, infiltration, occlusion, dislodgment, and catheter-associated bloodstream infection (CABSI), known to increase morbidity and mortality risk.2-9 Up to 90% of PIVCs are prematurely removed owing to failure before planned replacement or before intravenous (IV) therapy completion.3-6,10-12
PIVC complication and failure commonly triggers insertion of a replacement device and can entail significant costs.2-4 One example is PIVC-related CABSI, where treatment costs have been estimated to be between US$35,000 and US$56,000 per patient.6,13 Another important consideration is the pain and anxiety experienced by patients who need a replacement device, particularly those with difficult vascular access, who may require multiple cannulation attempts to replace a PIVC.12,14-16 In developing nations, serious adverse events related to PIVCs are even more concerning, because hospital acquired infection rates and associated mortality are nearly 20 times greater than in developed nations.17
A number of evidence-based interventions have been suggested to reduce PIVC failure rates. In addition to optimal hand hygiene when inserting or accessing a PIVC to prevent infection,18 recommended interventions include placement of the PIVC in an area of non-flexion such as the forearm to provide stability for the device and to reduce patient discomfort, securing the PIVC to reduce movement of the catheter at the insertion site and within the blood vessel, and use of occlusive dressings that reduce the risk of external contamination of the PIVC site.11,19,20 Best practice guidelines also recommend the prompt removal of devices that are symptomatic (when phlebitis or other complications are suspected) and when the catheter is no longer required.21,22
Recent evidence has demonstrated that catheter size can have an impact on device survival rates. In adults, large-bore catheters of 18 gauge (G) or higher were found to have an increased rate of thrombosis, and smaller-bore catheters of 22G or lower (in adults) were found to have higher rates of dislodgment and occlusion/infiltration. The catheter size recommended for adults based on the latest evidence for most clinical applications is 20G.3,20,23,24 In addition, the documentation of insertion, maintenance, and removal of PIVCs in the medical record is a requirement in most healthcare facilities worldwide and is recommended by best practice guidelines; however, adherence remains a challenge.1,19
The concerning prevalence of PIVC-related complications and the lack of comparative data internationally on organizational compliance with best practice guidelines formed the rationale for this study. Our study aim was to describe the insertion characteristics, management practices, and outcomes of PIVCs internationally and to compare these variables to recommended best practice.
MATERIALS AND METHODS
Study Design and Participants
In this international cross-sectional study, we recruited hospitals through professional networks, including vascular access, infection prevention, safety and quality, nursing, and hospital associations (Appendix 2). Healthcare organizations, government health departments, and intravascular device suppliers were informed of the study and requested to further disseminate information through their networks. A study website was developed,25 and social media outlets, including Twitter®, LinkedIn®, and Facebook®, were used to promote the study.
Approval was granted by the Griffith University Human Research Ethics Committee in Australia (reference number NRS/34/13/HREC). In addition, evidence of study site and local institutional review board/ethics committee approval was required prior to study commencement. Each participating site agreed to follow the study protocol and signed an authorship agreement form. No financial support was provided to any site.
Hospitalized adult and pediatric patients with a PIVC in situ on the day of the study were eligible for inclusion. Sample size was determined by local capacity. Hospitals were encouraged to audit their entire institution if possible; however, data were accepted from as little as one ward. Data collectors comprised nurses and doctors with experience in PIVC assessment. They were briefed on the study protocol and data collection forms by the local site coordinator, and they were supported by an overall global coordinator. Clinicians assessed the PIVC insertion site and accessed hospital records to collect data related to PIVC insertion, concurrent medications, and IV fluid orders. Further clarification of data was obtained if necessary by the clinicians from the patients and treating staff. No identifiable patient information was collected.
Data Collection
To assess whether clinical facilities were following best practice recommendations, the study team developed three data collection forms to collect information regarding site characteristics (site questionnaire), track participant recruitment (screening log), and collect data regarding PIVC characteristics and management practices (case report form [CRF]). All forms were internally and externally validated following a pilot study involving 14 sites in 13 countries.1
The CRF included variables used to assess best practice interventions, such as catheter insertion characteristics (date and time, reason, location, profession of inserter, anatomical site of placement), catheter type (gauge, brand, and product), insertion site assessment (adverse symptoms, dressing type and integrity), and information related to the IV therapy (types of IV fluids and medications, flushing solutions). Idle PIVCs were defined as not being used for blood sampling or IV therapy in the preceding 24 h.
Data collection forms were translated into 15 languages by professional translators and back-translated for validity. Translation of some languages included additional rigor. For example, Spanish-speaking members from the Spanish mainland as well as from South America were employed so that appropriate synonyms were used to capture local terms and practice. Three options were provided for data entry: directly into a purpose-developed electronic database (Lime Survey® Project, Hamburg, Germany); on paper, then transcribed into the survey database at a later time by the hospital site; or paper entry then sent (via email or post) to the coordinating center for data entry. Once cleaned and collated, all data were provided to each participating hospital to confirm accuracy and for site use in local quality improvement processes. Data were collected between June 1, 2014 and July 31, 2015.
Statistical Analysis
All data management was undertaken using SAS statistical software (SAS Institute Inc., Cary NC, USA). Results are presented for eight geographical regions using descriptive statistics (frequencies, percentages, and 95% CIs) for the variables of interest. To assess trends in catheter dwell time and rates of phlebitis, Poisson regression was used. All analyses were undertaken using the R language for statistical analysis (R Core Team, Vienna, Austria). The (STROBE (Strengthening the Reporting of Observational Studies in Epidemiology statement) guidelines for cross-sectional studies were followed, and results are presented according to these recommendations.26
RESULTS
Of the 415 hospitals that participated in this study, 406 had patients with PIVCs on the day of the study (the others being small rural centers). Thus, a total of 40,620 PIVCs in 38,161 patients from 406 hospitals in 51 countries were assessed, with no more than 5% missing data for any CRF question. There were 2459 patients (6.1%) with two or more PIVCs concurrently in situ. The median patient age was 59 y (interquartile range [IQR], 37–74 y), and just over half were male (n = 20,550, 51%). Hospital size ranged from fewer than 10 beds to over 1,000 beds, and hospitals were located in rural, regional, and metropolitan districts. The majority of countries (n = 31, 61%) contributed multiple sites, the highest being Australia with 79 hospitals. Countries with the most PIVCs studied were Spain (n = 5,553, 14%) and the United States (n = 5,048, 12%).
General surgical (n = 15,616, 39%) and medical (n = 15,448, 38%) patients represented most of the population observed. PIVCs were inserted primarily in general wards or clinics (n = 22,167, 55%) or in emergency departments (n = 7,388, 18%; Table) and for the administration of IV medication (n = 28,571, 70%) and IV fluids (n = 7,093, 18%; Table).
Globally, nurses were the primary PIVC inserters (n = 28,575, 71%); however, Australia/New Zealand had only 26% (n = 1,518) of PIVCs inserted by this group (Table). Only about one-third of PIVCs were placed in an area of non-flexion (forearm, n = 12,675, 31%, Table) the majority (n = 27,856, 69%) were placed in non-recommended anatomical sites (Figure 1). Most PIVCs were placed in the hand (n = 13,265, 32.7%) followed by the antecubital veins (n = 6176, 15.2%) and the wrist (n = 5,465, 13.5%). Site selection varied widely across the regions; 29% (n = 1686) of PIVCs in Australia/New Zealand were inserted into the antecubital veins, twice the study group average. Over half of the PIVCs inserted in the Middle East were placed in the hand (n = 295, 56%). This region also had the highest prevalence of devices placed in nonrecommended sites (n = 416, 79%; Figure 1).
The majority of PIVCs (n = 27,192, 67%; Table) were of recommended size (20–22G); however, some devices were observed to be large (14–18G; n = 6,802, 17%) or small (24-26g; n = 4,869, 12%) in adults. In Asia, 41% (n = 2,617) of devices inserted were 24-26G, more than three times the global rate. Half of all devices in Asia (n = 3,077, 48%) and the South Pacific (n = 67, 52%) were of a size not recommended for routine IV therapy (Figure 2).
The primary dressing material used was a transparent dressing (n = 31,596, 77.8%; Table); however, nearly 1 in 5 dressings used had either nonsterile tape alone (n = 5,169, 13%; Appendix 4), or a sterile gauze and tape (n = 2,592, 6%; Appendix 4.1). We found a wide variation in the use of nonsterile tape, including 1 in every 3 devices in South America dressed with nonsterile tape (n = 714, 30%) and a larger proportion in Africa (n = 543, 19%) and Europe (n = 3,056, 18%). Nonsterile tape was rarely used in North America and Australia/New Zealand. Although most PIVC dressings were clean, dry, and intact (n = 31,786, 79%; Table), one-fifth overall were compromised (moist, soiled, and/or lifting off the skin). Compromised dressings (Appendix 4.2) were more prevalent in Australia/New Zealand (n = 1,448; 25%) and in Africa (n = 707, 25%) than elsewhere.
Ten percent of PIVCs (n = 4,204) had signs and/or symptoms suggestive of phlebitis (characterized by pain, redness and/or swelling at the insertion site; Appendix 4.3). The highest prevalence of phlebitis occurred in Asia (n = 1,021, 16%), Africa (n = 360, 13%), and South America (n = 284, 12%). Pain and/or redness were the most common phlebitis symptoms. We found no association between dwell time of PIVCs and phlebitis rates (P = .085). Phlebitis rates were 12% (Days 1-3; n = 15,625), 16% (Days 4-7; n = 3,348), 10% (Days 8-21; n = 457), and 13% (Day21+; n = 174). Nearly 10% (n = 3,879) of catheters were observed to have signs of malfunction such as blood in the infusion tubing, leaking at the insertion site, or dislodgment (Appendix 4.4).
We observed 14% (n = 5,796) of PIVCs to be idle (Appendix 4.5), defined as not used in the preceding 24 h. Nearly one-fourth of all devices in North America (n = 1,230, 23%) and Australia/New Zealand (n = 1,335, 23%) were idle. PIVC documentation in hospital records was also poor, nearly half of all PIVCs (n = 19,768, 49%) had no documented date and time of insertion. The poorest compliance was in Australia/New Zealand (n = 3,428, 59%; Appendix 4.6). We also observed that 1 in 10 PIVCs had no documentation regarding who inserted the PIVC (n = 3,905). Thirty-six percent of PIVCs (n = 14,787) had no documented assessment of the PIVC site on the day of review (Appendix 4.7), including over half of all PIVCs in Asia (n = 3,364, 52%). Overall, the median dwell at the time of assessment for PIVCs with insertion date/time documented was 1.5 d (IQR, 1.0–2.5 d).
DISCUSSION
This international assessment of more than 40,000 PIVCs in 51 countries provides great insight into device characteristics and variation in management practices. Predominantly, PIVCs were inserted by nurses in the general ward environment for IV medication. One in ten PIVCs had at least one symptom of phlebitis, one in ten were dysfunctional, one in five PIVC dressings were compromised, and one in six PIVCs had not been used in the preceding 24 h. Nearly half of the PIVCs audited had the insertion date and time missing.
Regional variation was found in the professions inserting PIVCs, as well as in anatomical placement. In Australia/New Zealand, the proportion of nurses inserting PIVCs was much lower than the study group average (26% vs 71%). Because these countries contributed a substantial number of hospitals to the study, this seems a representative finding and suggests a need for education targeted at nurses for PIVC insertion in this region. The veins in the forearm are recommended as optimal for PIVC insertion in adults, rather than areas of high flexion, because the forearm provides a wide surface area to secure and dress PIVCs. Forearm placement can reduce pain during catheter dwell as well as decrease the risk of accidental removal or occlusion.3,19,27 We found only one-third of PIVCs were placed in the forearm, with most placed in the hand, antecubital veins, or wrist. This highlights an inconsistency with published recommendations and suggests that additional training and technology are required so that staff can better identify and insert PIVCs in the forearm for other than very short-term (procedural) PIVCp;s.19
Phlebitis triggering PIVC failure remains a global clinical challenge with numerous phlebitis definitions and varied assessment techniques.10 The prevalence of phlebitis has been difficult to approximate with varying estimates and definitions in the literature; however, it remains a key predictor of PIVC failure.6,10 Identification of this complication and prompt removal of the device is critical for patient comfort and reducing CABSI risk.5,28 The overall prevalence of phlebitis signs or symptoms (defined in this study as having one or more signs of redness, swelling, or pain surrounding the insertion site) was just over 10%, with pain and/or redness being most prevalent. These compromised PIVCs had not been removed as is recommended for such complications.19,28 Considering that our study was a snapshot at only one time point, the per-catheter incidence of phlebitis would be even higher; interestingly, among PIVCs with a documented insertion date and time, we observed that dwell time did not influence phlebitis rates.
Another concern is that nearly 10% (n = 3,879) of PIVCs were malfunctioning (eg, leaking) but were still in place. To bring these problems into context, around 2 billion PIVCs are used annually worldwide; as a consequence, millions of patients suffer from painful or malfunctioning PIVCs staff had not responded.1,29 The placement of large-bore catheters, and smaller-gauge ones in adults, is known to increase the incidence of malfunction that leads to failure. There are a number of sound clinical reasons for the use of large-bore (eg, resuscitation and rapid fluid replacement) or small-bore (eg, difficult venous access with small superficial veins only visible and palpable) catheters. However, it would be expected that only a small proportion of patients would require these devices, and not one in three devices as we identified. This finding suggests that some PIVCs were inappropriate in size for general IV therapy and may reflect antiquated hospital policies for some clinical cohorts.30,31
Overall, transparent dressings were used to cover the PIVC, but a number of patients were observed to have a sterile gauze and tape dressing (n = 2,592, 6%). Although the latter is less common, both dressing approaches are recommended in clinical practice guidelines because there is a lack of high-quality evidence regarding which is superior.21,22,32 Of concern was the use of nonsterile tape to dress the PIVC (n = 5,169, 12.7%). We found the prevalence of nonsterile tape use to be higher in lower-resourced countries in South America (n = 714, 30%), Africa (n = 543, 19%) and Europe (n = 3,056, 18%) and this was likely related to institutional cost reduction practices.
This finding illustrates an important issue regarding proper PIVC care and management practices in developing nations. It is widely known that access to safe health care in lower-resourced nations is challenging and that rates of mortality related to healthcare-associated infections are much higher. Thus, the differences we found in PIVC management practices in these countries are not surprising.33,34 International health networks such as the Infection Control Africa Network, the International Federation of Infection Control, and the Centers for Disease Control and Prevention can have great influence on ministries of health and clinicians in these countries to develop coordinated efforts for safe and sustainable IV practices to reduce the burden of hospital-acquired infections and related morbidity and mortality.
We found that 14% of all PIVCs had no documented IV medication or IV fluid administered in the previous 24 h, strongly indicating that they were no longer needed. Australia/New Zealand, Europe, and North America were observed to have a higher prevalence of idle catheters than the remaining regions. This suggests that an opportunity exists to develop surveillance systems that better identify idle devices for prompt removal to reduce infection risk and patient discomfort. Several randomized controlled trials, a Cochrane review, and clinical practice guidelines recommend prompt removal of PIVCs when not required, if there are any complications, or if the PIVC was inserted urgently without an aseptic insertion technique.21,28,35,36 Idle PIVCs have been implicated in adverse patient outcomes, including phlebitis and CABSI.13,27
The substantial proportion of patients with a PIVC in this study who had no clinical indication for a PIVC, a symptomatic insertion site, malfunctioning catheter, and suboptimal dressing quality suggests the need for physicians, advanced practitioners, and nurses to adopt evidence-based PIVC insertion and maintenance bundles and supporting checklists to reduce the prevalence of PIVC complications.19,21,38-40 Recommended strategies for inclusion in PIVC maintenance bundles are prompt removal of symptomatic and/or idle catheters, hand hygiene prior to accessing the catheter, regular assessment of the device, and replacement of suboptimal dressings.41,42 This approach should be implemented across all clinical specialties involved in PIVC insertion and care.
Our study findings need to be considered within the context of some limitations. The cross-sectional design prevented follow-up of PIVCs until removal to collect outcomes, including subsequent PIVC complications and/or failure, following the study observation. Ideally, data collection could have included patient-level preferences for PIVC insertion, history of PIVC use and/or failure, the number of PIVC insertion attempts, and the number of PIVCs used during that hospitalization. However, a cohort study of this magnitude was not feasible, particularly because all sites contributed staff time to complete the data collection. Only half of all initially registered sites eventually participated in the study; reasons for not participating were cited as local workload constraints and/or difficulties in applying for local approvals. Although efforts to enroll hospitals worldwide were exhaustive, our sample was not randomly selected but relied on self-selection and so is not representative, particularly for countries that contributed only one hospital site. Caution is also required when comparing inter regional differences, particularly developing regions, because better-resourced/academic sites were possibly over represented in the sample. Nevertheless, PIVC variables differed significantly between participating hospitals, suggesting that the data represent a reasonable reflection of hospital variability.
CONCLUSIONS
On the basis of this international investigation, we report variations in the characteristics, management practices, and outcomes of PIVCs inserted in hospital patients from 51 countries. Many PIVCs were idle, symptomatic, had substandard dressings, and were inserted in suboptimal anatomical sites. Despite international best practice guidelines, a large number of patients had PIVCs that were already failing or at risk of complications, including infection. A stronger focus is needed on compliance with PIVC insertion and management guidelines; better surveillance of PIVC sites; and improved assessment, decision-making, and documentation.
Acknowledgements
We are extremely grateful to colleagues from across the globe who committed their time and effort to this study (for full details of countries and team members see Appendix 1).
1. Alexandrou E, Ray-Barruel G, Carr PJ, et al. International prevalence of the use of peripheral intravenous catheters. J Hosp Med. 2015;10(8):530-533. https:/doi.org/10.1002/jhm.2389
2. Zingg W, Pittet D. Peripheral venous catheters: an under-evaluated problem. Int J Antimicrob Agents. 2009;34(suppl 4):S38-S42. https:/ doi.org/10.1016/S0924-8579(09)70565-5
3. Wallis MC, McGrail MR, Webster J, Gowardman JR, Playford G, Rickard CM. Risk factors for PIV catheter failure: a multivariate analysis from a randomized control trial. Infect. Control Hosp Epidemiol. 2014;35(1):63-68. https:/doi.org/10.1086/674398.
4. Pujol M, Hornero A, Saballs M, et al. Clinical epidemiology and outcomes of peripheral venous catheter-related bloodstream infections at a university-affiliated hospital. J Hosp Infect. 2007;67(1):22-29.
5. Fakih MG, Jones K, Rey JE, et al. Sustained improvements in peripheral venous catheter care in non–intensive care units: a quasi-experimental controlled study of education and feedback. Infect. Control Hosp Epidemiol. 2012;33(5):449-455. https:/doi.org/10.1086/665322.
6. Helm RE, Klausner JD, Klemperer JD, Flint LM, Huang E. Accepted but unacceptable: peripheral IV catheter failure. J Infus Nurs. 2015;38(3):189-203. https:/ doi.org/10.1097/NAN.0000000000000100.
7. Austin ED, Sullivan SB, Whittier S, Lowy FD, Uhlemann AC. Peripheral intravenous catheter placement is an underrecognized source of Staphylococcus aureus bloodstream infection. Open Forum Infect Dis. 2016;3(2):ofw072. https:/ doi.org/10.1093/ofid/ofw072.
8. Stuart RL, Cameron D, Scott C, et al. Peripheral intravenous catheter-associated Staphylococcus aureus bacteraemia: more than 5 years of prospective data from two tertiary health services. Med J Aust. 2013;198(10):551-553.
9. Trinh TT, Chan PA, Edwards O, et al. Peripheral venous catheter-related Staphylococcus aureus bacteremia. Infect Control Hosp Epidemiol. 2011;32(6):579-583. https:/doi.org/10.1086/660099.
10. Ray Barruel G, Polit DF, Murfield JE, Rickard CM. Infusion phlebitis assessment measures: a systematic review. J Eval Clin Pract. 2014;20(2):191-202. https:/ doi.org/ 10.1111/jep.12107
11. Marsh N, Webster J, Flynn J, et al. Securement methods for peripheral venous catheters to prevent failure: a randomised controlled pilot trial. J Vasc Access. 2015;16(3):237-244. https:/doi.org /10.5301/jva.5000348.
12. Carr PJ, Higgins NS, Cooke ML, Rippey J, Rickard CM. Tools, clinical prediction rules, and algorithms for the insertion of peripheral intravenous catheters in adult hospitalized patients: a systematic scoping review of literature. J Hosp Med. 2017;12(10):851-858. https:/doi.org/ 10.12788/jhm.2836
13. Becerra MB, Shirley D, Safdar N. Prevalence, risk factors, and outcomes of idle intravenous catheters: An integrative review. Am J Infect Control. 2016;44(10):e167-e172. https:/ doi.org/10.1016/j.ajic.2016.03.073.
14. Robinson-Reilly M, Paliadelis P, Cruickshank M. Venous access: the patient experience. Support Care Cancer. 2016;24(3):1181-1187. https:/ doi.org/10.1007/s00520-015-2900-9.
15. Petroski A, Frisch A, Joseph N, Carlson JN. Predictors of difficult pediatric intravenous access in a community Emergency Department. J Vasc Access. 2015;16(6):521-526. https:/doi.org/10.5301/jva.5000411
16. Sou V, McManus C, Mifflin N, Frost SA, Ale J, Alexandrou E. A clinical pathway for the management of difficult venous access. BMC Nurs. 2017;16(1):64. https:/ doi.org/10.1186/s12912-017-0261-z
17. World Health Organization. Report on the burden of endemic health care-associated infection worldwide. Geneva2011. 9241501502.
18. Hirschmann H, Fux L, Podusel J, et al. The influence of hand hygiene prior to insertion of peripheral venous catheters on the frequency of complications. J Hosp Infect. 2001;49(3):199-203. https:/doi.org/10.1053/jhin.2001.1077
19. Gorski L, Hadaway L, Hagle M, McGoldrick M, Orr M, Doellman D. Infusion therapy standards of practice. J Infus Nurs. 2016;39(suppl 1):S1-S159.
20. Abolfotouh MA, Salam M, Bani-Mustafa Aa, White D, Balkhy HH. Prospective study of incidence and predictors of peripheral intravenous catheter-induced complications. Ther Clin Risk Manag. 2014;10:993. https://doi.org/10.2147/TCRM.S74685.
21. Loveday H, Wilson J, Pratt R, et al. epic3: national evidence-based guidelines for preventing healthcare-associated infections in NHS hospitals in England. J Hosp Infect. 2014;86(suppl 1):S1-S70. https:/doi.org/10.1016/S0195-6701(13)60012-2.
22. O’Grady NP, Alexander M, Burns LA, et al. Guidelines for the prevention of intravascular catheter-related infections. Clin Infect Dis. 2011;52(9):e162-e193. https:/doi.org/10.1093/cid/cir257
23. Cicolini G, Bonghi AP, Di Labio L, Di Mascio R. Position of peripheral venous cannulae and the incidence of thrombophlebitis: an observational study. J Adv Nurs. 2009;65(6):1268-1273. https:/doi.org/10.1111/j.1365-2648.2009.04980.x.
24. Marsh N, Webster J, Larson E, Cooke M, Mihala G, Rickard C. Observational study of peripheral intravenous catheter outcomes in adult hospitalized patients: a multivariable analysis of peripheral intravenous catheter failure. J Hosp Med. 2018;13(2):83-89. https:/doi.org/10.12788/jhm.2867.
25. One Million Global Catheters PIVC Worldwide Prevalence study. OMG study website http://www.omgpivc.org/. Accessed 23 March, 2017.
26. Von Elm E, Altman DG, Egger M, et al. The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) Statement: guidelines for reporting observational studies. Int J Surg. 2014;12(12):1495-1499. https:/doi.org/ 10.1136/bmj.39335.541782.AD
27. Fields JM, Dean AJ, Todman RW, et al. The effect of vessel depth, diameter, and location on ultrasound-guided peripheral intravenous catheter longevity. Am J Emerg Med. 2012;30(7):1134-1140. https:/doi.org/10.1016/j.ajem.2011.07.027.
28. Patel SA, Alebich MM, Feldman LS. Choosing wisely: things we do for no reason. Routine replacement of peripheral intravenous catheters. J Hosp Med. 2017;12(1):42-45.
29. Newswire. Global Peripheral I.V. Catheter Market 2014 - 2018. New York, PR Newswire Assoc; 2014.
30. Webster J, Larsen E, Booker C, Laws J, Marsh N. Prophylactic insertion of large bore peripheral intravenous catheters in maternity patients for postpartum haemorrhage: A cohort study. Aust N Z J Obstet Gynaecol. 2017.https:/doi.org/10.1111/ajo.12759.
31. Rivera A, Strauss K, van Zundert A, Mortier E. Matching the peripheral intravenous catheter to the individual patient. Acta Anaesthesiol Belg. 2006;58(1):19.
32. Webster J, Gillies D, O’Riordan E, Sherriff KL, Rickard CM. Gauze and tape and transparent polyurethane dressings for central venous catheters. Cochrane Database Syst Rev. 2011;11:CD003827. https:/doi.org/10.1002/14651858.CD003827.pub2
33. Dieleman JL, Templin T, Sadat N, et al. National spending on health by source for 184 countries between 2013 and 2040. Lancet. 2016;387(10037):2521-2535. https:/ doi.org/10.1016/S0140-6736(16)30167-2.
34. Allegranzi B, Nejad SB, Combescure C, et al. Burden of endemic health-care-associated infection in developing countries: systematic review and meta-analysis. Lancet. 2011;377(9761):228-241. https:/ doi.org/10.1016/S0140-6736(10)61458-4.
35. Rickard CM, Webster J, Wallis MC, et al. Routine versus clinically indicated replacement of peripheral intravenous catheters: a randomised controlled equivalence trial. Lancet. 2012;380(9847):1066-1074. https:/doi.org/10.1016/S0140-6736(12)61082-4.
36. Webster J, Osborne S, Rickard CM, New K. Clinically indicated replacement versus routine replacement of peripheral venous catheters. Cochrane Database Syst Rev. 2015;8:CD007798. https://doi.org/10.1002/14651858.CD007798.pub4.
37. Yagnik L, Graves A, Thong K. Plastic in patient study: Prospective audit of adherence to peripheral intravenous cannula monitoring and documentation guidelines, with the aim of reducing future rates of intravenous cannula-related complications. Am J Infect Control. 2017;45(1):34-38. https:/doi.org/10.1016/j.ajic.2016.09.008.
38. Boyd S, Aggarwal I, Davey P, Logan M, Nathwani D. Peripheral intravenous catheters: the road to quality improvement and safer patient care. J Hosp Infect. 2011;77(1):37-41. https:/doi.org/10.1016/j.jhin.2010.09.011.
39. DeVries M, Valentine M, Mancos P. Protected clinical indication of peripheral intravenous lines: successful implementation. J Assoc Vasc Access. 2016;21(2):89-92. https://doi.org/10.1016/j.java.2016.03.001.
40. Rhodes D, Cheng A, McLellan S, et al. Reducing Staphylococcus aureus bloodstream infections associated with peripheral intravenous cannulae: successful implementation of a care bundle at a large Australian health service. J Hosp Infect. 2016;94(1):86-91. https:/doi.org/10.1016/j.jhin.2016.05.020.
41. Rinke ML, Chen AR, Bundy DG, et al. Implementation of a central line maintenance care bundle in hospitalized pediatric oncology patients. Pediatr. 2012;130(4):e996-e1004. https:/doi.org/10.1542/peds.2012-0295.
42. Marshall J, Mermel L, Fakih M, Hadaway L, Kallen A, O’Grady N. Strategies to prevent central line–associated bloodstream infections in acute care hospitals: 2014 update. Infect. Control Hosp Epidemiol. 2014;35(suppl 2):S89-107. https:/doi.org/10.1086/676533.
The majority of hospitalized patients worldwide have at least one peripheral intravenous catheter (PIVC),1 making PIVC insertion one of the most common clinical procedures. In the United States, physicians, advanced practitioners, and nurses insert over 300 million of these devices in hospitalized patients annually.2 Despite their prevalence, PIVCs are associated with high rates of complications, including insertion difficulty, phlebitis, infiltration, occlusion, dislodgment, and catheter-associated bloodstream infection (CABSI), known to increase morbidity and mortality risk.2-9 Up to 90% of PIVCs are prematurely removed owing to failure before planned replacement or before intravenous (IV) therapy completion.3-6,10-12
PIVC complication and failure commonly triggers insertion of a replacement device and can entail significant costs.2-4 One example is PIVC-related CABSI, where treatment costs have been estimated to be between US$35,000 and US$56,000 per patient.6,13 Another important consideration is the pain and anxiety experienced by patients who need a replacement device, particularly those with difficult vascular access, who may require multiple cannulation attempts to replace a PIVC.12,14-16 In developing nations, serious adverse events related to PIVCs are even more concerning, because hospital acquired infection rates and associated mortality are nearly 20 times greater than in developed nations.17
A number of evidence-based interventions have been suggested to reduce PIVC failure rates. In addition to optimal hand hygiene when inserting or accessing a PIVC to prevent infection,18 recommended interventions include placement of the PIVC in an area of non-flexion such as the forearm to provide stability for the device and to reduce patient discomfort, securing the PIVC to reduce movement of the catheter at the insertion site and within the blood vessel, and use of occlusive dressings that reduce the risk of external contamination of the PIVC site.11,19,20 Best practice guidelines also recommend the prompt removal of devices that are symptomatic (when phlebitis or other complications are suspected) and when the catheter is no longer required.21,22
Recent evidence has demonstrated that catheter size can have an impact on device survival rates. In adults, large-bore catheters of 18 gauge (G) or higher were found to have an increased rate of thrombosis, and smaller-bore catheters of 22G or lower (in adults) were found to have higher rates of dislodgment and occlusion/infiltration. The catheter size recommended for adults based on the latest evidence for most clinical applications is 20G.3,20,23,24 In addition, the documentation of insertion, maintenance, and removal of PIVCs in the medical record is a requirement in most healthcare facilities worldwide and is recommended by best practice guidelines; however, adherence remains a challenge.1,19
The concerning prevalence of PIVC-related complications and the lack of comparative data internationally on organizational compliance with best practice guidelines formed the rationale for this study. Our study aim was to describe the insertion characteristics, management practices, and outcomes of PIVCs internationally and to compare these variables to recommended best practice.
MATERIALS AND METHODS
Study Design and Participants
In this international cross-sectional study, we recruited hospitals through professional networks, including vascular access, infection prevention, safety and quality, nursing, and hospital associations (Appendix 2). Healthcare organizations, government health departments, and intravascular device suppliers were informed of the study and requested to further disseminate information through their networks. A study website was developed,25 and social media outlets, including Twitter®, LinkedIn®, and Facebook®, were used to promote the study.
Approval was granted by the Griffith University Human Research Ethics Committee in Australia (reference number NRS/34/13/HREC). In addition, evidence of study site and local institutional review board/ethics committee approval was required prior to study commencement. Each participating site agreed to follow the study protocol and signed an authorship agreement form. No financial support was provided to any site.
Hospitalized adult and pediatric patients with a PIVC in situ on the day of the study were eligible for inclusion. Sample size was determined by local capacity. Hospitals were encouraged to audit their entire institution if possible; however, data were accepted from as little as one ward. Data collectors comprised nurses and doctors with experience in PIVC assessment. They were briefed on the study protocol and data collection forms by the local site coordinator, and they were supported by an overall global coordinator. Clinicians assessed the PIVC insertion site and accessed hospital records to collect data related to PIVC insertion, concurrent medications, and IV fluid orders. Further clarification of data was obtained if necessary by the clinicians from the patients and treating staff. No identifiable patient information was collected.
Data Collection
To assess whether clinical facilities were following best practice recommendations, the study team developed three data collection forms to collect information regarding site characteristics (site questionnaire), track participant recruitment (screening log), and collect data regarding PIVC characteristics and management practices (case report form [CRF]). All forms were internally and externally validated following a pilot study involving 14 sites in 13 countries.1
The CRF included variables used to assess best practice interventions, such as catheter insertion characteristics (date and time, reason, location, profession of inserter, anatomical site of placement), catheter type (gauge, brand, and product), insertion site assessment (adverse symptoms, dressing type and integrity), and information related to the IV therapy (types of IV fluids and medications, flushing solutions). Idle PIVCs were defined as not being used for blood sampling or IV therapy in the preceding 24 h.
Data collection forms were translated into 15 languages by professional translators and back-translated for validity. Translation of some languages included additional rigor. For example, Spanish-speaking members from the Spanish mainland as well as from South America were employed so that appropriate synonyms were used to capture local terms and practice. Three options were provided for data entry: directly into a purpose-developed electronic database (Lime Survey® Project, Hamburg, Germany); on paper, then transcribed into the survey database at a later time by the hospital site; or paper entry then sent (via email or post) to the coordinating center for data entry. Once cleaned and collated, all data were provided to each participating hospital to confirm accuracy and for site use in local quality improvement processes. Data were collected between June 1, 2014 and July 31, 2015.
Statistical Analysis
All data management was undertaken using SAS statistical software (SAS Institute Inc., Cary NC, USA). Results are presented for eight geographical regions using descriptive statistics (frequencies, percentages, and 95% CIs) for the variables of interest. To assess trends in catheter dwell time and rates of phlebitis, Poisson regression was used. All analyses were undertaken using the R language for statistical analysis (R Core Team, Vienna, Austria). The (STROBE (Strengthening the Reporting of Observational Studies in Epidemiology statement) guidelines for cross-sectional studies were followed, and results are presented according to these recommendations.26
RESULTS
Of the 415 hospitals that participated in this study, 406 had patients with PIVCs on the day of the study (the others being small rural centers). Thus, a total of 40,620 PIVCs in 38,161 patients from 406 hospitals in 51 countries were assessed, with no more than 5% missing data for any CRF question. There were 2459 patients (6.1%) with two or more PIVCs concurrently in situ. The median patient age was 59 y (interquartile range [IQR], 37–74 y), and just over half were male (n = 20,550, 51%). Hospital size ranged from fewer than 10 beds to over 1,000 beds, and hospitals were located in rural, regional, and metropolitan districts. The majority of countries (n = 31, 61%) contributed multiple sites, the highest being Australia with 79 hospitals. Countries with the most PIVCs studied were Spain (n = 5,553, 14%) and the United States (n = 5,048, 12%).
General surgical (n = 15,616, 39%) and medical (n = 15,448, 38%) patients represented most of the population observed. PIVCs were inserted primarily in general wards or clinics (n = 22,167, 55%) or in emergency departments (n = 7,388, 18%; Table) and for the administration of IV medication (n = 28,571, 70%) and IV fluids (n = 7,093, 18%; Table).
Globally, nurses were the primary PIVC inserters (n = 28,575, 71%); however, Australia/New Zealand had only 26% (n = 1,518) of PIVCs inserted by this group (Table). Only about one-third of PIVCs were placed in an area of non-flexion (forearm, n = 12,675, 31%, Table) the majority (n = 27,856, 69%) were placed in non-recommended anatomical sites (Figure 1). Most PIVCs were placed in the hand (n = 13,265, 32.7%) followed by the antecubital veins (n = 6176, 15.2%) and the wrist (n = 5,465, 13.5%). Site selection varied widely across the regions; 29% (n = 1686) of PIVCs in Australia/New Zealand were inserted into the antecubital veins, twice the study group average. Over half of the PIVCs inserted in the Middle East were placed in the hand (n = 295, 56%). This region also had the highest prevalence of devices placed in nonrecommended sites (n = 416, 79%; Figure 1).
The majority of PIVCs (n = 27,192, 67%; Table) were of recommended size (20–22G); however, some devices were observed to be large (14–18G; n = 6,802, 17%) or small (24-26g; n = 4,869, 12%) in adults. In Asia, 41% (n = 2,617) of devices inserted were 24-26G, more than three times the global rate. Half of all devices in Asia (n = 3,077, 48%) and the South Pacific (n = 67, 52%) were of a size not recommended for routine IV therapy (Figure 2).
The primary dressing material used was a transparent dressing (n = 31,596, 77.8%; Table); however, nearly 1 in 5 dressings used had either nonsterile tape alone (n = 5,169, 13%; Appendix 4), or a sterile gauze and tape (n = 2,592, 6%; Appendix 4.1). We found a wide variation in the use of nonsterile tape, including 1 in every 3 devices in South America dressed with nonsterile tape (n = 714, 30%) and a larger proportion in Africa (n = 543, 19%) and Europe (n = 3,056, 18%). Nonsterile tape was rarely used in North America and Australia/New Zealand. Although most PIVC dressings were clean, dry, and intact (n = 31,786, 79%; Table), one-fifth overall were compromised (moist, soiled, and/or lifting off the skin). Compromised dressings (Appendix 4.2) were more prevalent in Australia/New Zealand (n = 1,448; 25%) and in Africa (n = 707, 25%) than elsewhere.
Ten percent of PIVCs (n = 4,204) had signs and/or symptoms suggestive of phlebitis (characterized by pain, redness and/or swelling at the insertion site; Appendix 4.3). The highest prevalence of phlebitis occurred in Asia (n = 1,021, 16%), Africa (n = 360, 13%), and South America (n = 284, 12%). Pain and/or redness were the most common phlebitis symptoms. We found no association between dwell time of PIVCs and phlebitis rates (P = .085). Phlebitis rates were 12% (Days 1-3; n = 15,625), 16% (Days 4-7; n = 3,348), 10% (Days 8-21; n = 457), and 13% (Day21+; n = 174). Nearly 10% (n = 3,879) of catheters were observed to have signs of malfunction such as blood in the infusion tubing, leaking at the insertion site, or dislodgment (Appendix 4.4).
We observed 14% (n = 5,796) of PIVCs to be idle (Appendix 4.5), defined as not used in the preceding 24 h. Nearly one-fourth of all devices in North America (n = 1,230, 23%) and Australia/New Zealand (n = 1,335, 23%) were idle. PIVC documentation in hospital records was also poor, nearly half of all PIVCs (n = 19,768, 49%) had no documented date and time of insertion. The poorest compliance was in Australia/New Zealand (n = 3,428, 59%; Appendix 4.6). We also observed that 1 in 10 PIVCs had no documentation regarding who inserted the PIVC (n = 3,905). Thirty-six percent of PIVCs (n = 14,787) had no documented assessment of the PIVC site on the day of review (Appendix 4.7), including over half of all PIVCs in Asia (n = 3,364, 52%). Overall, the median dwell at the time of assessment for PIVCs with insertion date/time documented was 1.5 d (IQR, 1.0–2.5 d).
DISCUSSION
This international assessment of more than 40,000 PIVCs in 51 countries provides great insight into device characteristics and variation in management practices. Predominantly, PIVCs were inserted by nurses in the general ward environment for IV medication. One in ten PIVCs had at least one symptom of phlebitis, one in ten were dysfunctional, one in five PIVC dressings were compromised, and one in six PIVCs had not been used in the preceding 24 h. Nearly half of the PIVCs audited had the insertion date and time missing.
Regional variation was found in the professions inserting PIVCs, as well as in anatomical placement. In Australia/New Zealand, the proportion of nurses inserting PIVCs was much lower than the study group average (26% vs 71%). Because these countries contributed a substantial number of hospitals to the study, this seems a representative finding and suggests a need for education targeted at nurses for PIVC insertion in this region. The veins in the forearm are recommended as optimal for PIVC insertion in adults, rather than areas of high flexion, because the forearm provides a wide surface area to secure and dress PIVCs. Forearm placement can reduce pain during catheter dwell as well as decrease the risk of accidental removal or occlusion.3,19,27 We found only one-third of PIVCs were placed in the forearm, with most placed in the hand, antecubital veins, or wrist. This highlights an inconsistency with published recommendations and suggests that additional training and technology are required so that staff can better identify and insert PIVCs in the forearm for other than very short-term (procedural) PIVCp;s.19
Phlebitis triggering PIVC failure remains a global clinical challenge with numerous phlebitis definitions and varied assessment techniques.10 The prevalence of phlebitis has been difficult to approximate with varying estimates and definitions in the literature; however, it remains a key predictor of PIVC failure.6,10 Identification of this complication and prompt removal of the device is critical for patient comfort and reducing CABSI risk.5,28 The overall prevalence of phlebitis signs or symptoms (defined in this study as having one or more signs of redness, swelling, or pain surrounding the insertion site) was just over 10%, with pain and/or redness being most prevalent. These compromised PIVCs had not been removed as is recommended for such complications.19,28 Considering that our study was a snapshot at only one time point, the per-catheter incidence of phlebitis would be even higher; interestingly, among PIVCs with a documented insertion date and time, we observed that dwell time did not influence phlebitis rates.
Another concern is that nearly 10% (n = 3,879) of PIVCs were malfunctioning (eg, leaking) but were still in place. To bring these problems into context, around 2 billion PIVCs are used annually worldwide; as a consequence, millions of patients suffer from painful or malfunctioning PIVCs staff had not responded.1,29 The placement of large-bore catheters, and smaller-gauge ones in adults, is known to increase the incidence of malfunction that leads to failure. There are a number of sound clinical reasons for the use of large-bore (eg, resuscitation and rapid fluid replacement) or small-bore (eg, difficult venous access with small superficial veins only visible and palpable) catheters. However, it would be expected that only a small proportion of patients would require these devices, and not one in three devices as we identified. This finding suggests that some PIVCs were inappropriate in size for general IV therapy and may reflect antiquated hospital policies for some clinical cohorts.30,31
Overall, transparent dressings were used to cover the PIVC, but a number of patients were observed to have a sterile gauze and tape dressing (n = 2,592, 6%). Although the latter is less common, both dressing approaches are recommended in clinical practice guidelines because there is a lack of high-quality evidence regarding which is superior.21,22,32 Of concern was the use of nonsterile tape to dress the PIVC (n = 5,169, 12.7%). We found the prevalence of nonsterile tape use to be higher in lower-resourced countries in South America (n = 714, 30%), Africa (n = 543, 19%) and Europe (n = 3,056, 18%) and this was likely related to institutional cost reduction practices.
This finding illustrates an important issue regarding proper PIVC care and management practices in developing nations. It is widely known that access to safe health care in lower-resourced nations is challenging and that rates of mortality related to healthcare-associated infections are much higher. Thus, the differences we found in PIVC management practices in these countries are not surprising.33,34 International health networks such as the Infection Control Africa Network, the International Federation of Infection Control, and the Centers for Disease Control and Prevention can have great influence on ministries of health and clinicians in these countries to develop coordinated efforts for safe and sustainable IV practices to reduce the burden of hospital-acquired infections and related morbidity and mortality.
We found that 14% of all PIVCs had no documented IV medication or IV fluid administered in the previous 24 h, strongly indicating that they were no longer needed. Australia/New Zealand, Europe, and North America were observed to have a higher prevalence of idle catheters than the remaining regions. This suggests that an opportunity exists to develop surveillance systems that better identify idle devices for prompt removal to reduce infection risk and patient discomfort. Several randomized controlled trials, a Cochrane review, and clinical practice guidelines recommend prompt removal of PIVCs when not required, if there are any complications, or if the PIVC was inserted urgently without an aseptic insertion technique.21,28,35,36 Idle PIVCs have been implicated in adverse patient outcomes, including phlebitis and CABSI.13,27
The substantial proportion of patients with a PIVC in this study who had no clinical indication for a PIVC, a symptomatic insertion site, malfunctioning catheter, and suboptimal dressing quality suggests the need for physicians, advanced practitioners, and nurses to adopt evidence-based PIVC insertion and maintenance bundles and supporting checklists to reduce the prevalence of PIVC complications.19,21,38-40 Recommended strategies for inclusion in PIVC maintenance bundles are prompt removal of symptomatic and/or idle catheters, hand hygiene prior to accessing the catheter, regular assessment of the device, and replacement of suboptimal dressings.41,42 This approach should be implemented across all clinical specialties involved in PIVC insertion and care.
Our study findings need to be considered within the context of some limitations. The cross-sectional design prevented follow-up of PIVCs until removal to collect outcomes, including subsequent PIVC complications and/or failure, following the study observation. Ideally, data collection could have included patient-level preferences for PIVC insertion, history of PIVC use and/or failure, the number of PIVC insertion attempts, and the number of PIVCs used during that hospitalization. However, a cohort study of this magnitude was not feasible, particularly because all sites contributed staff time to complete the data collection. Only half of all initially registered sites eventually participated in the study; reasons for not participating were cited as local workload constraints and/or difficulties in applying for local approvals. Although efforts to enroll hospitals worldwide were exhaustive, our sample was not randomly selected but relied on self-selection and so is not representative, particularly for countries that contributed only one hospital site. Caution is also required when comparing inter regional differences, particularly developing regions, because better-resourced/academic sites were possibly over represented in the sample. Nevertheless, PIVC variables differed significantly between participating hospitals, suggesting that the data represent a reasonable reflection of hospital variability.
CONCLUSIONS
On the basis of this international investigation, we report variations in the characteristics, management practices, and outcomes of PIVCs inserted in hospital patients from 51 countries. Many PIVCs were idle, symptomatic, had substandard dressings, and were inserted in suboptimal anatomical sites. Despite international best practice guidelines, a large number of patients had PIVCs that were already failing or at risk of complications, including infection. A stronger focus is needed on compliance with PIVC insertion and management guidelines; better surveillance of PIVC sites; and improved assessment, decision-making, and documentation.
Acknowledgements
We are extremely grateful to colleagues from across the globe who committed their time and effort to this study (for full details of countries and team members see Appendix 1).
The majority of hospitalized patients worldwide have at least one peripheral intravenous catheter (PIVC),1 making PIVC insertion one of the most common clinical procedures. In the United States, physicians, advanced practitioners, and nurses insert over 300 million of these devices in hospitalized patients annually.2 Despite their prevalence, PIVCs are associated with high rates of complications, including insertion difficulty, phlebitis, infiltration, occlusion, dislodgment, and catheter-associated bloodstream infection (CABSI), known to increase morbidity and mortality risk.2-9 Up to 90% of PIVCs are prematurely removed owing to failure before planned replacement or before intravenous (IV) therapy completion.3-6,10-12
PIVC complication and failure commonly triggers insertion of a replacement device and can entail significant costs.2-4 One example is PIVC-related CABSI, where treatment costs have been estimated to be between US$35,000 and US$56,000 per patient.6,13 Another important consideration is the pain and anxiety experienced by patients who need a replacement device, particularly those with difficult vascular access, who may require multiple cannulation attempts to replace a PIVC.12,14-16 In developing nations, serious adverse events related to PIVCs are even more concerning, because hospital acquired infection rates and associated mortality are nearly 20 times greater than in developed nations.17
A number of evidence-based interventions have been suggested to reduce PIVC failure rates. In addition to optimal hand hygiene when inserting or accessing a PIVC to prevent infection,18 recommended interventions include placement of the PIVC in an area of non-flexion such as the forearm to provide stability for the device and to reduce patient discomfort, securing the PIVC to reduce movement of the catheter at the insertion site and within the blood vessel, and use of occlusive dressings that reduce the risk of external contamination of the PIVC site.11,19,20 Best practice guidelines also recommend the prompt removal of devices that are symptomatic (when phlebitis or other complications are suspected) and when the catheter is no longer required.21,22
Recent evidence has demonstrated that catheter size can have an impact on device survival rates. In adults, large-bore catheters of 18 gauge (G) or higher were found to have an increased rate of thrombosis, and smaller-bore catheters of 22G or lower (in adults) were found to have higher rates of dislodgment and occlusion/infiltration. The catheter size recommended for adults based on the latest evidence for most clinical applications is 20G.3,20,23,24 In addition, the documentation of insertion, maintenance, and removal of PIVCs in the medical record is a requirement in most healthcare facilities worldwide and is recommended by best practice guidelines; however, adherence remains a challenge.1,19
The concerning prevalence of PIVC-related complications and the lack of comparative data internationally on organizational compliance with best practice guidelines formed the rationale for this study. Our study aim was to describe the insertion characteristics, management practices, and outcomes of PIVCs internationally and to compare these variables to recommended best practice.
MATERIALS AND METHODS
Study Design and Participants
In this international cross-sectional study, we recruited hospitals through professional networks, including vascular access, infection prevention, safety and quality, nursing, and hospital associations (Appendix 2). Healthcare organizations, government health departments, and intravascular device suppliers were informed of the study and requested to further disseminate information through their networks. A study website was developed,25 and social media outlets, including Twitter®, LinkedIn®, and Facebook®, were used to promote the study.
Approval was granted by the Griffith University Human Research Ethics Committee in Australia (reference number NRS/34/13/HREC). In addition, evidence of study site and local institutional review board/ethics committee approval was required prior to study commencement. Each participating site agreed to follow the study protocol and signed an authorship agreement form. No financial support was provided to any site.
Hospitalized adult and pediatric patients with a PIVC in situ on the day of the study were eligible for inclusion. Sample size was determined by local capacity. Hospitals were encouraged to audit their entire institution if possible; however, data were accepted from as little as one ward. Data collectors comprised nurses and doctors with experience in PIVC assessment. They were briefed on the study protocol and data collection forms by the local site coordinator, and they were supported by an overall global coordinator. Clinicians assessed the PIVC insertion site and accessed hospital records to collect data related to PIVC insertion, concurrent medications, and IV fluid orders. Further clarification of data was obtained if necessary by the clinicians from the patients and treating staff. No identifiable patient information was collected.
Data Collection
To assess whether clinical facilities were following best practice recommendations, the study team developed three data collection forms to collect information regarding site characteristics (site questionnaire), track participant recruitment (screening log), and collect data regarding PIVC characteristics and management practices (case report form [CRF]). All forms were internally and externally validated following a pilot study involving 14 sites in 13 countries.1
The CRF included variables used to assess best practice interventions, such as catheter insertion characteristics (date and time, reason, location, profession of inserter, anatomical site of placement), catheter type (gauge, brand, and product), insertion site assessment (adverse symptoms, dressing type and integrity), and information related to the IV therapy (types of IV fluids and medications, flushing solutions). Idle PIVCs were defined as not being used for blood sampling or IV therapy in the preceding 24 h.
Data collection forms were translated into 15 languages by professional translators and back-translated for validity. Translation of some languages included additional rigor. For example, Spanish-speaking members from the Spanish mainland as well as from South America were employed so that appropriate synonyms were used to capture local terms and practice. Three options were provided for data entry: directly into a purpose-developed electronic database (Lime Survey® Project, Hamburg, Germany); on paper, then transcribed into the survey database at a later time by the hospital site; or paper entry then sent (via email or post) to the coordinating center for data entry. Once cleaned and collated, all data were provided to each participating hospital to confirm accuracy and for site use in local quality improvement processes. Data were collected between June 1, 2014 and July 31, 2015.
Statistical Analysis
All data management was undertaken using SAS statistical software (SAS Institute Inc., Cary NC, USA). Results are presented for eight geographical regions using descriptive statistics (frequencies, percentages, and 95% CIs) for the variables of interest. To assess trends in catheter dwell time and rates of phlebitis, Poisson regression was used. All analyses were undertaken using the R language for statistical analysis (R Core Team, Vienna, Austria). The (STROBE (Strengthening the Reporting of Observational Studies in Epidemiology statement) guidelines for cross-sectional studies were followed, and results are presented according to these recommendations.26
RESULTS
Of the 415 hospitals that participated in this study, 406 had patients with PIVCs on the day of the study (the others being small rural centers). Thus, a total of 40,620 PIVCs in 38,161 patients from 406 hospitals in 51 countries were assessed, with no more than 5% missing data for any CRF question. There were 2459 patients (6.1%) with two or more PIVCs concurrently in situ. The median patient age was 59 y (interquartile range [IQR], 37–74 y), and just over half were male (n = 20,550, 51%). Hospital size ranged from fewer than 10 beds to over 1,000 beds, and hospitals were located in rural, regional, and metropolitan districts. The majority of countries (n = 31, 61%) contributed multiple sites, the highest being Australia with 79 hospitals. Countries with the most PIVCs studied were Spain (n = 5,553, 14%) and the United States (n = 5,048, 12%).
General surgical (n = 15,616, 39%) and medical (n = 15,448, 38%) patients represented most of the population observed. PIVCs were inserted primarily in general wards or clinics (n = 22,167, 55%) or in emergency departments (n = 7,388, 18%; Table) and for the administration of IV medication (n = 28,571, 70%) and IV fluids (n = 7,093, 18%; Table).
Globally, nurses were the primary PIVC inserters (n = 28,575, 71%); however, Australia/New Zealand had only 26% (n = 1,518) of PIVCs inserted by this group (Table). Only about one-third of PIVCs were placed in an area of non-flexion (forearm, n = 12,675, 31%, Table) the majority (n = 27,856, 69%) were placed in non-recommended anatomical sites (Figure 1). Most PIVCs were placed in the hand (n = 13,265, 32.7%) followed by the antecubital veins (n = 6176, 15.2%) and the wrist (n = 5,465, 13.5%). Site selection varied widely across the regions; 29% (n = 1686) of PIVCs in Australia/New Zealand were inserted into the antecubital veins, twice the study group average. Over half of the PIVCs inserted in the Middle East were placed in the hand (n = 295, 56%). This region also had the highest prevalence of devices placed in nonrecommended sites (n = 416, 79%; Figure 1).
The majority of PIVCs (n = 27,192, 67%; Table) were of recommended size (20–22G); however, some devices were observed to be large (14–18G; n = 6,802, 17%) or small (24-26g; n = 4,869, 12%) in adults. In Asia, 41% (n = 2,617) of devices inserted were 24-26G, more than three times the global rate. Half of all devices in Asia (n = 3,077, 48%) and the South Pacific (n = 67, 52%) were of a size not recommended for routine IV therapy (Figure 2).
The primary dressing material used was a transparent dressing (n = 31,596, 77.8%; Table); however, nearly 1 in 5 dressings used had either nonsterile tape alone (n = 5,169, 13%; Appendix 4), or a sterile gauze and tape (n = 2,592, 6%; Appendix 4.1). We found a wide variation in the use of nonsterile tape, including 1 in every 3 devices in South America dressed with nonsterile tape (n = 714, 30%) and a larger proportion in Africa (n = 543, 19%) and Europe (n = 3,056, 18%). Nonsterile tape was rarely used in North America and Australia/New Zealand. Although most PIVC dressings were clean, dry, and intact (n = 31,786, 79%; Table), one-fifth overall were compromised (moist, soiled, and/or lifting off the skin). Compromised dressings (Appendix 4.2) were more prevalent in Australia/New Zealand (n = 1,448; 25%) and in Africa (n = 707, 25%) than elsewhere.
Ten percent of PIVCs (n = 4,204) had signs and/or symptoms suggestive of phlebitis (characterized by pain, redness and/or swelling at the insertion site; Appendix 4.3). The highest prevalence of phlebitis occurred in Asia (n = 1,021, 16%), Africa (n = 360, 13%), and South America (n = 284, 12%). Pain and/or redness were the most common phlebitis symptoms. We found no association between dwell time of PIVCs and phlebitis rates (P = .085). Phlebitis rates were 12% (Days 1-3; n = 15,625), 16% (Days 4-7; n = 3,348), 10% (Days 8-21; n = 457), and 13% (Day21+; n = 174). Nearly 10% (n = 3,879) of catheters were observed to have signs of malfunction such as blood in the infusion tubing, leaking at the insertion site, or dislodgment (Appendix 4.4).
We observed 14% (n = 5,796) of PIVCs to be idle (Appendix 4.5), defined as not used in the preceding 24 h. Nearly one-fourth of all devices in North America (n = 1,230, 23%) and Australia/New Zealand (n = 1,335, 23%) were idle. PIVC documentation in hospital records was also poor, nearly half of all PIVCs (n = 19,768, 49%) had no documented date and time of insertion. The poorest compliance was in Australia/New Zealand (n = 3,428, 59%; Appendix 4.6). We also observed that 1 in 10 PIVCs had no documentation regarding who inserted the PIVC (n = 3,905). Thirty-six percent of PIVCs (n = 14,787) had no documented assessment of the PIVC site on the day of review (Appendix 4.7), including over half of all PIVCs in Asia (n = 3,364, 52%). Overall, the median dwell at the time of assessment for PIVCs with insertion date/time documented was 1.5 d (IQR, 1.0–2.5 d).
DISCUSSION
This international assessment of more than 40,000 PIVCs in 51 countries provides great insight into device characteristics and variation in management practices. Predominantly, PIVCs were inserted by nurses in the general ward environment for IV medication. One in ten PIVCs had at least one symptom of phlebitis, one in ten were dysfunctional, one in five PIVC dressings were compromised, and one in six PIVCs had not been used in the preceding 24 h. Nearly half of the PIVCs audited had the insertion date and time missing.
Regional variation was found in the professions inserting PIVCs, as well as in anatomical placement. In Australia/New Zealand, the proportion of nurses inserting PIVCs was much lower than the study group average (26% vs 71%). Because these countries contributed a substantial number of hospitals to the study, this seems a representative finding and suggests a need for education targeted at nurses for PIVC insertion in this region. The veins in the forearm are recommended as optimal for PIVC insertion in adults, rather than areas of high flexion, because the forearm provides a wide surface area to secure and dress PIVCs. Forearm placement can reduce pain during catheter dwell as well as decrease the risk of accidental removal or occlusion.3,19,27 We found only one-third of PIVCs were placed in the forearm, with most placed in the hand, antecubital veins, or wrist. This highlights an inconsistency with published recommendations and suggests that additional training and technology are required so that staff can better identify and insert PIVCs in the forearm for other than very short-term (procedural) PIVCp;s.19
Phlebitis triggering PIVC failure remains a global clinical challenge with numerous phlebitis definitions and varied assessment techniques.10 The prevalence of phlebitis has been difficult to approximate with varying estimates and definitions in the literature; however, it remains a key predictor of PIVC failure.6,10 Identification of this complication and prompt removal of the device is critical for patient comfort and reducing CABSI risk.5,28 The overall prevalence of phlebitis signs or symptoms (defined in this study as having one or more signs of redness, swelling, or pain surrounding the insertion site) was just over 10%, with pain and/or redness being most prevalent. These compromised PIVCs had not been removed as is recommended for such complications.19,28 Considering that our study was a snapshot at only one time point, the per-catheter incidence of phlebitis would be even higher; interestingly, among PIVCs with a documented insertion date and time, we observed that dwell time did not influence phlebitis rates.
Another concern is that nearly 10% (n = 3,879) of PIVCs were malfunctioning (eg, leaking) but were still in place. To bring these problems into context, around 2 billion PIVCs are used annually worldwide; as a consequence, millions of patients suffer from painful or malfunctioning PIVCs staff had not responded.1,29 The placement of large-bore catheters, and smaller-gauge ones in adults, is known to increase the incidence of malfunction that leads to failure. There are a number of sound clinical reasons for the use of large-bore (eg, resuscitation and rapid fluid replacement) or small-bore (eg, difficult venous access with small superficial veins only visible and palpable) catheters. However, it would be expected that only a small proportion of patients would require these devices, and not one in three devices as we identified. This finding suggests that some PIVCs were inappropriate in size for general IV therapy and may reflect antiquated hospital policies for some clinical cohorts.30,31
Overall, transparent dressings were used to cover the PIVC, but a number of patients were observed to have a sterile gauze and tape dressing (n = 2,592, 6%). Although the latter is less common, both dressing approaches are recommended in clinical practice guidelines because there is a lack of high-quality evidence regarding which is superior.21,22,32 Of concern was the use of nonsterile tape to dress the PIVC (n = 5,169, 12.7%). We found the prevalence of nonsterile tape use to be higher in lower-resourced countries in South America (n = 714, 30%), Africa (n = 543, 19%) and Europe (n = 3,056, 18%) and this was likely related to institutional cost reduction practices.
This finding illustrates an important issue regarding proper PIVC care and management practices in developing nations. It is widely known that access to safe health care in lower-resourced nations is challenging and that rates of mortality related to healthcare-associated infections are much higher. Thus, the differences we found in PIVC management practices in these countries are not surprising.33,34 International health networks such as the Infection Control Africa Network, the International Federation of Infection Control, and the Centers for Disease Control and Prevention can have great influence on ministries of health and clinicians in these countries to develop coordinated efforts for safe and sustainable IV practices to reduce the burden of hospital-acquired infections and related morbidity and mortality.
We found that 14% of all PIVCs had no documented IV medication or IV fluid administered in the previous 24 h, strongly indicating that they were no longer needed. Australia/New Zealand, Europe, and North America were observed to have a higher prevalence of idle catheters than the remaining regions. This suggests that an opportunity exists to develop surveillance systems that better identify idle devices for prompt removal to reduce infection risk and patient discomfort. Several randomized controlled trials, a Cochrane review, and clinical practice guidelines recommend prompt removal of PIVCs when not required, if there are any complications, or if the PIVC was inserted urgently without an aseptic insertion technique.21,28,35,36 Idle PIVCs have been implicated in adverse patient outcomes, including phlebitis and CABSI.13,27
The substantial proportion of patients with a PIVC in this study who had no clinical indication for a PIVC, a symptomatic insertion site, malfunctioning catheter, and suboptimal dressing quality suggests the need for physicians, advanced practitioners, and nurses to adopt evidence-based PIVC insertion and maintenance bundles and supporting checklists to reduce the prevalence of PIVC complications.19,21,38-40 Recommended strategies for inclusion in PIVC maintenance bundles are prompt removal of symptomatic and/or idle catheters, hand hygiene prior to accessing the catheter, regular assessment of the device, and replacement of suboptimal dressings.41,42 This approach should be implemented across all clinical specialties involved in PIVC insertion and care.
Our study findings need to be considered within the context of some limitations. The cross-sectional design prevented follow-up of PIVCs until removal to collect outcomes, including subsequent PIVC complications and/or failure, following the study observation. Ideally, data collection could have included patient-level preferences for PIVC insertion, history of PIVC use and/or failure, the number of PIVC insertion attempts, and the number of PIVCs used during that hospitalization. However, a cohort study of this magnitude was not feasible, particularly because all sites contributed staff time to complete the data collection. Only half of all initially registered sites eventually participated in the study; reasons for not participating were cited as local workload constraints and/or difficulties in applying for local approvals. Although efforts to enroll hospitals worldwide were exhaustive, our sample was not randomly selected but relied on self-selection and so is not representative, particularly for countries that contributed only one hospital site. Caution is also required when comparing inter regional differences, particularly developing regions, because better-resourced/academic sites were possibly over represented in the sample. Nevertheless, PIVC variables differed significantly between participating hospitals, suggesting that the data represent a reasonable reflection of hospital variability.
CONCLUSIONS
On the basis of this international investigation, we report variations in the characteristics, management practices, and outcomes of PIVCs inserted in hospital patients from 51 countries. Many PIVCs were idle, symptomatic, had substandard dressings, and were inserted in suboptimal anatomical sites. Despite international best practice guidelines, a large number of patients had PIVCs that were already failing or at risk of complications, including infection. A stronger focus is needed on compliance with PIVC insertion and management guidelines; better surveillance of PIVC sites; and improved assessment, decision-making, and documentation.
Acknowledgements
We are extremely grateful to colleagues from across the globe who committed their time and effort to this study (for full details of countries and team members see Appendix 1).
1. Alexandrou E, Ray-Barruel G, Carr PJ, et al. International prevalence of the use of peripheral intravenous catheters. J Hosp Med. 2015;10(8):530-533. https:/doi.org/10.1002/jhm.2389
2. Zingg W, Pittet D. Peripheral venous catheters: an under-evaluated problem. Int J Antimicrob Agents. 2009;34(suppl 4):S38-S42. https:/ doi.org/10.1016/S0924-8579(09)70565-5
3. Wallis MC, McGrail MR, Webster J, Gowardman JR, Playford G, Rickard CM. Risk factors for PIV catheter failure: a multivariate analysis from a randomized control trial. Infect. Control Hosp Epidemiol. 2014;35(1):63-68. https:/doi.org/10.1086/674398.
4. Pujol M, Hornero A, Saballs M, et al. Clinical epidemiology and outcomes of peripheral venous catheter-related bloodstream infections at a university-affiliated hospital. J Hosp Infect. 2007;67(1):22-29.
5. Fakih MG, Jones K, Rey JE, et al. Sustained improvements in peripheral venous catheter care in non–intensive care units: a quasi-experimental controlled study of education and feedback. Infect. Control Hosp Epidemiol. 2012;33(5):449-455. https:/doi.org/10.1086/665322.
6. Helm RE, Klausner JD, Klemperer JD, Flint LM, Huang E. Accepted but unacceptable: peripheral IV catheter failure. J Infus Nurs. 2015;38(3):189-203. https:/ doi.org/10.1097/NAN.0000000000000100.
7. Austin ED, Sullivan SB, Whittier S, Lowy FD, Uhlemann AC. Peripheral intravenous catheter placement is an underrecognized source of Staphylococcus aureus bloodstream infection. Open Forum Infect Dis. 2016;3(2):ofw072. https:/ doi.org/10.1093/ofid/ofw072.
8. Stuart RL, Cameron D, Scott C, et al. Peripheral intravenous catheter-associated Staphylococcus aureus bacteraemia: more than 5 years of prospective data from two tertiary health services. Med J Aust. 2013;198(10):551-553.
9. Trinh TT, Chan PA, Edwards O, et al. Peripheral venous catheter-related Staphylococcus aureus bacteremia. Infect Control Hosp Epidemiol. 2011;32(6):579-583. https:/doi.org/10.1086/660099.
10. Ray Barruel G, Polit DF, Murfield JE, Rickard CM. Infusion phlebitis assessment measures: a systematic review. J Eval Clin Pract. 2014;20(2):191-202. https:/ doi.org/ 10.1111/jep.12107
11. Marsh N, Webster J, Flynn J, et al. Securement methods for peripheral venous catheters to prevent failure: a randomised controlled pilot trial. J Vasc Access. 2015;16(3):237-244. https:/doi.org /10.5301/jva.5000348.
12. Carr PJ, Higgins NS, Cooke ML, Rippey J, Rickard CM. Tools, clinical prediction rules, and algorithms for the insertion of peripheral intravenous catheters in adult hospitalized patients: a systematic scoping review of literature. J Hosp Med. 2017;12(10):851-858. https:/doi.org/ 10.12788/jhm.2836
13. Becerra MB, Shirley D, Safdar N. Prevalence, risk factors, and outcomes of idle intravenous catheters: An integrative review. Am J Infect Control. 2016;44(10):e167-e172. https:/ doi.org/10.1016/j.ajic.2016.03.073.
14. Robinson-Reilly M, Paliadelis P, Cruickshank M. Venous access: the patient experience. Support Care Cancer. 2016;24(3):1181-1187. https:/ doi.org/10.1007/s00520-015-2900-9.
15. Petroski A, Frisch A, Joseph N, Carlson JN. Predictors of difficult pediatric intravenous access in a community Emergency Department. J Vasc Access. 2015;16(6):521-526. https:/doi.org/10.5301/jva.5000411
16. Sou V, McManus C, Mifflin N, Frost SA, Ale J, Alexandrou E. A clinical pathway for the management of difficult venous access. BMC Nurs. 2017;16(1):64. https:/ doi.org/10.1186/s12912-017-0261-z
17. World Health Organization. Report on the burden of endemic health care-associated infection worldwide. Geneva2011. 9241501502.
18. Hirschmann H, Fux L, Podusel J, et al. The influence of hand hygiene prior to insertion of peripheral venous catheters on the frequency of complications. J Hosp Infect. 2001;49(3):199-203. https:/doi.org/10.1053/jhin.2001.1077
19. Gorski L, Hadaway L, Hagle M, McGoldrick M, Orr M, Doellman D. Infusion therapy standards of practice. J Infus Nurs. 2016;39(suppl 1):S1-S159.
20. Abolfotouh MA, Salam M, Bani-Mustafa Aa, White D, Balkhy HH. Prospective study of incidence and predictors of peripheral intravenous catheter-induced complications. Ther Clin Risk Manag. 2014;10:993. https://doi.org/10.2147/TCRM.S74685.
21. Loveday H, Wilson J, Pratt R, et al. epic3: national evidence-based guidelines for preventing healthcare-associated infections in NHS hospitals in England. J Hosp Infect. 2014;86(suppl 1):S1-S70. https:/doi.org/10.1016/S0195-6701(13)60012-2.
22. O’Grady NP, Alexander M, Burns LA, et al. Guidelines for the prevention of intravascular catheter-related infections. Clin Infect Dis. 2011;52(9):e162-e193. https:/doi.org/10.1093/cid/cir257
23. Cicolini G, Bonghi AP, Di Labio L, Di Mascio R. Position of peripheral venous cannulae and the incidence of thrombophlebitis: an observational study. J Adv Nurs. 2009;65(6):1268-1273. https:/doi.org/10.1111/j.1365-2648.2009.04980.x.
24. Marsh N, Webster J, Larson E, Cooke M, Mihala G, Rickard C. Observational study of peripheral intravenous catheter outcomes in adult hospitalized patients: a multivariable analysis of peripheral intravenous catheter failure. J Hosp Med. 2018;13(2):83-89. https:/doi.org/10.12788/jhm.2867.
25. One Million Global Catheters PIVC Worldwide Prevalence study. OMG study website http://www.omgpivc.org/. Accessed 23 March, 2017.
26. Von Elm E, Altman DG, Egger M, et al. The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) Statement: guidelines for reporting observational studies. Int J Surg. 2014;12(12):1495-1499. https:/doi.org/ 10.1136/bmj.39335.541782.AD
27. Fields JM, Dean AJ, Todman RW, et al. The effect of vessel depth, diameter, and location on ultrasound-guided peripheral intravenous catheter longevity. Am J Emerg Med. 2012;30(7):1134-1140. https:/doi.org/10.1016/j.ajem.2011.07.027.
28. Patel SA, Alebich MM, Feldman LS. Choosing wisely: things we do for no reason. Routine replacement of peripheral intravenous catheters. J Hosp Med. 2017;12(1):42-45.
29. Newswire. Global Peripheral I.V. Catheter Market 2014 - 2018. New York, PR Newswire Assoc; 2014.
30. Webster J, Larsen E, Booker C, Laws J, Marsh N. Prophylactic insertion of large bore peripheral intravenous catheters in maternity patients for postpartum haemorrhage: A cohort study. Aust N Z J Obstet Gynaecol. 2017.https:/doi.org/10.1111/ajo.12759.
31. Rivera A, Strauss K, van Zundert A, Mortier E. Matching the peripheral intravenous catheter to the individual patient. Acta Anaesthesiol Belg. 2006;58(1):19.
32. Webster J, Gillies D, O’Riordan E, Sherriff KL, Rickard CM. Gauze and tape and transparent polyurethane dressings for central venous catheters. Cochrane Database Syst Rev. 2011;11:CD003827. https:/doi.org/10.1002/14651858.CD003827.pub2
33. Dieleman JL, Templin T, Sadat N, et al. National spending on health by source for 184 countries between 2013 and 2040. Lancet. 2016;387(10037):2521-2535. https:/ doi.org/10.1016/S0140-6736(16)30167-2.
34. Allegranzi B, Nejad SB, Combescure C, et al. Burden of endemic health-care-associated infection in developing countries: systematic review and meta-analysis. Lancet. 2011;377(9761):228-241. https:/ doi.org/10.1016/S0140-6736(10)61458-4.
35. Rickard CM, Webster J, Wallis MC, et al. Routine versus clinically indicated replacement of peripheral intravenous catheters: a randomised controlled equivalence trial. Lancet. 2012;380(9847):1066-1074. https:/doi.org/10.1016/S0140-6736(12)61082-4.
36. Webster J, Osborne S, Rickard CM, New K. Clinically indicated replacement versus routine replacement of peripheral venous catheters. Cochrane Database Syst Rev. 2015;8:CD007798. https://doi.org/10.1002/14651858.CD007798.pub4.
37. Yagnik L, Graves A, Thong K. Plastic in patient study: Prospective audit of adherence to peripheral intravenous cannula monitoring and documentation guidelines, with the aim of reducing future rates of intravenous cannula-related complications. Am J Infect Control. 2017;45(1):34-38. https:/doi.org/10.1016/j.ajic.2016.09.008.
38. Boyd S, Aggarwal I, Davey P, Logan M, Nathwani D. Peripheral intravenous catheters: the road to quality improvement and safer patient care. J Hosp Infect. 2011;77(1):37-41. https:/doi.org/10.1016/j.jhin.2010.09.011.
39. DeVries M, Valentine M, Mancos P. Protected clinical indication of peripheral intravenous lines: successful implementation. J Assoc Vasc Access. 2016;21(2):89-92. https://doi.org/10.1016/j.java.2016.03.001.
40. Rhodes D, Cheng A, McLellan S, et al. Reducing Staphylococcus aureus bloodstream infections associated with peripheral intravenous cannulae: successful implementation of a care bundle at a large Australian health service. J Hosp Infect. 2016;94(1):86-91. https:/doi.org/10.1016/j.jhin.2016.05.020.
41. Rinke ML, Chen AR, Bundy DG, et al. Implementation of a central line maintenance care bundle in hospitalized pediatric oncology patients. Pediatr. 2012;130(4):e996-e1004. https:/doi.org/10.1542/peds.2012-0295.
42. Marshall J, Mermel L, Fakih M, Hadaway L, Kallen A, O’Grady N. Strategies to prevent central line–associated bloodstream infections in acute care hospitals: 2014 update. Infect. Control Hosp Epidemiol. 2014;35(suppl 2):S89-107. https:/doi.org/10.1086/676533.
1. Alexandrou E, Ray-Barruel G, Carr PJ, et al. International prevalence of the use of peripheral intravenous catheters. J Hosp Med. 2015;10(8):530-533. https:/doi.org/10.1002/jhm.2389
2. Zingg W, Pittet D. Peripheral venous catheters: an under-evaluated problem. Int J Antimicrob Agents. 2009;34(suppl 4):S38-S42. https:/ doi.org/10.1016/S0924-8579(09)70565-5
3. Wallis MC, McGrail MR, Webster J, Gowardman JR, Playford G, Rickard CM. Risk factors for PIV catheter failure: a multivariate analysis from a randomized control trial. Infect. Control Hosp Epidemiol. 2014;35(1):63-68. https:/doi.org/10.1086/674398.
4. Pujol M, Hornero A, Saballs M, et al. Clinical epidemiology and outcomes of peripheral venous catheter-related bloodstream infections at a university-affiliated hospital. J Hosp Infect. 2007;67(1):22-29.
5. Fakih MG, Jones K, Rey JE, et al. Sustained improvements in peripheral venous catheter care in non–intensive care units: a quasi-experimental controlled study of education and feedback. Infect. Control Hosp Epidemiol. 2012;33(5):449-455. https:/doi.org/10.1086/665322.
6. Helm RE, Klausner JD, Klemperer JD, Flint LM, Huang E. Accepted but unacceptable: peripheral IV catheter failure. J Infus Nurs. 2015;38(3):189-203. https:/ doi.org/10.1097/NAN.0000000000000100.
7. Austin ED, Sullivan SB, Whittier S, Lowy FD, Uhlemann AC. Peripheral intravenous catheter placement is an underrecognized source of Staphylococcus aureus bloodstream infection. Open Forum Infect Dis. 2016;3(2):ofw072. https:/ doi.org/10.1093/ofid/ofw072.
8. Stuart RL, Cameron D, Scott C, et al. Peripheral intravenous catheter-associated Staphylococcus aureus bacteraemia: more than 5 years of prospective data from two tertiary health services. Med J Aust. 2013;198(10):551-553.
9. Trinh TT, Chan PA, Edwards O, et al. Peripheral venous catheter-related Staphylococcus aureus bacteremia. Infect Control Hosp Epidemiol. 2011;32(6):579-583. https:/doi.org/10.1086/660099.
10. Ray Barruel G, Polit DF, Murfield JE, Rickard CM. Infusion phlebitis assessment measures: a systematic review. J Eval Clin Pract. 2014;20(2):191-202. https:/ doi.org/ 10.1111/jep.12107
11. Marsh N, Webster J, Flynn J, et al. Securement methods for peripheral venous catheters to prevent failure: a randomised controlled pilot trial. J Vasc Access. 2015;16(3):237-244. https:/doi.org /10.5301/jva.5000348.
12. Carr PJ, Higgins NS, Cooke ML, Rippey J, Rickard CM. Tools, clinical prediction rules, and algorithms for the insertion of peripheral intravenous catheters in adult hospitalized patients: a systematic scoping review of literature. J Hosp Med. 2017;12(10):851-858. https:/doi.org/ 10.12788/jhm.2836
13. Becerra MB, Shirley D, Safdar N. Prevalence, risk factors, and outcomes of idle intravenous catheters: An integrative review. Am J Infect Control. 2016;44(10):e167-e172. https:/ doi.org/10.1016/j.ajic.2016.03.073.
14. Robinson-Reilly M, Paliadelis P, Cruickshank M. Venous access: the patient experience. Support Care Cancer. 2016;24(3):1181-1187. https:/ doi.org/10.1007/s00520-015-2900-9.
15. Petroski A, Frisch A, Joseph N, Carlson JN. Predictors of difficult pediatric intravenous access in a community Emergency Department. J Vasc Access. 2015;16(6):521-526. https:/doi.org/10.5301/jva.5000411
16. Sou V, McManus C, Mifflin N, Frost SA, Ale J, Alexandrou E. A clinical pathway for the management of difficult venous access. BMC Nurs. 2017;16(1):64. https:/ doi.org/10.1186/s12912-017-0261-z
17. World Health Organization. Report on the burden of endemic health care-associated infection worldwide. Geneva2011. 9241501502.
18. Hirschmann H, Fux L, Podusel J, et al. The influence of hand hygiene prior to insertion of peripheral venous catheters on the frequency of complications. J Hosp Infect. 2001;49(3):199-203. https:/doi.org/10.1053/jhin.2001.1077
19. Gorski L, Hadaway L, Hagle M, McGoldrick M, Orr M, Doellman D. Infusion therapy standards of practice. J Infus Nurs. 2016;39(suppl 1):S1-S159.
20. Abolfotouh MA, Salam M, Bani-Mustafa Aa, White D, Balkhy HH. Prospective study of incidence and predictors of peripheral intravenous catheter-induced complications. Ther Clin Risk Manag. 2014;10:993. https://doi.org/10.2147/TCRM.S74685.
21. Loveday H, Wilson J, Pratt R, et al. epic3: national evidence-based guidelines for preventing healthcare-associated infections in NHS hospitals in England. J Hosp Infect. 2014;86(suppl 1):S1-S70. https:/doi.org/10.1016/S0195-6701(13)60012-2.
22. O’Grady NP, Alexander M, Burns LA, et al. Guidelines for the prevention of intravascular catheter-related infections. Clin Infect Dis. 2011;52(9):e162-e193. https:/doi.org/10.1093/cid/cir257
23. Cicolini G, Bonghi AP, Di Labio L, Di Mascio R. Position of peripheral venous cannulae and the incidence of thrombophlebitis: an observational study. J Adv Nurs. 2009;65(6):1268-1273. https:/doi.org/10.1111/j.1365-2648.2009.04980.x.
24. Marsh N, Webster J, Larson E, Cooke M, Mihala G, Rickard C. Observational study of peripheral intravenous catheter outcomes in adult hospitalized patients: a multivariable analysis of peripheral intravenous catheter failure. J Hosp Med. 2018;13(2):83-89. https:/doi.org/10.12788/jhm.2867.
25. One Million Global Catheters PIVC Worldwide Prevalence study. OMG study website http://www.omgpivc.org/. Accessed 23 March, 2017.
26. Von Elm E, Altman DG, Egger M, et al. The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) Statement: guidelines for reporting observational studies. Int J Surg. 2014;12(12):1495-1499. https:/doi.org/ 10.1136/bmj.39335.541782.AD
27. Fields JM, Dean AJ, Todman RW, et al. The effect of vessel depth, diameter, and location on ultrasound-guided peripheral intravenous catheter longevity. Am J Emerg Med. 2012;30(7):1134-1140. https:/doi.org/10.1016/j.ajem.2011.07.027.
28. Patel SA, Alebich MM, Feldman LS. Choosing wisely: things we do for no reason. Routine replacement of peripheral intravenous catheters. J Hosp Med. 2017;12(1):42-45.
29. Newswire. Global Peripheral I.V. Catheter Market 2014 - 2018. New York, PR Newswire Assoc; 2014.
30. Webster J, Larsen E, Booker C, Laws J, Marsh N. Prophylactic insertion of large bore peripheral intravenous catheters in maternity patients for postpartum haemorrhage: A cohort study. Aust N Z J Obstet Gynaecol. 2017.https:/doi.org/10.1111/ajo.12759.
31. Rivera A, Strauss K, van Zundert A, Mortier E. Matching the peripheral intravenous catheter to the individual patient. Acta Anaesthesiol Belg. 2006;58(1):19.
32. Webster J, Gillies D, O’Riordan E, Sherriff KL, Rickard CM. Gauze and tape and transparent polyurethane dressings for central venous catheters. Cochrane Database Syst Rev. 2011;11:CD003827. https:/doi.org/10.1002/14651858.CD003827.pub2
33. Dieleman JL, Templin T, Sadat N, et al. National spending on health by source for 184 countries between 2013 and 2040. Lancet. 2016;387(10037):2521-2535. https:/ doi.org/10.1016/S0140-6736(16)30167-2.
34. Allegranzi B, Nejad SB, Combescure C, et al. Burden of endemic health-care-associated infection in developing countries: systematic review and meta-analysis. Lancet. 2011;377(9761):228-241. https:/ doi.org/10.1016/S0140-6736(10)61458-4.
35. Rickard CM, Webster J, Wallis MC, et al. Routine versus clinically indicated replacement of peripheral intravenous catheters: a randomised controlled equivalence trial. Lancet. 2012;380(9847):1066-1074. https:/doi.org/10.1016/S0140-6736(12)61082-4.
36. Webster J, Osborne S, Rickard CM, New K. Clinically indicated replacement versus routine replacement of peripheral venous catheters. Cochrane Database Syst Rev. 2015;8:CD007798. https://doi.org/10.1002/14651858.CD007798.pub4.
37. Yagnik L, Graves A, Thong K. Plastic in patient study: Prospective audit of adherence to peripheral intravenous cannula monitoring and documentation guidelines, with the aim of reducing future rates of intravenous cannula-related complications. Am J Infect Control. 2017;45(1):34-38. https:/doi.org/10.1016/j.ajic.2016.09.008.
38. Boyd S, Aggarwal I, Davey P, Logan M, Nathwani D. Peripheral intravenous catheters: the road to quality improvement and safer patient care. J Hosp Infect. 2011;77(1):37-41. https:/doi.org/10.1016/j.jhin.2010.09.011.
39. DeVries M, Valentine M, Mancos P. Protected clinical indication of peripheral intravenous lines: successful implementation. J Assoc Vasc Access. 2016;21(2):89-92. https://doi.org/10.1016/j.java.2016.03.001.
40. Rhodes D, Cheng A, McLellan S, et al. Reducing Staphylococcus aureus bloodstream infections associated with peripheral intravenous cannulae: successful implementation of a care bundle at a large Australian health service. J Hosp Infect. 2016;94(1):86-91. https:/doi.org/10.1016/j.jhin.2016.05.020.
41. Rinke ML, Chen AR, Bundy DG, et al. Implementation of a central line maintenance care bundle in hospitalized pediatric oncology patients. Pediatr. 2012;130(4):e996-e1004. https:/doi.org/10.1542/peds.2012-0295.
42. Marshall J, Mermel L, Fakih M, Hadaway L, Kallen A, O’Grady N. Strategies to prevent central line–associated bloodstream infections in acute care hospitals: 2014 update. Infect. Control Hosp Epidemiol. 2014;35(suppl 2):S89-107. https:/doi.org/10.1086/676533.
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