Inspired by the ABIM Foundation’s Choosing Wisely^® campaign, the “Things We Do for No Reason^™” (TWDFNR) series reviews practices that have become common parts of hospital care but may provide little value to our patients. Practices reviewed in the TWDFNR series do not represent clear-cut conclusions or clinical practice standards but are meant as a starting place for research and active discussions among hospitalists and patients. We invite you to be part of that discussion.

A 65-year-old woman with hypertension presents to the emergency department with three days of dyspnea, malaise, and pleuritic chest pain. Her temperature is 100.1°F, heart rate 110 beats per minute, and blood pressure 110/60 mm Hg. She is breathing 24 times per minute and has an oxygen saturation (SpO₂) of 94% on room air. Her exam is remarkable for dry mucous membranes and right lower lung crackles. Her nurse places her on 3 L of oxygen per minute via nasal cannula, and her SpO₂ rises to 99%.

Shortly after the discovery of oxygen in the late 18th century, physicians began using it to treat a variety of conditions including tuberculosis, pneumonia, respiratory failure, and angina. By the 1970s, most medical texts recommended oxygen use in suspected myocardial infarction (MI) because of the theoretical appeal of increasing delivery of oxygen to the heart and other vital organs.¹ Additionally, there is a tendency to believe that supplemental oxygen alleviates dyspnea regardless of etiology or oxygen saturation. Recent studies have shown widespread use of oxygen in scenarios without clear indications and without oxygen saturation goals. A 2010 survey of clinicians managing acute MI found that 98% “always or usually” used oxygen and 55% believed that oxygen “definitely or probably reduces the risk of death.”² In a Danish prehospital study, supplemental oxygen was used in 34% of ambulance patients even though only 17% of these patients had an SpO₂ less than 94%.³ A study of critically ill patients found that most of the time, SpO₂ exceeded 98%. Even when the fraction of inspired oxygen (FiO₂) was between 0.3 and 0.4, no one adjusted the oxygen dose.⁴

The reflexive use of oxygen in patients with acute respiratory or cardiovascular illness is problematic for several reasons. First, when oxygen saturation is near-normal, the potential benefit from supplemental oxygen lacks physiologic plausibility. More compellingly, evidence exists that hyperoxemia may cause significant harm. Finally, the unnecessary use of supplemental oxygen incurs practical inconveniences and expenses.

To understand why the physiologic basis for reflexive oxygen use is weak, it is important to distinguish hypoxemia (low arterial oxygen tension and hemoglobin oxygen saturation), tissue hypoxia (which can occur from hypoxemia or focal abnormalities in perfusion), and dyspnea (a subjective experience of breathing discomfort). A variety of mechanisms cause dyspnea, most of which do not involve hypoxemia. A patient with acute heart failure may experience severe dyspnea caused by activation of pressure-sensitive J-receptors in the lung, even if oxygen saturation and tissue perfusion are intact. This process will be relieved by reducing pulmonary capillary pressures, but it is unaffected by supplemental oxygen. Coronary occlusion causes hypoxia of the heart muscle, but restoring perfusion is the most effective treatment. The instinct to maximize the oxygen-carrying capacity of the remaining blood flow is understandable. However, in a normoxemic patient, increasing the inspired fraction of oxygen has a marginal effect on oxygen-carrying capacity, since hemoglobin saturation and concentration rather than arterial oxygen tension (PaO₂) predominantly determine oxygen-carrying capacity. On the other hand, supraphysiologic levels of dissolved oxygen may lead to toxicity.⁵

For over a century, we have known the potential harms of hyperoxia. Original studies in animal models showed that hyperoxia led to lung injury, altered hemodynamics, endothelial cell dysfunction, and inflammatory activation.⁵ Many of these detrimental effects involve the generation of reactive oxygen species and oxidative stress.⁵ High levels of inspired oxygen can also cause increased pulmonary shunting through inhibition of physiologic hypoxic vasoconstriction and due to absorption atelectasis.⁶ Oxygen negatively affects cardiovascular function by reducing coronary blood flow, increasing systemic vascular resistance, and reducing cardiac output.¹

Chronic obstructive pulmonary disease (COPD) is the clinical setting in which risks of supplemental oxygen are most well-recognized historically. In patients with COPD at risk for hypercarbia, oxygen titrated to a goal SpO₂ outside 88%-92% is associated with a two-fold risk of mortality.⁷ Worsening ventilation-perfusion matching and the Haldane effect (decreased affinity of hemoglobin for carbon dioxide as the PaO₂ rises), rather than the previously theorized decrease in hypoxic drive, are now believed to contribute most to hyperoxia-induced hypercarbia. These unintended consequences may also occur in patients with other forms of acute and chronic lung disease.

The British Medical Journal published the first randomized controlled trial of oxygen use in suspected MI in 1976.¹ Patients who received oxygen at 6 L per minute for 24 hours had more episodes of sinus tachycardia without any improvement in mortality, analgesic use, or infarct size.¹ More recent and robust trials comparing outcomes in normoxemic patients randomized to supplemental oxygen versus room air have had similar findings: no difference in mortality, infarct size, or pain ratings.^8,9 One found a significantly increased rate of MI recurrence with the use of oxygen.⁸ These data have led the latest guidelines for the management of ST-elevation MI from the European Society of Cardiology to discourage the use of supplemental oxygen unless SpO₂ is <90%.¹⁰

Two recent trials investigated the effects of hyperoxia in critically ill patients.^11,12 Girardis and colleagues randomized 480 critically ill patients in an Italian medical-surgical intensive care unit to conservative (SpO₂ between 94% and 98% or PaO₂ between 70 and 100 mm Hg) versus conventional oxygenation targets (SpO₂ between 97% and 100% and PaO₂ up to 150 mm Hg). Compared with conventional oxygen targets, conservative oxygen use was associated with an absolute risk reduction in mortality of 8.6% (11.6% vs 20.2%; P =.01).¹¹ Another trial from 22 centers in France compared outcomes in mechanically ventilated patients with septic shock who received FiO₂ at 1.0 compared with those with oxygen titration to SpO₂ between 88% and 95%. The trial was stopped early for safety concerns. Those in the hyperoxemia group had a higher incidence of serious adverse events (85% vs 76%; P =.02), including pneumothorax, clinically relevant bleeding, myocardial infarction, and arrhythmias, as well as a trend toward increased mortality.¹²

Trials of liberal oxygen use in other settings of acute illness,¹³ including ischemic stroke,¹⁴ traumatic brain injury,¹⁵ and postcardiac arrest,¹⁶ have also linked liberal oxygen use with increased risk of mortality and other adverse events. “Liberal” use in these trials ranged from an FiO₂ of 0.28 (equivalent to 2 L of nasal cannula) to 1.0. Significant secondary outcomes included fewer hospital-free and ventilator-free days in patients with liberal oxygen use. Furthermore, a meta-analysis of 25 trials including over 16,000 patients found dose-dependent toxicity: for every 1% increase in SpO₂ above 94%-96% (the median SpO₂ in the liberal oxygen groups), there was a 25% relative increase in in-hospital mortality.¹³

In addition to the data above, there are practical reasons to avoid unnecessary use of supplemental oxygen. Providing supplemental oxygen to a patient who is not hypoxemic may delay the recognition of cardiopulmonary decompensation by delaying detection of hypoxemia.⁶ Beyond the effects of oxygen itself, oxygen delivery methods carry their own potential adverse effects. These include epistaxis (with nasal cannula), claustrophobia (with face masks), decreased mobility, falls, and delirium.¹⁷ Finally, oxygen administration has direct and indirect financial costs, including those of supplies, care coordination, and monitoring.

Importantly, the above discussion pertains to normoxemic patients receiving supplemental oxygen. There is no dispute that significantly hypoxemic patients should receive supplemental oxygen. There are also instances where the use of supplemental oxygen in normoxemic patients may be beneficial, such as in carbon monoxide poisoning, decompression injury, gas embolism, cluster headaches, sickle cell crisis, and pneumothorax.¹⁷

Like any other drug, oxygen should be administered after assessment of its indications, intended benefits, and possible harms. Both significant hypoxemia and hyperoxemia should be avoided. In patients with neither hypoxemia nor the indications above, clinicians should not administer supplemental oxygen. Recent society guidelines can be applied in various clinical contexts. In patients with suspected MI, oxygen should be administered if SpO₂ is <90%.¹⁰ For most other acutely ill patients, clinicians should administer supplemental oxygen if SpO₂ <90%-92% and target an SpO₂ of no higher than 94%-96%,^18-19 as meta-analyses found evidence of harm above this level.¹³ Results of randomized trials currently underway should add supporting evidence for more specific oxygenation targets in different patient populations. With respect to implementation, it must be noted that factors beyond physician decision influence the use of supplemental oxygen. Appropriate institutional policies, standards of care, and educational efforts to all hospital providers must be enacted in order to reduce the unnecessary use of supplemental oxygen.

• For most acutely ill patients, do not administer supplemental oxygen when SpO₂ >92%. If supplemental oxygen is used, the SpO₂ should not exceed 94%-96%.
• For patients with suspected MI, only start supplemental oxygen for SpO₂ <90%.
• For patients at risk for hypercapnic respiratory failure (eg, COPD patients), target SpO₂ of 88%-92%.
• Provide supplemental oxygen to normoxemic patients with carbon monoxide poisoning, decompression injury, gas embolism, cluster headache, sickle cell crisis, and pneumothorax.
• Review and revise institutional practices and policies that contribute to unnecessary use of supplemental oxygen.

In the opening case, the patient is acutely ill and requires further workup. Her current SpO₂ of 99% puts her at risk for adverse events and death, and supplemental oxygen should be titrated down or stopped to avoid SpO₂ greater than 94%-96%. For years, clinicians have erred on the side of using supplemental oxygen, without recognizing its dangers. However, over a century of evidence from pathophysiologic experiments and randomized trials across multiple clinical settings have associated hyperoxemia with adverse outcomes and increased mortality. Professional societies are adopting this evidence into their guideline recommendations, and clinicians should use supplemental oxygen judiciously in their daily practice.

Do you think this is a low-value practice? Is this truly a “Thing We Do for No Reason^™”? Share what you do in your practice and join in the conversation online by retweeting it on Twitter (#TWDFNR) and liking it on Facebook. We invite you to propose ideas for other “Things We Do for No Reason^™” topics by emailing TWDFNR@hospitalmedicine.org.

Inspired by the ABIM Foundation’s Choosing Wisely^® campaign, the “Things We Do for No Reason^™” (TWDFNR) series reviews practices that have become common parts of hospital care but may provide little value to our patients. Practices reviewed in the TWDFNR series do not represent clear-cut conclusions or clinical practice standards but are meant as a starting place for research and active discussions among hospitalists and patients. We invite you to be part of that discussion.

A 65-year-old woman with hypertension presents to the emergency department with three days of dyspnea, malaise, and pleuritic chest pain. Her temperature is 100.1°F, heart rate 110 beats per minute, and blood pressure 110/60 mm Hg. She is breathing 24 times per minute and has an oxygen saturation (SpO₂) of 94% on room air. Her exam is remarkable for dry mucous membranes and right lower lung crackles. Her nurse places her on 3 L of oxygen per minute via nasal cannula, and her SpO₂ rises to 99%.

Shortly after the discovery of oxygen in the late 18th century, physicians began using it to treat a variety of conditions including tuberculosis, pneumonia, respiratory failure, and angina. By the 1970s, most medical texts recommended oxygen use in suspected myocardial infarction (MI) because of the theoretical appeal of increasing delivery of oxygen to the heart and other vital organs.¹ Additionally, there is a tendency to believe that supplemental oxygen alleviates dyspnea regardless of etiology or oxygen saturation. Recent studies have shown widespread use of oxygen in scenarios without clear indications and without oxygen saturation goals. A 2010 survey of clinicians managing acute MI found that 98% “always or usually” used oxygen and 55% believed that oxygen “definitely or probably reduces the risk of death.”² In a Danish prehospital study, supplemental oxygen was used in 34% of ambulance patients even though only 17% of these patients had an SpO₂ less than 94%.³ A study of critically ill patients found that most of the time, SpO₂ exceeded 98%. Even when the fraction of inspired oxygen (FiO₂) was between 0.3 and 0.4, no one adjusted the oxygen dose.⁴

The reflexive use of oxygen in patients with acute respiratory or cardiovascular illness is problematic for several reasons. First, when oxygen saturation is near-normal, the potential benefit from supplemental oxygen lacks physiologic plausibility. More compellingly, evidence exists that hyperoxemia may cause significant harm. Finally, the unnecessary use of supplemental oxygen incurs practical inconveniences and expenses.

To understand why the physiologic basis for reflexive oxygen use is weak, it is important to distinguish hypoxemia (low arterial oxygen tension and hemoglobin oxygen saturation), tissue hypoxia (which can occur from hypoxemia or focal abnormalities in perfusion), and dyspnea (a subjective experience of breathing discomfort). A variety of mechanisms cause dyspnea, most of which do not involve hypoxemia. A patient with acute heart failure may experience severe dyspnea caused by activation of pressure-sensitive J-receptors in the lung, even if oxygen saturation and tissue perfusion are intact. This process will be relieved by reducing pulmonary capillary pressures, but it is unaffected by supplemental oxygen. Coronary occlusion causes hypoxia of the heart muscle, but restoring perfusion is the most effective treatment. The instinct to maximize the oxygen-carrying capacity of the remaining blood flow is understandable. However, in a normoxemic patient, increasing the inspired fraction of oxygen has a marginal effect on oxygen-carrying capacity, since hemoglobin saturation and concentration rather than arterial oxygen tension (PaO₂) predominantly determine oxygen-carrying capacity. On the other hand, supraphysiologic levels of dissolved oxygen may lead to toxicity.⁵

For over a century, we have known the potential harms of hyperoxia. Original studies in animal models showed that hyperoxia led to lung injury, altered hemodynamics, endothelial cell dysfunction, and inflammatory activation.⁵ Many of these detrimental effects involve the generation of reactive oxygen species and oxidative stress.⁵ High levels of inspired oxygen can also cause increased pulmonary shunting through inhibition of physiologic hypoxic vasoconstriction and due to absorption atelectasis.⁶ Oxygen negatively affects cardiovascular function by reducing coronary blood flow, increasing systemic vascular resistance, and reducing cardiac output.¹

Chronic obstructive pulmonary disease (COPD) is the clinical setting in which risks of supplemental oxygen are most well-recognized historically. In patients with COPD at risk for hypercarbia, oxygen titrated to a goal SpO₂ outside 88%-92% is associated with a two-fold risk of mortality.⁷ Worsening ventilation-perfusion matching and the Haldane effect (decreased affinity of hemoglobin for carbon dioxide as the PaO₂ rises), rather than the previously theorized decrease in hypoxic drive, are now believed to contribute most to hyperoxia-induced hypercarbia. These unintended consequences may also occur in patients with other forms of acute and chronic lung disease.

The British Medical Journal published the first randomized controlled trial of oxygen use in suspected MI in 1976.¹ Patients who received oxygen at 6 L per minute for 24 hours had more episodes of sinus tachycardia without any improvement in mortality, analgesic use, or infarct size.¹ More recent and robust trials comparing outcomes in normoxemic patients randomized to supplemental oxygen versus room air have had similar findings: no difference in mortality, infarct size, or pain ratings.^8,9 One found a significantly increased rate of MI recurrence with the use of oxygen.⁸ These data have led the latest guidelines for the management of ST-elevation MI from the European Society of Cardiology to discourage the use of supplemental oxygen unless SpO₂ is <90%.¹⁰

Two recent trials investigated the effects of hyperoxia in critically ill patients.^11,12 Girardis and colleagues randomized 480 critically ill patients in an Italian medical-surgical intensive care unit to conservative (SpO₂ between 94% and 98% or PaO₂ between 70 and 100 mm Hg) versus conventional oxygenation targets (SpO₂ between 97% and 100% and PaO₂ up to 150 mm Hg). Compared with conventional oxygen targets, conservative oxygen use was associated with an absolute risk reduction in mortality of 8.6% (11.6% vs 20.2%; P =.01).¹¹ Another trial from 22 centers in France compared outcomes in mechanically ventilated patients with septic shock who received FiO₂ at 1.0 compared with those with oxygen titration to SpO₂ between 88% and 95%. The trial was stopped early for safety concerns. Those in the hyperoxemia group had a higher incidence of serious adverse events (85% vs 76%; P =.02), including pneumothorax, clinically relevant bleeding, myocardial infarction, and arrhythmias, as well as a trend toward increased mortality.¹²

Trials of liberal oxygen use in other settings of acute illness,¹³ including ischemic stroke,¹⁴ traumatic brain injury,¹⁵ and postcardiac arrest,¹⁶ have also linked liberal oxygen use with increased risk of mortality and other adverse events. “Liberal” use in these trials ranged from an FiO₂ of 0.28 (equivalent to 2 L of nasal cannula) to 1.0. Significant secondary outcomes included fewer hospital-free and ventilator-free days in patients with liberal oxygen use. Furthermore, a meta-analysis of 25 trials including over 16,000 patients found dose-dependent toxicity: for every 1% increase in SpO₂ above 94%-96% (the median SpO₂ in the liberal oxygen groups), there was a 25% relative increase in in-hospital mortality.¹³

In addition to the data above, there are practical reasons to avoid unnecessary use of supplemental oxygen. Providing supplemental oxygen to a patient who is not hypoxemic may delay the recognition of cardiopulmonary decompensation by delaying detection of hypoxemia.⁶ Beyond the effects of oxygen itself, oxygen delivery methods carry their own potential adverse effects. These include epistaxis (with nasal cannula), claustrophobia (with face masks), decreased mobility, falls, and delirium.¹⁷ Finally, oxygen administration has direct and indirect financial costs, including those of supplies, care coordination, and monitoring.

Importantly, the above discussion pertains to normoxemic patients receiving supplemental oxygen. There is no dispute that significantly hypoxemic patients should receive supplemental oxygen. There are also instances where the use of supplemental oxygen in normoxemic patients may be beneficial, such as in carbon monoxide poisoning, decompression injury, gas embolism, cluster headaches, sickle cell crisis, and pneumothorax.¹⁷

Like any other drug, oxygen should be administered after assessment of its indications, intended benefits, and possible harms. Both significant hypoxemia and hyperoxemia should be avoided. In patients with neither hypoxemia nor the indications above, clinicians should not administer supplemental oxygen. Recent society guidelines can be applied in various clinical contexts. In patients with suspected MI, oxygen should be administered if SpO₂ is <90%.¹⁰ For most other acutely ill patients, clinicians should administer supplemental oxygen if SpO₂ <90%-92% and target an SpO₂ of no higher than 94%-96%,^18-19 as meta-analyses found evidence of harm above this level.¹³ Results of randomized trials currently underway should add supporting evidence for more specific oxygenation targets in different patient populations. With respect to implementation, it must be noted that factors beyond physician decision influence the use of supplemental oxygen. Appropriate institutional policies, standards of care, and educational efforts to all hospital providers must be enacted in order to reduce the unnecessary use of supplemental oxygen.

• For most acutely ill patients, do not administer supplemental oxygen when SpO₂ >92%. If supplemental oxygen is used, the SpO₂ should not exceed 94%-96%.
• For patients with suspected MI, only start supplemental oxygen for SpO₂ <90%.
• For patients at risk for hypercapnic respiratory failure (eg, COPD patients), target SpO₂ of 88%-92%.
• Provide supplemental oxygen to normoxemic patients with carbon monoxide poisoning, decompression injury, gas embolism, cluster headache, sickle cell crisis, and pneumothorax.
• Review and revise institutional practices and policies that contribute to unnecessary use of supplemental oxygen.

In the opening case, the patient is acutely ill and requires further workup. Her current SpO₂ of 99% puts her at risk for adverse events and death, and supplemental oxygen should be titrated down or stopped to avoid SpO₂ greater than 94%-96%. For years, clinicians have erred on the side of using supplemental oxygen, without recognizing its dangers. However, over a century of evidence from pathophysiologic experiments and randomized trials across multiple clinical settings have associated hyperoxemia with adverse outcomes and increased mortality. Professional societies are adopting this evidence into their guideline recommendations, and clinicians should use supplemental oxygen judiciously in their daily practice.

Do you think this is a low-value practice? Is this truly a “Thing We Do for No Reason^™”? Share what you do in your practice and join in the conversation online by retweeting it on Twitter (#TWDFNR) and liking it on Facebook. We invite you to propose ideas for other “Things We Do for No Reason^™” topics by emailing TWDFNR@hospitalmedicine.org.

Inspired by the ABIM Foundation’s Choosing Wisely^® campaign, the “Things We Do for No Reason^™” (TWDFNR) series reviews practices that have become common parts of hospital care but may provide little value to our patients. Practices reviewed in the TWDFNR series do not represent clear-cut conclusions or clinical practice standards but are meant as a starting place for research and active discussions among hospitalists and patients. We invite you to be part of that discussion.

A 65-year-old woman with hypertension presents to the emergency department with three days of dyspnea, malaise, and pleuritic chest pain. Her temperature is 100.1°F, heart rate 110 beats per minute, and blood pressure 110/60 mm Hg. She is breathing 24 times per minute and has an oxygen saturation (SpO₂) of 94% on room air. Her exam is remarkable for dry mucous membranes and right lower lung crackles. Her nurse places her on 3 L of oxygen per minute via nasal cannula, and her SpO₂ rises to 99%.

Shortly after the discovery of oxygen in the late 18th century, physicians began using it to treat a variety of conditions including tuberculosis, pneumonia, respiratory failure, and angina. By the 1970s, most medical texts recommended oxygen use in suspected myocardial infarction (MI) because of the theoretical appeal of increasing delivery of oxygen to the heart and other vital organs.¹ Additionally, there is a tendency to believe that supplemental oxygen alleviates dyspnea regardless of etiology or oxygen saturation. Recent studies have shown widespread use of oxygen in scenarios without clear indications and without oxygen saturation goals. A 2010 survey of clinicians managing acute MI found that 98% “always or usually” used oxygen and 55% believed that oxygen “definitely or probably reduces the risk of death.”² In a Danish prehospital study, supplemental oxygen was used in 34% of ambulance patients even though only 17% of these patients had an SpO₂ less than 94%.³ A study of critically ill patients found that most of the time, SpO₂ exceeded 98%. Even when the fraction of inspired oxygen (FiO₂) was between 0.3 and 0.4, no one adjusted the oxygen dose.⁴

The reflexive use of oxygen in patients with acute respiratory or cardiovascular illness is problematic for several reasons. First, when oxygen saturation is near-normal, the potential benefit from supplemental oxygen lacks physiologic plausibility. More compellingly, evidence exists that hyperoxemia may cause significant harm. Finally, the unnecessary use of supplemental oxygen incurs practical inconveniences and expenses.

To understand why the physiologic basis for reflexive oxygen use is weak, it is important to distinguish hypoxemia (low arterial oxygen tension and hemoglobin oxygen saturation), tissue hypoxia (which can occur from hypoxemia or focal abnormalities in perfusion), and dyspnea (a subjective experience of breathing discomfort). A variety of mechanisms cause dyspnea, most of which do not involve hypoxemia. A patient with acute heart failure may experience severe dyspnea caused by activation of pressure-sensitive J-receptors in the lung, even if oxygen saturation and tissue perfusion are intact. This process will be relieved by reducing pulmonary capillary pressures, but it is unaffected by supplemental oxygen. Coronary occlusion causes hypoxia of the heart muscle, but restoring perfusion is the most effective treatment. The instinct to maximize the oxygen-carrying capacity of the remaining blood flow is understandable. However, in a normoxemic patient, increasing the inspired fraction of oxygen has a marginal effect on oxygen-carrying capacity, since hemoglobin saturation and concentration rather than arterial oxygen tension (PaO₂) predominantly determine oxygen-carrying capacity. On the other hand, supraphysiologic levels of dissolved oxygen may lead to toxicity.⁵

For over a century, we have known the potential harms of hyperoxia. Original studies in animal models showed that hyperoxia led to lung injury, altered hemodynamics, endothelial cell dysfunction, and inflammatory activation.⁵ Many of these detrimental effects involve the generation of reactive oxygen species and oxidative stress.⁵ High levels of inspired oxygen can also cause increased pulmonary shunting through inhibition of physiologic hypoxic vasoconstriction and due to absorption atelectasis.⁶ Oxygen negatively affects cardiovascular function by reducing coronary blood flow, increasing systemic vascular resistance, and reducing cardiac output.¹

Chronic obstructive pulmonary disease (COPD) is the clinical setting in which risks of supplemental oxygen are most well-recognized historically. In patients with COPD at risk for hypercarbia, oxygen titrated to a goal SpO₂ outside 88%-92% is associated with a two-fold risk of mortality.⁷ Worsening ventilation-perfusion matching and the Haldane effect (decreased affinity of hemoglobin for carbon dioxide as the PaO₂ rises), rather than the previously theorized decrease in hypoxic drive, are now believed to contribute most to hyperoxia-induced hypercarbia. These unintended consequences may also occur in patients with other forms of acute and chronic lung disease.

The British Medical Journal published the first randomized controlled trial of oxygen use in suspected MI in 1976.¹ Patients who received oxygen at 6 L per minute for 24 hours had more episodes of sinus tachycardia without any improvement in mortality, analgesic use, or infarct size.¹ More recent and robust trials comparing outcomes in normoxemic patients randomized to supplemental oxygen versus room air have had similar findings: no difference in mortality, infarct size, or pain ratings.^8,9 One found a significantly increased rate of MI recurrence with the use of oxygen.⁸ These data have led the latest guidelines for the management of ST-elevation MI from the European Society of Cardiology to discourage the use of supplemental oxygen unless SpO₂ is <90%.¹⁰

Two recent trials investigated the effects of hyperoxia in critically ill patients.^11,12 Girardis and colleagues randomized 480 critically ill patients in an Italian medical-surgical intensive care unit to conservative (SpO₂ between 94% and 98% or PaO₂ between 70 and 100 mm Hg) versus conventional oxygenation targets (SpO₂ between 97% and 100% and PaO₂ up to 150 mm Hg). Compared with conventional oxygen targets, conservative oxygen use was associated with an absolute risk reduction in mortality of 8.6% (11.6% vs 20.2%; P =.01).¹¹ Another trial from 22 centers in France compared outcomes in mechanically ventilated patients with septic shock who received FiO₂ at 1.0 compared with those with oxygen titration to SpO₂ between 88% and 95%. The trial was stopped early for safety concerns. Those in the hyperoxemia group had a higher incidence of serious adverse events (85% vs 76%; P =.02), including pneumothorax, clinically relevant bleeding, myocardial infarction, and arrhythmias, as well as a trend toward increased mortality.¹²

Trials of liberal oxygen use in other settings of acute illness,¹³ including ischemic stroke,¹⁴ traumatic brain injury,¹⁵ and postcardiac arrest,¹⁶ have also linked liberal oxygen use with increased risk of mortality and other adverse events. “Liberal” use in these trials ranged from an FiO₂ of 0.28 (equivalent to 2 L of nasal cannula) to 1.0. Significant secondary outcomes included fewer hospital-free and ventilator-free days in patients with liberal oxygen use. Furthermore, a meta-analysis of 25 trials including over 16,000 patients found dose-dependent toxicity: for every 1% increase in SpO₂ above 94%-96% (the median SpO₂ in the liberal oxygen groups), there was a 25% relative increase in in-hospital mortality.¹³

In addition to the data above, there are practical reasons to avoid unnecessary use of supplemental oxygen. Providing supplemental oxygen to a patient who is not hypoxemic may delay the recognition of cardiopulmonary decompensation by delaying detection of hypoxemia.⁶ Beyond the effects of oxygen itself, oxygen delivery methods carry their own potential adverse effects. These include epistaxis (with nasal cannula), claustrophobia (with face masks), decreased mobility, falls, and delirium.¹⁷ Finally, oxygen administration has direct and indirect financial costs, including those of supplies, care coordination, and monitoring.

Importantly, the above discussion pertains to normoxemic patients receiving supplemental oxygen. There is no dispute that significantly hypoxemic patients should receive supplemental oxygen. There are also instances where the use of supplemental oxygen in normoxemic patients may be beneficial, such as in carbon monoxide poisoning, decompression injury, gas embolism, cluster headaches, sickle cell crisis, and pneumothorax.¹⁷

Like any other drug, oxygen should be administered after assessment of its indications, intended benefits, and possible harms. Both significant hypoxemia and hyperoxemia should be avoided. In patients with neither hypoxemia nor the indications above, clinicians should not administer supplemental oxygen. Recent society guidelines can be applied in various clinical contexts. In patients with suspected MI, oxygen should be administered if SpO₂ is <90%.¹⁰ For most other acutely ill patients, clinicians should administer supplemental oxygen if SpO₂ <90%-92% and target an SpO₂ of no higher than 94%-96%,^18-19 as meta-analyses found evidence of harm above this level.¹³ Results of randomized trials currently underway should add supporting evidence for more specific oxygenation targets in different patient populations. With respect to implementation, it must be noted that factors beyond physician decision influence the use of supplemental oxygen. Appropriate institutional policies, standards of care, and educational efforts to all hospital providers must be enacted in order to reduce the unnecessary use of supplemental oxygen.

• For most acutely ill patients, do not administer supplemental oxygen when SpO₂ >92%. If supplemental oxygen is used, the SpO₂ should not exceed 94%-96%.
• For patients with suspected MI, only start supplemental oxygen for SpO₂ <90%.
• For patients at risk for hypercapnic respiratory failure (eg, COPD patients), target SpO₂ of 88%-92%.
• Provide supplemental oxygen to normoxemic patients with carbon monoxide poisoning, decompression injury, gas embolism, cluster headache, sickle cell crisis, and pneumothorax.
• Review and revise institutional practices and policies that contribute to unnecessary use of supplemental oxygen.

In the opening case, the patient is acutely ill and requires further workup. Her current SpO₂ of 99% puts her at risk for adverse events and death, and supplemental oxygen should be titrated down or stopped to avoid SpO₂ greater than 94%-96%. For years, clinicians have erred on the side of using supplemental oxygen, without recognizing its dangers. However, over a century of evidence from pathophysiologic experiments and randomized trials across multiple clinical settings have associated hyperoxemia with adverse outcomes and increased mortality. Professional societies are adopting this evidence into their guideline recommendations, and clinicians should use supplemental oxygen judiciously in their daily practice.

Do you think this is a low-value practice? Is this truly a “Thing We Do for No Reason^™”? Share what you do in your practice and join in the conversation online by retweeting it on Twitter (#TWDFNR) and liking it on Facebook. We invite you to propose ideas for other “Things We Do for No Reason^™” topics by emailing TWDFNR@hospitalmedicine.org.

Introduced in the 1950s, midline catheters have become a popular option for intravenous (IV) access.^1,2 Ranging from 8 to 25 cm in length, they are inserted in the veins of the upper arm. Unlike peripherally inserted central catheters (PICCs), the tip of midline catheters terminates proximal to the axillary vein; thus, midlines are peripheral, not central venous access devices.^1-3 One popular variation of a midline catheter, though nebulously defined, is the long peripheral catheter (LPC), a device ranging from 6 to 15 cm in length.^4,5

Concerns regarding inappropriate use and complications such as thrombosis and central line-associated bloodstream infection (CLABSI) have spurred growth in the use of LPCs.⁶ However, data regarding complication rates with these devices are limited. Whether LPCs are a safe and viable option for IV access is unclear. We conducted a retrospective study to examine indications, patterns of use, and complications following LPC insertion in hospitalized patients.

Device Selection

Our institution is a 470-bed tertiary care, safety-net hospital in Chicago, Illinois. Our vascular access team (VAT) performs a patient assessment and selects IV devices based upon published standards for device appropriateness. ⁷ We retrospectively collated electronic requests for LPC insertion on adult inpatients between October 2015 and June 2017. Cases where (1) duplicate orders, (2) patient refusal, (3) peripheral intravenous catheter of any length, or (4) PICCs were placed were excluded from this analysis.

VAT and Device Characteristics

We used Bard PowerGlide^® (Bard Access Systems, Inc., Salt Lake City, Utah), an 18-gauge, 8-10 cm long, power-injectable, polyurethane LPC. Bundled kits (ie, device, gown, dressing, etc.) were utilized, and VAT providers underwent two weeks of training prior to the study period. All LPCs were inserted in the upper extremities under sterile technique using ultrasound guidance (accelerated Seldinger technique). Placement confirmation was verified by aspiration, flush, and ultrasound visualization of the catheter tip within the vein. An antimicrobial dressing was applied to the catheter insertion site, and daily saline flushes and weekly dressing changes by bedside nurses were used for device maintenance. LPC placement was available on all nonholiday weekdays from 8 am to 5 pm.

Data Selection

For each LPC recipient, demographic and comorbidity data were collected to calculate the Charlson Comorbidity Index (Table 1). Every LPC recipient’s history of deep vein thrombosis (DVT) and catheter-related infection (CRI) was recorded. Procedural information (eg, inserter, vein, and number of attempts) was obtained from insertion notes. All data were extracted from the electronic medical record via chart review. Two reviewers verified outcomes to ensure concordance with stated definitions (ie, DVT, CRI). Device parameters, including dwell time, indication, and time to complication(s) were also collected.

Primary Outcomes

The primary outcome was the incidence of DVT and CRI (Table 2). DVT was defined as radiographically confirmed (eg, ultrasound, computed tomography) thrombosis in the presence of patient signs or symptoms. CRI was defined in accordance with Timsit et al.⁸ as follows: catheter-related clinical sepsis without bloodstream infection defined as (1) combination of fever (body temperature >38.5°C) or hypothermia (body temperature <36.5°C), (2) catheter-tip culture yielding ≥103 CFUs/mL, (3) pus at the insertion site or resolution of clinical sepsis after catheter removal, and (4) absence of any other infectious focus or catheter-related bloodstream infection (CRBSI). CRBSI was defined as a combination of (1) one or more positive peripheral blood cultures sampled immediately before or within 48 hours after catheter removal, (2) a quantitative catheter-tip culture testing positive for the same microorganisms (same species and susceptibility pattern) or a differential time to positivity of blood cultures ≥2 hours, and (3) no other infectious focus explaining the positive blood culture result.

Secondary Outcomes

Secondary outcomes, defined as minor complications, included infiltration, thrombophlebitis, and catheter occlusion. Infiltration was defined as localized swelling due to infusate or site leakage. Thrombophlebitis was defined as one or more of the following: localized erythema, palpable cord, tenderness, or streaking. Occlusion was defined as nonpatency of the catheter due to the inability to flush or aspirate. Definitions for secondary outcomes are consistent with those used in prior studies.⁹

Statistical Analysis

Patient and LPC characteristics were analyzed using descriptive statistics. Results were reported as percentages, means, medians (interquartile range [IQR]), and rates per 1,000 catheter days. All analyses were conducted in Stata v.15 (StataCorp, College Station, Texas).

Within the 20-month study period, a total of 539 LPCs representing 5,543 catheter days were available for analysis. The mean patient age was 53 years. A total of 90 patients (16.7%) had a history of DVT, while 6 (1.1%) had a history of CRI. We calculated a median Charlson index of 4 (interquartile range [IQR], 2-7), suggesting an estimated one-year postdischarge survival of 53% (Table 1).

The majority of LPCs (99.6% [537/539]) were single lumen catheters. No patient had more than one concurrent LPC. The cannulation success rate on the first attempt was 93.9% (507/539). The brachial or basilic veins were primarily targeted (98.7%, [532/539]). Difficult intravenous access represented 48.8% (263/539) of indications, and postdischarge parenteral antibiotics constituted 47.9% (258/539). The median catheter dwell time was eight days (IQR, 4-14 days).

Nine DVTs (1.7% [9/539]) occurred in patients with LPCs. The incidence of DVT was higher in patients with a history of DVT (5.7%, 5/90). The median time from insertion to DVT was 11 (IQR, 5-14) days. DVTs were managed with LPC removal and systemic anticoagulation in accordance with catheter-related DVT guidelines. The rate of CRI was 0.6% (3/539), or 0.54 per 1,000 catheter days. Two CRIs had positive blood cultures, while one had negative cultures. Infections occurred after a median of 12 (IQR, 8-15) days of catheter dwell. Each was treated with LPC removal and IV antibiotics, with two patients receiving two weeks and one receiving six weeks of antibiotic therapy (Table 2).

With respect to secondary outcomes, the incidence of infiltration was 0.4% (2/539), thrombophlebitis 0.7% (4/539), and catheter occlusion 0.9% (5/539). The time to event was 8.5, 3.75, and 5.4 days, respectively. Collectively, 2.0% of devices experienced a minor complication.

In our single-center study, LPCs were primarily inserted for difficult venous access or parenteral antibiotics. Despite a clinically complex population with a high number of comorbidities, rates of major and minor complications associated with LPCs were low. These data suggest that LPCs are a safe alternative to PICCs and other central access devices for short-term use.

Our incidence of CRI of 0.6% (0.54 per 1,000 catheter days) is similar to or lower than other studies.^2,10,11 An incidence of 0%-1.5% was observed in two recent publications about midline catheters, with rates across individual studies and hospital sites varying widely.^12,13 A systematic review of intravascular devices reported CRI rates of 0.4% (0.2 per 1,000 catheter days) for midlines and 0.1% (0.5 per 1,000 catheter days for peripheral IVs), in contrast to PICCs at 3.1% (1.1 per 1,000 catheter days).¹⁴ However, catheters of varying lengths and diameters were used in studies within the review, potentially leading to heterogeneous outcomes. In accordance with existing data, CRI incidence in our study increased with catheter dwell time.¹⁰

The 1.7% rate of DVT observed in our study is on the lower end of existing data (1.4%-5.9%).^12-15 Compared with PICCs (2%-15%), the incidence of venous thrombosis appears to be lower with midlines/LPCs—justifying their use as an alternative device for IV access.^7,9,12,14 There was an overall low rate of minor complications, similar to recently published results.¹⁰ As rates were greater in patients with a history of DVT (5.7%), caution is warranted when using these devices in this population.

Our experience with LPCs suggests financial and patient benefits. The cost of LPCs is lower than central access devices.⁴ As rates of CRI were low, costs related to CLABSIs from PICC use may be reduced by appropriate LPC use. LPCs may allow the ability to draw blood routinely, which could improve the patient experience—albeit with its own risks. Current recommendations support the use of PICCs or LPCs, somewhat interchangeably, for patients with appropriate indications needing IV therapy for more than five to six days.^2,7 However, LPCs now account for 57% of vascular access procedures in our center and have led to a decrease in reliance on PICCs and attendant complications.

Our study has several limitations. First, LPCs and midlines are often used interchangeably in the literature.^4,5 Therefore, reported complication rates may not reflect those of LPCs alone and may limit comparisons. Second, ours was a single-center study with experts assessing device appropriateness and performing ultrasound-guided insertions; our findings may not be generalizable to dissimilar settings. Third, we did not track LPC complications such as nonpatency and leakage. As prior studies reported high rates of complications such as these events, caution is advised when interpreting our findings.¹⁵ Finally, we retrospectively extracted data from our medical records; limitations in documentation may influence our findings.

In patients requiring short-term IV therapy, these data suggest LPCs have low complication rates and may be safely used as an alternative option for venous access.

Acknowledgments

The authors thank Drs. Laura Hernandez, Andres Mendez Hernandez, and Victor Prado for their assistance in data collection. The authors also thank Mr. Onofre Donceras and Dr. Sharon Welbel from the John H. Stroger, Jr. Hospital of Cook County Department of Infection Control & Epidemiology for their assistance in reviewing local line infection data.

Drs. Patel and Chopra developed the study design. Drs. Patel, Araujo, Parra Rodriguez, Ramirez Sanchez, and Chopra contributed to manuscript writing. Ms. Snyder provided statistical analysis. All authors have seen and approved the final manuscript for submission.

Disclosures

The authors have nothing to disclose.

Introduced in the 1950s, midline catheters have become a popular option for intravenous (IV) access.^1,2 Ranging from 8 to 25 cm in length, they are inserted in the veins of the upper arm. Unlike peripherally inserted central catheters (PICCs), the tip of midline catheters terminates proximal to the axillary vein; thus, midlines are peripheral, not central venous access devices.^1-3 One popular variation of a midline catheter, though nebulously defined, is the long peripheral catheter (LPC), a device ranging from 6 to 15 cm in length.^4,5

Concerns regarding inappropriate use and complications such as thrombosis and central line-associated bloodstream infection (CLABSI) have spurred growth in the use of LPCs.⁶ However, data regarding complication rates with these devices are limited. Whether LPCs are a safe and viable option for IV access is unclear. We conducted a retrospective study to examine indications, patterns of use, and complications following LPC insertion in hospitalized patients.

Device Selection

Our institution is a 470-bed tertiary care, safety-net hospital in Chicago, Illinois. Our vascular access team (VAT) performs a patient assessment and selects IV devices based upon published standards for device appropriateness. ⁷ We retrospectively collated electronic requests for LPC insertion on adult inpatients between October 2015 and June 2017. Cases where (1) duplicate orders, (2) patient refusal, (3) peripheral intravenous catheter of any length, or (4) PICCs were placed were excluded from this analysis.

VAT and Device Characteristics

We used Bard PowerGlide^® (Bard Access Systems, Inc., Salt Lake City, Utah), an 18-gauge, 8-10 cm long, power-injectable, polyurethane LPC. Bundled kits (ie, device, gown, dressing, etc.) were utilized, and VAT providers underwent two weeks of training prior to the study period. All LPCs were inserted in the upper extremities under sterile technique using ultrasound guidance (accelerated Seldinger technique). Placement confirmation was verified by aspiration, flush, and ultrasound visualization of the catheter tip within the vein. An antimicrobial dressing was applied to the catheter insertion site, and daily saline flushes and weekly dressing changes by bedside nurses were used for device maintenance. LPC placement was available on all nonholiday weekdays from 8 am to 5 pm.

Data Selection

For each LPC recipient, demographic and comorbidity data were collected to calculate the Charlson Comorbidity Index (Table 1). Every LPC recipient’s history of deep vein thrombosis (DVT) and catheter-related infection (CRI) was recorded. Procedural information (eg, inserter, vein, and number of attempts) was obtained from insertion notes. All data were extracted from the electronic medical record via chart review. Two reviewers verified outcomes to ensure concordance with stated definitions (ie, DVT, CRI). Device parameters, including dwell time, indication, and time to complication(s) were also collected.

Primary Outcomes

The primary outcome was the incidence of DVT and CRI (Table 2). DVT was defined as radiographically confirmed (eg, ultrasound, computed tomography) thrombosis in the presence of patient signs or symptoms. CRI was defined in accordance with Timsit et al.⁸ as follows: catheter-related clinical sepsis without bloodstream infection defined as (1) combination of fever (body temperature >38.5°C) or hypothermia (body temperature <36.5°C), (2) catheter-tip culture yielding ≥103 CFUs/mL, (3) pus at the insertion site or resolution of clinical sepsis after catheter removal, and (4) absence of any other infectious focus or catheter-related bloodstream infection (CRBSI). CRBSI was defined as a combination of (1) one or more positive peripheral blood cultures sampled immediately before or within 48 hours after catheter removal, (2) a quantitative catheter-tip culture testing positive for the same microorganisms (same species and susceptibility pattern) or a differential time to positivity of blood cultures ≥2 hours, and (3) no other infectious focus explaining the positive blood culture result.

Secondary Outcomes

Secondary outcomes, defined as minor complications, included infiltration, thrombophlebitis, and catheter occlusion. Infiltration was defined as localized swelling due to infusate or site leakage. Thrombophlebitis was defined as one or more of the following: localized erythema, palpable cord, tenderness, or streaking. Occlusion was defined as nonpatency of the catheter due to the inability to flush or aspirate. Definitions for secondary outcomes are consistent with those used in prior studies.⁹

Statistical Analysis

Patient and LPC characteristics were analyzed using descriptive statistics. Results were reported as percentages, means, medians (interquartile range [IQR]), and rates per 1,000 catheter days. All analyses were conducted in Stata v.15 (StataCorp, College Station, Texas).

Within the 20-month study period, a total of 539 LPCs representing 5,543 catheter days were available for analysis. The mean patient age was 53 years. A total of 90 patients (16.7%) had a history of DVT, while 6 (1.1%) had a history of CRI. We calculated a median Charlson index of 4 (interquartile range [IQR], 2-7), suggesting an estimated one-year postdischarge survival of 53% (Table 1).

The majority of LPCs (99.6% [537/539]) were single lumen catheters. No patient had more than one concurrent LPC. The cannulation success rate on the first attempt was 93.9% (507/539). The brachial or basilic veins were primarily targeted (98.7%, [532/539]). Difficult intravenous access represented 48.8% (263/539) of indications, and postdischarge parenteral antibiotics constituted 47.9% (258/539). The median catheter dwell time was eight days (IQR, 4-14 days).

Nine DVTs (1.7% [9/539]) occurred in patients with LPCs. The incidence of DVT was higher in patients with a history of DVT (5.7%, 5/90). The median time from insertion to DVT was 11 (IQR, 5-14) days. DVTs were managed with LPC removal and systemic anticoagulation in accordance with catheter-related DVT guidelines. The rate of CRI was 0.6% (3/539), or 0.54 per 1,000 catheter days. Two CRIs had positive blood cultures, while one had negative cultures. Infections occurred after a median of 12 (IQR, 8-15) days of catheter dwell. Each was treated with LPC removal and IV antibiotics, with two patients receiving two weeks and one receiving six weeks of antibiotic therapy (Table 2).

With respect to secondary outcomes, the incidence of infiltration was 0.4% (2/539), thrombophlebitis 0.7% (4/539), and catheter occlusion 0.9% (5/539). The time to event was 8.5, 3.75, and 5.4 days, respectively. Collectively, 2.0% of devices experienced a minor complication.

In our single-center study, LPCs were primarily inserted for difficult venous access or parenteral antibiotics. Despite a clinically complex population with a high number of comorbidities, rates of major and minor complications associated with LPCs were low. These data suggest that LPCs are a safe alternative to PICCs and other central access devices for short-term use.

Our incidence of CRI of 0.6% (0.54 per 1,000 catheter days) is similar to or lower than other studies.^2,10,11 An incidence of 0%-1.5% was observed in two recent publications about midline catheters, with rates across individual studies and hospital sites varying widely.^12,13 A systematic review of intravascular devices reported CRI rates of 0.4% (0.2 per 1,000 catheter days) for midlines and 0.1% (0.5 per 1,000 catheter days for peripheral IVs), in contrast to PICCs at 3.1% (1.1 per 1,000 catheter days).¹⁴ However, catheters of varying lengths and diameters were used in studies within the review, potentially leading to heterogeneous outcomes. In accordance with existing data, CRI incidence in our study increased with catheter dwell time.¹⁰

The 1.7% rate of DVT observed in our study is on the lower end of existing data (1.4%-5.9%).^12-15 Compared with PICCs (2%-15%), the incidence of venous thrombosis appears to be lower with midlines/LPCs—justifying their use as an alternative device for IV access.^7,9,12,14 There was an overall low rate of minor complications, similar to recently published results.¹⁰ As rates were greater in patients with a history of DVT (5.7%), caution is warranted when using these devices in this population.

Our experience with LPCs suggests financial and patient benefits. The cost of LPCs is lower than central access devices.⁴ As rates of CRI were low, costs related to CLABSIs from PICC use may be reduced by appropriate LPC use. LPCs may allow the ability to draw blood routinely, which could improve the patient experience—albeit with its own risks. Current recommendations support the use of PICCs or LPCs, somewhat interchangeably, for patients with appropriate indications needing IV therapy for more than five to six days.^2,7 However, LPCs now account for 57% of vascular access procedures in our center and have led to a decrease in reliance on PICCs and attendant complications.

Our study has several limitations. First, LPCs and midlines are often used interchangeably in the literature.^4,5 Therefore, reported complication rates may not reflect those of LPCs alone and may limit comparisons. Second, ours was a single-center study with experts assessing device appropriateness and performing ultrasound-guided insertions; our findings may not be generalizable to dissimilar settings. Third, we did not track LPC complications such as nonpatency and leakage. As prior studies reported high rates of complications such as these events, caution is advised when interpreting our findings.¹⁵ Finally, we retrospectively extracted data from our medical records; limitations in documentation may influence our findings.

In patients requiring short-term IV therapy, these data suggest LPCs have low complication rates and may be safely used as an alternative option for venous access.

Acknowledgments

The authors thank Drs. Laura Hernandez, Andres Mendez Hernandez, and Victor Prado for their assistance in data collection. The authors also thank Mr. Onofre Donceras and Dr. Sharon Welbel from the John H. Stroger, Jr. Hospital of Cook County Department of Infection Control & Epidemiology for their assistance in reviewing local line infection data.

Drs. Patel and Chopra developed the study design. Drs. Patel, Araujo, Parra Rodriguez, Ramirez Sanchez, and Chopra contributed to manuscript writing. Ms. Snyder provided statistical analysis. All authors have seen and approved the final manuscript for submission.

Disclosures

The authors have nothing to disclose.

Introduced in the 1950s, midline catheters have become a popular option for intravenous (IV) access.^1,2 Ranging from 8 to 25 cm in length, they are inserted in the veins of the upper arm. Unlike peripherally inserted central catheters (PICCs), the tip of midline catheters terminates proximal to the axillary vein; thus, midlines are peripheral, not central venous access devices.^1-3 One popular variation of a midline catheter, though nebulously defined, is the long peripheral catheter (LPC), a device ranging from 6 to 15 cm in length.^4,5

Concerns regarding inappropriate use and complications such as thrombosis and central line-associated bloodstream infection (CLABSI) have spurred growth in the use of LPCs.⁶ However, data regarding complication rates with these devices are limited. Whether LPCs are a safe and viable option for IV access is unclear. We conducted a retrospective study to examine indications, patterns of use, and complications following LPC insertion in hospitalized patients.

Device Selection

Our institution is a 470-bed tertiary care, safety-net hospital in Chicago, Illinois. Our vascular access team (VAT) performs a patient assessment and selects IV devices based upon published standards for device appropriateness. ⁷ We retrospectively collated electronic requests for LPC insertion on adult inpatients between October 2015 and June 2017. Cases where (1) duplicate orders, (2) patient refusal, (3) peripheral intravenous catheter of any length, or (4) PICCs were placed were excluded from this analysis.

VAT and Device Characteristics

We used Bard PowerGlide^® (Bard Access Systems, Inc., Salt Lake City, Utah), an 18-gauge, 8-10 cm long, power-injectable, polyurethane LPC. Bundled kits (ie, device, gown, dressing, etc.) were utilized, and VAT providers underwent two weeks of training prior to the study period. All LPCs were inserted in the upper extremities under sterile technique using ultrasound guidance (accelerated Seldinger technique). Placement confirmation was verified by aspiration, flush, and ultrasound visualization of the catheter tip within the vein. An antimicrobial dressing was applied to the catheter insertion site, and daily saline flushes and weekly dressing changes by bedside nurses were used for device maintenance. LPC placement was available on all nonholiday weekdays from 8 am to 5 pm.

Data Selection

For each LPC recipient, demographic and comorbidity data were collected to calculate the Charlson Comorbidity Index (Table 1). Every LPC recipient’s history of deep vein thrombosis (DVT) and catheter-related infection (CRI) was recorded. Procedural information (eg, inserter, vein, and number of attempts) was obtained from insertion notes. All data were extracted from the electronic medical record via chart review. Two reviewers verified outcomes to ensure concordance with stated definitions (ie, DVT, CRI). Device parameters, including dwell time, indication, and time to complication(s) were also collected.

Primary Outcomes

The primary outcome was the incidence of DVT and CRI (Table 2). DVT was defined as radiographically confirmed (eg, ultrasound, computed tomography) thrombosis in the presence of patient signs or symptoms. CRI was defined in accordance with Timsit et al.⁸ as follows: catheter-related clinical sepsis without bloodstream infection defined as (1) combination of fever (body temperature >38.5°C) or hypothermia (body temperature <36.5°C), (2) catheter-tip culture yielding ≥103 CFUs/mL, (3) pus at the insertion site or resolution of clinical sepsis after catheter removal, and (4) absence of any other infectious focus or catheter-related bloodstream infection (CRBSI). CRBSI was defined as a combination of (1) one or more positive peripheral blood cultures sampled immediately before or within 48 hours after catheter removal, (2) a quantitative catheter-tip culture testing positive for the same microorganisms (same species and susceptibility pattern) or a differential time to positivity of blood cultures ≥2 hours, and (3) no other infectious focus explaining the positive blood culture result.

Secondary Outcomes

Secondary outcomes, defined as minor complications, included infiltration, thrombophlebitis, and catheter occlusion. Infiltration was defined as localized swelling due to infusate or site leakage. Thrombophlebitis was defined as one or more of the following: localized erythema, palpable cord, tenderness, or streaking. Occlusion was defined as nonpatency of the catheter due to the inability to flush or aspirate. Definitions for secondary outcomes are consistent with those used in prior studies.⁹

Statistical Analysis

Patient and LPC characteristics were analyzed using descriptive statistics. Results were reported as percentages, means, medians (interquartile range [IQR]), and rates per 1,000 catheter days. All analyses were conducted in Stata v.15 (StataCorp, College Station, Texas).

Within the 20-month study period, a total of 539 LPCs representing 5,543 catheter days were available for analysis. The mean patient age was 53 years. A total of 90 patients (16.7%) had a history of DVT, while 6 (1.1%) had a history of CRI. We calculated a median Charlson index of 4 (interquartile range [IQR], 2-7), suggesting an estimated one-year postdischarge survival of 53% (Table 1).

The majority of LPCs (99.6% [537/539]) were single lumen catheters. No patient had more than one concurrent LPC. The cannulation success rate on the first attempt was 93.9% (507/539). The brachial or basilic veins were primarily targeted (98.7%, [532/539]). Difficult intravenous access represented 48.8% (263/539) of indications, and postdischarge parenteral antibiotics constituted 47.9% (258/539). The median catheter dwell time was eight days (IQR, 4-14 days).

Nine DVTs (1.7% [9/539]) occurred in patients with LPCs. The incidence of DVT was higher in patients with a history of DVT (5.7%, 5/90). The median time from insertion to DVT was 11 (IQR, 5-14) days. DVTs were managed with LPC removal and systemic anticoagulation in accordance with catheter-related DVT guidelines. The rate of CRI was 0.6% (3/539), or 0.54 per 1,000 catheter days. Two CRIs had positive blood cultures, while one had negative cultures. Infections occurred after a median of 12 (IQR, 8-15) days of catheter dwell. Each was treated with LPC removal and IV antibiotics, with two patients receiving two weeks and one receiving six weeks of antibiotic therapy (Table 2).

With respect to secondary outcomes, the incidence of infiltration was 0.4% (2/539), thrombophlebitis 0.7% (4/539), and catheter occlusion 0.9% (5/539). The time to event was 8.5, 3.75, and 5.4 days, respectively. Collectively, 2.0% of devices experienced a minor complication.

In our single-center study, LPCs were primarily inserted for difficult venous access or parenteral antibiotics. Despite a clinically complex population with a high number of comorbidities, rates of major and minor complications associated with LPCs were low. These data suggest that LPCs are a safe alternative to PICCs and other central access devices for short-term use.

Our incidence of CRI of 0.6% (0.54 per 1,000 catheter days) is similar to or lower than other studies.^2,10,11 An incidence of 0%-1.5% was observed in two recent publications about midline catheters, with rates across individual studies and hospital sites varying widely.^12,13 A systematic review of intravascular devices reported CRI rates of 0.4% (0.2 per 1,000 catheter days) for midlines and 0.1% (0.5 per 1,000 catheter days for peripheral IVs), in contrast to PICCs at 3.1% (1.1 per 1,000 catheter days).¹⁴ However, catheters of varying lengths and diameters were used in studies within the review, potentially leading to heterogeneous outcomes. In accordance with existing data, CRI incidence in our study increased with catheter dwell time.¹⁰

The 1.7% rate of DVT observed in our study is on the lower end of existing data (1.4%-5.9%).^12-15 Compared with PICCs (2%-15%), the incidence of venous thrombosis appears to be lower with midlines/LPCs—justifying their use as an alternative device for IV access.^7,9,12,14 There was an overall low rate of minor complications, similar to recently published results.¹⁰ As rates were greater in patients with a history of DVT (5.7%), caution is warranted when using these devices in this population.

Our experience with LPCs suggests financial and patient benefits. The cost of LPCs is lower than central access devices.⁴ As rates of CRI were low, costs related to CLABSIs from PICC use may be reduced by appropriate LPC use. LPCs may allow the ability to draw blood routinely, which could improve the patient experience—albeit with its own risks. Current recommendations support the use of PICCs or LPCs, somewhat interchangeably, for patients with appropriate indications needing IV therapy for more than five to six days.^2,7 However, LPCs now account for 57% of vascular access procedures in our center and have led to a decrease in reliance on PICCs and attendant complications.

Our study has several limitations. First, LPCs and midlines are often used interchangeably in the literature.^4,5 Therefore, reported complication rates may not reflect those of LPCs alone and may limit comparisons. Second, ours was a single-center study with experts assessing device appropriateness and performing ultrasound-guided insertions; our findings may not be generalizable to dissimilar settings. Third, we did not track LPC complications such as nonpatency and leakage. As prior studies reported high rates of complications such as these events, caution is advised when interpreting our findings.¹⁵ Finally, we retrospectively extracted data from our medical records; limitations in documentation may influence our findings.

In patients requiring short-term IV therapy, these data suggest LPCs have low complication rates and may be safely used as an alternative option for venous access.

Acknowledgments

The authors thank Drs. Laura Hernandez, Andres Mendez Hernandez, and Victor Prado for their assistance in data collection. The authors also thank Mr. Onofre Donceras and Dr. Sharon Welbel from the John H. Stroger, Jr. Hospital of Cook County Department of Infection Control & Epidemiology for their assistance in reviewing local line infection data.

Drs. Patel and Chopra developed the study design. Drs. Patel, Araujo, Parra Rodriguez, Ramirez Sanchez, and Chopra contributed to manuscript writing. Ms. Snyder provided statistical analysis. All authors have seen and approved the final manuscript for submission.

Disclosures

The authors have nothing to disclose.

Clostridium difficile (name changed to Clostridioides difficile [CDI]) are a major public health problem, with 500,000 infections annually in the United States, 15,000-30,000 associated deaths, and acute care costs exceeding $4.8 billion. The recent clinical practice guideline for CDI provides recommendations about the epidemiology, diagnosis, treatment, prevention, and environmental management. A total of 52 recommendations are included, and we will review 11 with pertinence to pediatrics in this highlight.

Recommendation 1. In infants ≤12 months of age, testing for CDI should never be routinely recommended because of the high prevalence of asymptomatic carriage of toxigenic C. difficile in infants (strong recommendation, moderate quality of evidence).

Recommendation 2. In children 1-2 years of age, testing should not be routinely performed unless other causes have been excluded (weak recommendation, low quality of evidence).Recommendation 3. In children ≥2 years of age, testing is recommended for patients with prolonged or worsening diarrhea and risk factors (eg, underlying inflammatory bowel disease) or immunocompromising conditions) or relevant exposures (eg, contact with the healthcare system or recent antibiotics) (weak recommendation, moderate quality of evidence).

The rate of C. difficile colonization among asymptomatic infants can exceed 40%. This rate declines over the first year but remains 15% at 12 months of age.¹ Therefore, the guideline recommends against routinely testing infants ≤12 months of age as a positive test probably reflects colonization rather than disease. Testing in infants is recommended only when other causes have been excluded and a concern for pseudomembranous colitis, toxic megacolon, or clinically significant diarrhea exists.

The rate of asymptomatic colonization remains elevated in the second year of life. By 2-3 years, the rate is 1%-3% which is similar to that in healthy adults. However, the role of C. difficile in community-onset diarrhea in otherwise healthy children is controversial. In a study of 100 hospitalized children aged <2 years with CDI and diarrhea, all had resolution of diarrhea regardless of whether therapy was administered.² Another study found an alternative pathogen in >50% of hospitalized children with CDI.³ Therefore, the guideline recommends against testing in children aged 1-2 years unless other causes have been excluded and in children aged >2 years only when they have prolonged or worsening diarrhea along with risk factors or exposures.

Recommendation 4. In institutions without specific required criteria for stool submissions, use a stool toxin test as part of a multistep algorithm (ie, glutamate dehydrogenase [GDH] plus toxin, GDH plus toxin arbitrated by nucleic-acid amplification tests [NAAT], or NAAT plus toxin) rather than a NAAT alone (weak recommendation, low quality of evidence).

Recommendation 5. In institutions with specific required criteria for stool submissions, use a NAAT alone or a multistep algorithm for testing (ie, GDH plus toxin, GDH plus toxin arbitrated by NAAT, or NAAT plus toxin) rather than a toxin test alone (weak recommendation, low quality of evidence).

There are a variety of testing approaches for CDI and recommendations vary based on local practice. If laboratories accept all stools, a more specific approach is recommended, including a toxin test as part of a multistep algorithm to limit false positives. If laboratories first screen for symptoms and antibiotic exposure before accepting stool samples, a more sensitive approach is recommended including NAAT alone or a multistep algorithm rather than toxin alone.

Infection Prevention and Control

Recommendation 6. There is insufficient evidence for discontinuation of PPIs (proton pump inhibitors) as a measure for preventing CDI (no recommendation).

The guideline acknowledges data suggesting an association between PPI use and CDI, but not a causal relationship. Due to the lack of high-quality evidence, it does not recommend stopping PPIs to prevent CDI.

Recommendation 7. There are insufficient data to recommend probiotics for primary prevention of CDI outside of clinical trials (no recommendation).

The guideline notes that although several meta-analyses indicate that probiotics may prevent CDI; however there were limitations, including a high incidence of CDI in placebo arms and differences in probiotic formulations and duration of use, leading to insufficient data to recommend probiotic use to prevent CDI.

Treatment

Recommendation 8. Either per os (PO) metronidazole or PO vancomycin is recommended for an initial episode or first recurrence of nonsevere pediatric CDI (weak recommendation, low quality of evidence).

Data assessing the optimal treatment for nonsevere pediatric CDI are limited. Emerging data support the use of vancomycin,⁴ which is now recommended for initial episodes of CDI in adults. However, there are insufficient data to recommend vancomycin over metronidazole for nonsevere pediatric CDI; therefore, either option is recommended.

Recommendation 9. For children with an initial episode of severe CDI, oral vancomycin with or without IV metronidazole is recommended over metronidazole alone (strong recommendation, moderate quality of evidence).

Recommendation 10. For children with a second or greater episode of recurrent CDI, oral vancomycin is recommended over metronidazole (weak recommendation, low quality of evidence).

There is no well-designed trial comparing metronidazole and vancomycin for severe or recurrent pediatric CDI. For children previously treated with metronidazole, vancomycin is recommended based on adult literature.⁴ For children previously treated with metronidazole and vancomycin, an extended course of tapered or pulse regimen vancomycin or vancomycin followed by rifaximin is recommended.

Recommendations must weigh potential harms. Metronidazole has been associated with neuropathies,⁵ cramping, and nausea. PO vancomycin has poor enteral absorption, minimizing systemic effects. Both vancomycin and metronidazole may promote carriage of resistant enterococci.

Recommendation 11. Fecal microbiota transplantation (FMT) should be considered for pediatric patients with multiple recurrences of CDI following standard treatments (weak recommendation, very low quality of evidence).

There are no robust data examining the effectiveness of pediatric FMT. Recommendations are guided by adult studies. Limited evidence suggests that FMT can be effective in children with multiple recurrent CDI.⁶ Concerns include procedure-related risks, transmission of resistant organisms and blood-borne pathogens, and induced metabolic or immunologic disorders.

Methods in Preparing a Guideline

The strength of a guideline includes representation from a diverse panel, including the Infectious Diseases Society of America (IDSA), the Society for Healthcare Epidemiology of America, the American Society of Health-Systems Pharmacists, the Society of Infectious Diseases Pharmacists, and the Pediatric Infectious Diseases Society.

The panel utilized the Grading of Recommendations Assessment, Development, and Evaluation system to weigh the strength and quality of evidence.

From a pediatric perspective, the current guideline added pediatric-specific recommendations based on a comprehensive review of the literature from 1977 to 2016. The strength of these recommendations is somewhat limited by the lack of well-designed pediatric studies. An additional limitation is that treatment recommendations are based on illness severity, although the definitions used to classify severity are not pediatric-specific and are based on unvalidated expert opinion.

Sources of Potential Conflicts or Interest or Bias

The panel complied with the IDSA policy on conflicts of interest and disclosed any interest that might be construed as a conflict, regardless of relevancy. These were evaluated by the IDSA Standards and Practice Guidelines Committee.

Generalizability

Guideline generalizability may be impacted by testing availabilities within a particular setting. Cost factors and local formularies may also limit treatment options within a given setting.

Areas in Need of Future Study

Research gaps exist regarding at what age C. difficile is pathogenic given the prevalence of asymptomatic carriage. Future studies can also focus on a newly available molecular polymerase chain reaction test platform that detects C. difficile.⁷

There is limited pediatric evidence to recommend metronidazole versus vancomycin in children, particularly in nonsevere cases. There is also an opportunity to further explore alternative therapies, including fidaxomicin (not currently approved for children) and bezlotoxumab, a new agent approved as adult adjunctive therapy.⁸

Clostridium difficile (name changed to Clostridioides difficile [CDI]) are a major public health problem, with 500,000 infections annually in the United States, 15,000-30,000 associated deaths, and acute care costs exceeding $4.8 billion. The recent clinical practice guideline for CDI provides recommendations about the epidemiology, diagnosis, treatment, prevention, and environmental management. A total of 52 recommendations are included, and we will review 11 with pertinence to pediatrics in this highlight.

Recommendation 1. In infants ≤12 months of age, testing for CDI should never be routinely recommended because of the high prevalence of asymptomatic carriage of toxigenic C. difficile in infants (strong recommendation, moderate quality of evidence).

Recommendation 2. In children 1-2 years of age, testing should not be routinely performed unless other causes have been excluded (weak recommendation, low quality of evidence).Recommendation 3. In children ≥2 years of age, testing is recommended for patients with prolonged or worsening diarrhea and risk factors (eg, underlying inflammatory bowel disease) or immunocompromising conditions) or relevant exposures (eg, contact with the healthcare system or recent antibiotics) (weak recommendation, moderate quality of evidence).

The rate of C. difficile colonization among asymptomatic infants can exceed 40%. This rate declines over the first year but remains 15% at 12 months of age.¹ Therefore, the guideline recommends against routinely testing infants ≤12 months of age as a positive test probably reflects colonization rather than disease. Testing in infants is recommended only when other causes have been excluded and a concern for pseudomembranous colitis, toxic megacolon, or clinically significant diarrhea exists.

The rate of asymptomatic colonization remains elevated in the second year of life. By 2-3 years, the rate is 1%-3% which is similar to that in healthy adults. However, the role of C. difficile in community-onset diarrhea in otherwise healthy children is controversial. In a study of 100 hospitalized children aged <2 years with CDI and diarrhea, all had resolution of diarrhea regardless of whether therapy was administered.² Another study found an alternative pathogen in >50% of hospitalized children with CDI.³ Therefore, the guideline recommends against testing in children aged 1-2 years unless other causes have been excluded and in children aged >2 years only when they have prolonged or worsening diarrhea along with risk factors or exposures.

Recommendation 4. In institutions without specific required criteria for stool submissions, use a stool toxin test as part of a multistep algorithm (ie, glutamate dehydrogenase [GDH] plus toxin, GDH plus toxin arbitrated by nucleic-acid amplification tests [NAAT], or NAAT plus toxin) rather than a NAAT alone (weak recommendation, low quality of evidence).

Recommendation 5. In institutions with specific required criteria for stool submissions, use a NAAT alone or a multistep algorithm for testing (ie, GDH plus toxin, GDH plus toxin arbitrated by NAAT, or NAAT plus toxin) rather than a toxin test alone (weak recommendation, low quality of evidence).

There are a variety of testing approaches for CDI and recommendations vary based on local practice. If laboratories accept all stools, a more specific approach is recommended, including a toxin test as part of a multistep algorithm to limit false positives. If laboratories first screen for symptoms and antibiotic exposure before accepting stool samples, a more sensitive approach is recommended including NAAT alone or a multistep algorithm rather than toxin alone.

Infection Prevention and Control

Recommendation 6. There is insufficient evidence for discontinuation of PPIs (proton pump inhibitors) as a measure for preventing CDI (no recommendation).

The guideline acknowledges data suggesting an association between PPI use and CDI, but not a causal relationship. Due to the lack of high-quality evidence, it does not recommend stopping PPIs to prevent CDI.

Recommendation 7. There are insufficient data to recommend probiotics for primary prevention of CDI outside of clinical trials (no recommendation).

The guideline notes that although several meta-analyses indicate that probiotics may prevent CDI; however there were limitations, including a high incidence of CDI in placebo arms and differences in probiotic formulations and duration of use, leading to insufficient data to recommend probiotic use to prevent CDI.

Treatment

Recommendation 8. Either per os (PO) metronidazole or PO vancomycin is recommended for an initial episode or first recurrence of nonsevere pediatric CDI (weak recommendation, low quality of evidence).

Data assessing the optimal treatment for nonsevere pediatric CDI are limited. Emerging data support the use of vancomycin,⁴ which is now recommended for initial episodes of CDI in adults. However, there are insufficient data to recommend vancomycin over metronidazole for nonsevere pediatric CDI; therefore, either option is recommended.

Recommendation 9. For children with an initial episode of severe CDI, oral vancomycin with or without IV metronidazole is recommended over metronidazole alone (strong recommendation, moderate quality of evidence).

Recommendation 10. For children with a second or greater episode of recurrent CDI, oral vancomycin is recommended over metronidazole (weak recommendation, low quality of evidence).

There is no well-designed trial comparing metronidazole and vancomycin for severe or recurrent pediatric CDI. For children previously treated with metronidazole, vancomycin is recommended based on adult literature.⁴ For children previously treated with metronidazole and vancomycin, an extended course of tapered or pulse regimen vancomycin or vancomycin followed by rifaximin is recommended.

Recommendations must weigh potential harms. Metronidazole has been associated with neuropathies,⁵ cramping, and nausea. PO vancomycin has poor enteral absorption, minimizing systemic effects. Both vancomycin and metronidazole may promote carriage of resistant enterococci.

Recommendation 11. Fecal microbiota transplantation (FMT) should be considered for pediatric patients with multiple recurrences of CDI following standard treatments (weak recommendation, very low quality of evidence).

There are no robust data examining the effectiveness of pediatric FMT. Recommendations are guided by adult studies. Limited evidence suggests that FMT can be effective in children with multiple recurrent CDI.⁶ Concerns include procedure-related risks, transmission of resistant organisms and blood-borne pathogens, and induced metabolic or immunologic disorders.

Methods in Preparing a Guideline

The strength of a guideline includes representation from a diverse panel, including the Infectious Diseases Society of America (IDSA), the Society for Healthcare Epidemiology of America, the American Society of Health-Systems Pharmacists, the Society of Infectious Diseases Pharmacists, and the Pediatric Infectious Diseases Society.

The panel utilized the Grading of Recommendations Assessment, Development, and Evaluation system to weigh the strength and quality of evidence.

From a pediatric perspective, the current guideline added pediatric-specific recommendations based on a comprehensive review of the literature from 1977 to 2016. The strength of these recommendations is somewhat limited by the lack of well-designed pediatric studies. An additional limitation is that treatment recommendations are based on illness severity, although the definitions used to classify severity are not pediatric-specific and are based on unvalidated expert opinion.

Sources of Potential Conflicts or Interest or Bias

The panel complied with the IDSA policy on conflicts of interest and disclosed any interest that might be construed as a conflict, regardless of relevancy. These were evaluated by the IDSA Standards and Practice Guidelines Committee.

Generalizability

Guideline generalizability may be impacted by testing availabilities within a particular setting. Cost factors and local formularies may also limit treatment options within a given setting.

Areas in Need of Future Study

Research gaps exist regarding at what age C. difficile is pathogenic given the prevalence of asymptomatic carriage. Future studies can also focus on a newly available molecular polymerase chain reaction test platform that detects C. difficile.⁷

There is limited pediatric evidence to recommend metronidazole versus vancomycin in children, particularly in nonsevere cases. There is also an opportunity to further explore alternative therapies, including fidaxomicin (not currently approved for children) and bezlotoxumab, a new agent approved as adult adjunctive therapy.⁸

Clostridium difficile (name changed to Clostridioides difficile [CDI]) are a major public health problem, with 500,000 infections annually in the United States, 15,000-30,000 associated deaths, and acute care costs exceeding $4.8 billion. The recent clinical practice guideline for CDI provides recommendations about the epidemiology, diagnosis, treatment, prevention, and environmental management. A total of 52 recommendations are included, and we will review 11 with pertinence to pediatrics in this highlight.

Recommendation 1. In infants ≤12 months of age, testing for CDI should never be routinely recommended because of the high prevalence of asymptomatic carriage of toxigenic C. difficile in infants (strong recommendation, moderate quality of evidence).

Recommendation 2. In children 1-2 years of age, testing should not be routinely performed unless other causes have been excluded (weak recommendation, low quality of evidence).Recommendation 3. In children ≥2 years of age, testing is recommended for patients with prolonged or worsening diarrhea and risk factors (eg, underlying inflammatory bowel disease) or immunocompromising conditions) or relevant exposures (eg, contact with the healthcare system or recent antibiotics) (weak recommendation, moderate quality of evidence).

The rate of C. difficile colonization among asymptomatic infants can exceed 40%. This rate declines over the first year but remains 15% at 12 months of age.¹ Therefore, the guideline recommends against routinely testing infants ≤12 months of age as a positive test probably reflects colonization rather than disease. Testing in infants is recommended only when other causes have been excluded and a concern for pseudomembranous colitis, toxic megacolon, or clinically significant diarrhea exists.

The rate of asymptomatic colonization remains elevated in the second year of life. By 2-3 years, the rate is 1%-3% which is similar to that in healthy adults. However, the role of C. difficile in community-onset diarrhea in otherwise healthy children is controversial. In a study of 100 hospitalized children aged <2 years with CDI and diarrhea, all had resolution of diarrhea regardless of whether therapy was administered.² Another study found an alternative pathogen in >50% of hospitalized children with CDI.³ Therefore, the guideline recommends against testing in children aged 1-2 years unless other causes have been excluded and in children aged >2 years only when they have prolonged or worsening diarrhea along with risk factors or exposures.

Recommendation 4. In institutions without specific required criteria for stool submissions, use a stool toxin test as part of a multistep algorithm (ie, glutamate dehydrogenase [GDH] plus toxin, GDH plus toxin arbitrated by nucleic-acid amplification tests [NAAT], or NAAT plus toxin) rather than a NAAT alone (weak recommendation, low quality of evidence).

Recommendation 5. In institutions with specific required criteria for stool submissions, use a NAAT alone or a multistep algorithm for testing (ie, GDH plus toxin, GDH plus toxin arbitrated by NAAT, or NAAT plus toxin) rather than a toxin test alone (weak recommendation, low quality of evidence).

There are a variety of testing approaches for CDI and recommendations vary based on local practice. If laboratories accept all stools, a more specific approach is recommended, including a toxin test as part of a multistep algorithm to limit false positives. If laboratories first screen for symptoms and antibiotic exposure before accepting stool samples, a more sensitive approach is recommended including NAAT alone or a multistep algorithm rather than toxin alone.

Infection Prevention and Control

Recommendation 6. There is insufficient evidence for discontinuation of PPIs (proton pump inhibitors) as a measure for preventing CDI (no recommendation).

The guideline acknowledges data suggesting an association between PPI use and CDI, but not a causal relationship. Due to the lack of high-quality evidence, it does not recommend stopping PPIs to prevent CDI.

Recommendation 7. There are insufficient data to recommend probiotics for primary prevention of CDI outside of clinical trials (no recommendation).

The guideline notes that although several meta-analyses indicate that probiotics may prevent CDI; however there were limitations, including a high incidence of CDI in placebo arms and differences in probiotic formulations and duration of use, leading to insufficient data to recommend probiotic use to prevent CDI.

Treatment

Recommendation 8. Either per os (PO) metronidazole or PO vancomycin is recommended for an initial episode or first recurrence of nonsevere pediatric CDI (weak recommendation, low quality of evidence).

Data assessing the optimal treatment for nonsevere pediatric CDI are limited. Emerging data support the use of vancomycin,⁴ which is now recommended for initial episodes of CDI in adults. However, there are insufficient data to recommend vancomycin over metronidazole for nonsevere pediatric CDI; therefore, either option is recommended.

Recommendation 9. For children with an initial episode of severe CDI, oral vancomycin with or without IV metronidazole is recommended over metronidazole alone (strong recommendation, moderate quality of evidence).

Recommendation 10. For children with a second or greater episode of recurrent CDI, oral vancomycin is recommended over metronidazole (weak recommendation, low quality of evidence).

There is no well-designed trial comparing metronidazole and vancomycin for severe or recurrent pediatric CDI. For children previously treated with metronidazole, vancomycin is recommended based on adult literature.⁴ For children previously treated with metronidazole and vancomycin, an extended course of tapered or pulse regimen vancomycin or vancomycin followed by rifaximin is recommended.

Recommendations must weigh potential harms. Metronidazole has been associated with neuropathies,⁵ cramping, and nausea. PO vancomycin has poor enteral absorption, minimizing systemic effects. Both vancomycin and metronidazole may promote carriage of resistant enterococci.

Recommendation 11. Fecal microbiota transplantation (FMT) should be considered for pediatric patients with multiple recurrences of CDI following standard treatments (weak recommendation, very low quality of evidence).

There are no robust data examining the effectiveness of pediatric FMT. Recommendations are guided by adult studies. Limited evidence suggests that FMT can be effective in children with multiple recurrent CDI.⁶ Concerns include procedure-related risks, transmission of resistant organisms and blood-borne pathogens, and induced metabolic or immunologic disorders.

Methods in Preparing a Guideline

The strength of a guideline includes representation from a diverse panel, including the Infectious Diseases Society of America (IDSA), the Society for Healthcare Epidemiology of America, the American Society of Health-Systems Pharmacists, the Society of Infectious Diseases Pharmacists, and the Pediatric Infectious Diseases Society.

The panel utilized the Grading of Recommendations Assessment, Development, and Evaluation system to weigh the strength and quality of evidence.

From a pediatric perspective, the current guideline added pediatric-specific recommendations based on a comprehensive review of the literature from 1977 to 2016. The strength of these recommendations is somewhat limited by the lack of well-designed pediatric studies. An additional limitation is that treatment recommendations are based on illness severity, although the definitions used to classify severity are not pediatric-specific and are based on unvalidated expert opinion.

Sources of Potential Conflicts or Interest or Bias

The panel complied with the IDSA policy on conflicts of interest and disclosed any interest that might be construed as a conflict, regardless of relevancy. These were evaluated by the IDSA Standards and Practice Guidelines Committee.

Generalizability

Guideline generalizability may be impacted by testing availabilities within a particular setting. Cost factors and local formularies may also limit treatment options within a given setting.

Areas in Need of Future Study

Research gaps exist regarding at what age C. difficile is pathogenic given the prevalence of asymptomatic carriage. Future studies can also focus on a newly available molecular polymerase chain reaction test platform that detects C. difficile.⁷

There is limited pediatric evidence to recommend metronidazole versus vancomycin in children, particularly in nonsevere cases. There is also an opportunity to further explore alternative therapies, including fidaxomicin (not currently approved for children) and bezlotoxumab, a new agent approved as adult adjunctive therapy.⁸

In 2017, the death toll from drug overdoses reached a record high, killing more Americans than the entire Vietnam War or the HIV/AIDS epidemic at its peak.¹ Up to one-quarter of hospitalized patients have a substance use disorder (SUD) and SUD-related^2,3 hospitalizations are surging. People with SUD have longer hospital stays, higher costs, and more readmissions.^3,4 While the burden of SUD is staggering, it is far from hopeless. There are multiple evidence-based and highly effective interventions to treat SUD, including medications, behavioral interventions, and harm reduction strategies.

Hospitalization can be a reachable moment to initiate and coordinate addictions care.⁵ Hospital-based addictions care has the potential to engage sicker, highly vulnerable patients, many who are not engaged in primary care or outpatient addictions care.⁶ Studied effects of hospital-based addictions care include improved SUD treatment engagement, reduced alcohol and drug use, lower hospital readmissions, and improved provider experience.^7-9

Most hospitals, however, do not treat SUD during hospitalization and do not connect people to treatment after discharge. Hospitals may lack staffing or financial resources to implement addiction care, may believe that SUDs are an outpatient concern, may want to avoid caring for people with SUD, or may simply not know where to begin. Whatever the reason, unaddressed SUD can lead to untreated withdrawal, disruptive patient behaviors, failure to complete recommended medical therapy, high rates of against medical advice discharge, poor patient experience, and widespread provider distress.⁸

Hospitalists—individually and collectively—are uniquely positioned to address this gap. By treating addiction effectively and compassionately, hospitalists can engage patients, improve care, improve patient and provider experience, and lower costs. This paper is a call to action that describes the current state of hospital-based addictions care, outlines key challenges to implementing SUD care in the hospital, debunks common misconceptions, and identifies actionable steps for hospitalists, hospital leaders, and hospitalist organizations.

Hospital-based addiction medicine consult services are emerging; they include a range of models, with variations in how patients are identified, team composition, service availability, and financing.¹⁰ Existing addiction medicine consult services commonly offer SUD assessments, psychological intervention, medical management of SUDs (eg, initiating methadone or buprenorphine), medical pain management, and linkage to SUD care after hospitalization. Some services also explicitly integrate harm reduction principles (eg, naloxone distribution, safe injection education, permitting patients to smoke).¹¹ Additional consult service activities include hospital-wide SUD education, and creation and implementation of hospital guidance documents (eg, methadone policies).¹⁰ Some consult services utilize only physicians, while others include interprofessional providers, such as nurses, social workers, and peers with lived experience of addiction. Whereas addiction medicine physicians staff some consult services, hospitalists with less formal addiction credentials staff others.

Broadly, hospital-based addictions care cannot depend solely on consult services. Just as not all hospitals have cardiology consult services, not all hospitals will have addiction consult services. As such, hospitalists can play an even greater role by implementing order sets and guidelines, supporting partnerships with community SUD treatment, and independently initiating evidence-based medications.

Pervasive individual and structural stigmas¹² are perhaps the most critical barriers to incorporating addiction medicine into routine hospital practice, and they are both cause and consequence of our system failures. Most medical schools and residencies lack SUD training, which means that the understanding of addiction as a moral deficiency or lack of willpower may remain unchallenged. Stigma surrounding SUDs contributes to hospitalists’ and hospital leaders’ aversion to treating patients with SUD, and to fears that providing quality SUD care will attract patients suffering from these conditions.

Recent national efforts have focused on the problem of opioid overprescribing. Without an equal emphasis on treatment, this focus can lead to undertreatment of pain and/or opioid use disorder in hospitalized patients, particularly since most hospitalists have little to no training in diagnosing SUD, prescribing life-saving medications for opioid use disorder, or managing acute pain in patients with SUD. The focus on overprescribing also diverts attention away from trends involving stimulants,² fentanyl contamination of the drug supply,¹³ and alcohol, all of which have important implications for the care of hospitalized adults.

Hospital policies are often not grounded in evidence (eg, recommending clonidine for first-line treatment of opioid withdrawal and not buprenorphine/methadone), and there are widespread misconceptions about perceived legal barriers to treating opioid use disorder in the hospital, which is both safe and legal.¹⁰ People with SUD may be unjustly viewed through a criminal justice lens. Policies focused on controlling visitors and conducting room searches disproportionately burden people with SUD, which may create further harms through reinforcing negative provider cognitive biases about SUDs. Finally, hospitals may lack inpatient social work and pharmacy supports, and they rarely have pathways to connect people to SUD care after discharge.

Funding remains a widespread challenge. While some hospital administrators support addiction medicine services because of the pressing medical need and public health crisis, most services depend on billing or demonstrated savings through reduced hospital days or readmissions.

Individual hospitalists, hospitalist leaders, and hospitalist organizations can engage by improving individual practice, driving systems change, and through advocacy and policy change (Table).

Individual Hospitalists

Providing basic addiction medicine care should be a core competency for all hospitalists, just as every hospitalist can initiate a goals-of-care conversation or prescribe insulin. For opioid use disorder, hospitalists should treat withdrawal and offer treatment initiation with opioid agonist therapy (ie, methadone, buprenorphine), which reduces mortality by over half. Commonly, hospitalized patients are subjected to harmful, nonevidence-based treatments, such as mandated rapid methadone tapers,²⁵ which can lead to undertreated withdrawal, increased pain, and opioid cravings. This increases patients’ risk for overdose after discharge and precludes them from receiving life-saving, evidence-based methadone maintenance, or buprenorphine treatment. Though widely misunderstood, prescribing methadone in the hospital is legal, and providers need no special waiver to prescribe buprenorphine during admission. Current laws require that hospitalists have a waiver to prescribe buprenorphine at discharge and prohibit hospitalists (or anyone outside of an opioid treatment program) from prescribing methadone for the treatment of opioid use disorder at discharge. Further, hospitalists should offer medication for alcohol use disorder (eg, naltrexone) and be good stewards of opioids during hospitalization, avoiding intravenous opioids where appropriate and curbing excessive prescribing at discharge. Given high rates of overdose and fentanyl contamination of stimulants, opioids, and benzodiazepines, hospitalists should prescribe naloxone at discharge to every patient with SUD, on chronic opioids, or who uses any nonmedical substances.

Resources exist for individual hospitalists seeking mentorship or additional training (Table). Though not necessary for in-hospital prescribing, hospitalists can obtain a waiver to prescribe buprenorphine at discharge (commonly called the X-waiver). To qualify, physicians must complete eight hours of accredited training (online and/or in-person), after which they must request a waiver from the Drug Enforcement Administration. Advanced-practice practitioners must complete 24 hours of training. Many have argued that policymakers should end this waiver requirement.²⁶ While we support efforts to “X the X” and urgently expand treatment access, additional training can enrich providers’ knowledge and confidence to prescribe buprenorphine, and is a relatively simple way that all hospitalists could act. Finally, by treating addiction and modeling patient-centered addictions care, hospitalists can legitimize and destigmatize the disease of addiction,⁸ and have the potential to mentor and train students, residents, nurses, and other staff.²⁷

Hospitalist Leaders

As leaders, hospitalists can play a key role in promoting hospital-based addictions care and tailoring solutions to meet local needs. Leaders can promote a cultural shift away from stigma, and promote evidence-based, life-saving care. Hospitalist leaders could require all hospitalists to obtain buprenorphine waivers. Leaders could initiate quality improvement projects related to SUD service delivery, develop policies that support inpatient SUD treatment, develop order sets for medication initiation, engage community substance use treatment partners, build pathways to timely addiction care after discharge, and champion development of addiction medicine consult services.

Hospitalist leaders can reference open-source guidelines, order sets, assessment and treatment tools, patient materials, pharmacy and therapeutics committee materials, and other resources for implementing services for hospitalized patients with SUD (Table).^21,22 Hospitalist leaders who understand financial and quality drivers can also champion the business and quality case for hospital-based addictions care, and help pursue local and national funding opportunities.

Hospitalist Organizations

Hospitalist societies could provide training at regional and national conferences to upskill hospitalists to care for people with SUD; support addiction medicine interest groups; and partner with addiction medicine societies, harm reduction organizations, and organizations focused on trauma-informed care. They could endorse practice guidelines and position statements describing the crucial role of hospitalists in addressing the overdose crisis and offering medication for addiction (Table). Hospitalist organizations can engage national and state hospital associations, lobby medical specialties to include addiction medicine competencies in board certification requirements, and advocate with governmental leaders to reduce barriers that restrict treatment access such as the X-waiver.

Regardless of whether a hospitalist is serving as an individual provider, a hospitalist leader, or as part of a hospitalist organization, hospitalists can take critical steps to advance the care of people with SUD. These steps shift the culture of hospitals from one where patients are afraid to discuss their substance use, to one that creates space for connection, treatment engagement, and healing. By starting medications, utilizing widely accessible resources, and collaborating with community treatment and harm reduction organizations, each one of us can play a part in addressing the epidemic.

Acknowledgments

The authors thank Alisa Patten for help preparing this manuscript. Dr. Englander would like to thank Dr. David Bangsberg and Dr. Christina Nicolaidis for their mentorship.

In 2017, the death toll from drug overdoses reached a record high, killing more Americans than the entire Vietnam War or the HIV/AIDS epidemic at its peak.¹ Up to one-quarter of hospitalized patients have a substance use disorder (SUD) and SUD-related^2,3 hospitalizations are surging. People with SUD have longer hospital stays, higher costs, and more readmissions.^3,4 While the burden of SUD is staggering, it is far from hopeless. There are multiple evidence-based and highly effective interventions to treat SUD, including medications, behavioral interventions, and harm reduction strategies.

Hospitalization can be a reachable moment to initiate and coordinate addictions care.⁵ Hospital-based addictions care has the potential to engage sicker, highly vulnerable patients, many who are not engaged in primary care or outpatient addictions care.⁶ Studied effects of hospital-based addictions care include improved SUD treatment engagement, reduced alcohol and drug use, lower hospital readmissions, and improved provider experience.^7-9

Most hospitals, however, do not treat SUD during hospitalization and do not connect people to treatment after discharge. Hospitals may lack staffing or financial resources to implement addiction care, may believe that SUDs are an outpatient concern, may want to avoid caring for people with SUD, or may simply not know where to begin. Whatever the reason, unaddressed SUD can lead to untreated withdrawal, disruptive patient behaviors, failure to complete recommended medical therapy, high rates of against medical advice discharge, poor patient experience, and widespread provider distress.⁸

Hospitalists—individually and collectively—are uniquely positioned to address this gap. By treating addiction effectively and compassionately, hospitalists can engage patients, improve care, improve patient and provider experience, and lower costs. This paper is a call to action that describes the current state of hospital-based addictions care, outlines key challenges to implementing SUD care in the hospital, debunks common misconceptions, and identifies actionable steps for hospitalists, hospital leaders, and hospitalist organizations.

Hospital-based addiction medicine consult services are emerging; they include a range of models, with variations in how patients are identified, team composition, service availability, and financing.¹⁰ Existing addiction medicine consult services commonly offer SUD assessments, psychological intervention, medical management of SUDs (eg, initiating methadone or buprenorphine), medical pain management, and linkage to SUD care after hospitalization. Some services also explicitly integrate harm reduction principles (eg, naloxone distribution, safe injection education, permitting patients to smoke).¹¹ Additional consult service activities include hospital-wide SUD education, and creation and implementation of hospital guidance documents (eg, methadone policies).¹⁰ Some consult services utilize only physicians, while others include interprofessional providers, such as nurses, social workers, and peers with lived experience of addiction. Whereas addiction medicine physicians staff some consult services, hospitalists with less formal addiction credentials staff others.

Broadly, hospital-based addictions care cannot depend solely on consult services. Just as not all hospitals have cardiology consult services, not all hospitals will have addiction consult services. As such, hospitalists can play an even greater role by implementing order sets and guidelines, supporting partnerships with community SUD treatment, and independently initiating evidence-based medications.

Pervasive individual and structural stigmas¹² are perhaps the most critical barriers to incorporating addiction medicine into routine hospital practice, and they are both cause and consequence of our system failures. Most medical schools and residencies lack SUD training, which means that the understanding of addiction as a moral deficiency or lack of willpower may remain unchallenged. Stigma surrounding SUDs contributes to hospitalists’ and hospital leaders’ aversion to treating patients with SUD, and to fears that providing quality SUD care will attract patients suffering from these conditions.

Recent national efforts have focused on the problem of opioid overprescribing. Without an equal emphasis on treatment, this focus can lead to undertreatment of pain and/or opioid use disorder in hospitalized patients, particularly since most hospitalists have little to no training in diagnosing SUD, prescribing life-saving medications for opioid use disorder, or managing acute pain in patients with SUD. The focus on overprescribing also diverts attention away from trends involving stimulants,² fentanyl contamination of the drug supply,¹³ and alcohol, all of which have important implications for the care of hospitalized adults.

Hospital policies are often not grounded in evidence (eg, recommending clonidine for first-line treatment of opioid withdrawal and not buprenorphine/methadone), and there are widespread misconceptions about perceived legal barriers to treating opioid use disorder in the hospital, which is both safe and legal.¹⁰ People with SUD may be unjustly viewed through a criminal justice lens. Policies focused on controlling visitors and conducting room searches disproportionately burden people with SUD, which may create further harms through reinforcing negative provider cognitive biases about SUDs. Finally, hospitals may lack inpatient social work and pharmacy supports, and they rarely have pathways to connect people to SUD care after discharge.

Funding remains a widespread challenge. While some hospital administrators support addiction medicine services because of the pressing medical need and public health crisis, most services depend on billing or demonstrated savings through reduced hospital days or readmissions.

Individual hospitalists, hospitalist leaders, and hospitalist organizations can engage by improving individual practice, driving systems change, and through advocacy and policy change (Table).

Individual Hospitalists

Providing basic addiction medicine care should be a core competency for all hospitalists, just as every hospitalist can initiate a goals-of-care conversation or prescribe insulin. For opioid use disorder, hospitalists should treat withdrawal and offer treatment initiation with opioid agonist therapy (ie, methadone, buprenorphine), which reduces mortality by over half. Commonly, hospitalized patients are subjected to harmful, nonevidence-based treatments, such as mandated rapid methadone tapers,²⁵ which can lead to undertreated withdrawal, increased pain, and opioid cravings. This increases patients’ risk for overdose after discharge and precludes them from receiving life-saving, evidence-based methadone maintenance, or buprenorphine treatment. Though widely misunderstood, prescribing methadone in the hospital is legal, and providers need no special waiver to prescribe buprenorphine during admission. Current laws require that hospitalists have a waiver to prescribe buprenorphine at discharge and prohibit hospitalists (or anyone outside of an opioid treatment program) from prescribing methadone for the treatment of opioid use disorder at discharge. Further, hospitalists should offer medication for alcohol use disorder (eg, naltrexone) and be good stewards of opioids during hospitalization, avoiding intravenous opioids where appropriate and curbing excessive prescribing at discharge. Given high rates of overdose and fentanyl contamination of stimulants, opioids, and benzodiazepines, hospitalists should prescribe naloxone at discharge to every patient with SUD, on chronic opioids, or who uses any nonmedical substances.

Resources exist for individual hospitalists seeking mentorship or additional training (Table). Though not necessary for in-hospital prescribing, hospitalists can obtain a waiver to prescribe buprenorphine at discharge (commonly called the X-waiver). To qualify, physicians must complete eight hours of accredited training (online and/or in-person), after which they must request a waiver from the Drug Enforcement Administration. Advanced-practice practitioners must complete 24 hours of training. Many have argued that policymakers should end this waiver requirement.²⁶ While we support efforts to “X the X” and urgently expand treatment access, additional training can enrich providers’ knowledge and confidence to prescribe buprenorphine, and is a relatively simple way that all hospitalists could act. Finally, by treating addiction and modeling patient-centered addictions care, hospitalists can legitimize and destigmatize the disease of addiction,⁸ and have the potential to mentor and train students, residents, nurses, and other staff.²⁷

Hospitalist Leaders

As leaders, hospitalists can play a key role in promoting hospital-based addictions care and tailoring solutions to meet local needs. Leaders can promote a cultural shift away from stigma, and promote evidence-based, life-saving care. Hospitalist leaders could require all hospitalists to obtain buprenorphine waivers. Leaders could initiate quality improvement projects related to SUD service delivery, develop policies that support inpatient SUD treatment, develop order sets for medication initiation, engage community substance use treatment partners, build pathways to timely addiction care after discharge, and champion development of addiction medicine consult services.

Hospitalist leaders can reference open-source guidelines, order sets, assessment and treatment tools, patient materials, pharmacy and therapeutics committee materials, and other resources for implementing services for hospitalized patients with SUD (Table).^21,22 Hospitalist leaders who understand financial and quality drivers can also champion the business and quality case for hospital-based addictions care, and help pursue local and national funding opportunities.

Hospitalist Organizations

Hospitalist societies could provide training at regional and national conferences to upskill hospitalists to care for people with SUD; support addiction medicine interest groups; and partner with addiction medicine societies, harm reduction organizations, and organizations focused on trauma-informed care. They could endorse practice guidelines and position statements describing the crucial role of hospitalists in addressing the overdose crisis and offering medication for addiction (Table). Hospitalist organizations can engage national and state hospital associations, lobby medical specialties to include addiction medicine competencies in board certification requirements, and advocate with governmental leaders to reduce barriers that restrict treatment access such as the X-waiver.

Regardless of whether a hospitalist is serving as an individual provider, a hospitalist leader, or as part of a hospitalist organization, hospitalists can take critical steps to advance the care of people with SUD. These steps shift the culture of hospitals from one where patients are afraid to discuss their substance use, to one that creates space for connection, treatment engagement, and healing. By starting medications, utilizing widely accessible resources, and collaborating with community treatment and harm reduction organizations, each one of us can play a part in addressing the epidemic.

Acknowledgments

The authors thank Alisa Patten for help preparing this manuscript. Dr. Englander would like to thank Dr. David Bangsberg and Dr. Christina Nicolaidis for their mentorship.

In 2017, the death toll from drug overdoses reached a record high, killing more Americans than the entire Vietnam War or the HIV/AIDS epidemic at its peak.¹ Up to one-quarter of hospitalized patients have a substance use disorder (SUD) and SUD-related^2,3 hospitalizations are surging. People with SUD have longer hospital stays, higher costs, and more readmissions.^3,4 While the burden of SUD is staggering, it is far from hopeless. There are multiple evidence-based and highly effective interventions to treat SUD, including medications, behavioral interventions, and harm reduction strategies.

Hospitalization can be a reachable moment to initiate and coordinate addictions care.⁵ Hospital-based addictions care has the potential to engage sicker, highly vulnerable patients, many who are not engaged in primary care or outpatient addictions care.⁶ Studied effects of hospital-based addictions care include improved SUD treatment engagement, reduced alcohol and drug use, lower hospital readmissions, and improved provider experience.^7-9

Most hospitals, however, do not treat SUD during hospitalization and do not connect people to treatment after discharge. Hospitals may lack staffing or financial resources to implement addiction care, may believe that SUDs are an outpatient concern, may want to avoid caring for people with SUD, or may simply not know where to begin. Whatever the reason, unaddressed SUD can lead to untreated withdrawal, disruptive patient behaviors, failure to complete recommended medical therapy, high rates of against medical advice discharge, poor patient experience, and widespread provider distress.⁸

Hospitalists—individually and collectively—are uniquely positioned to address this gap. By treating addiction effectively and compassionately, hospitalists can engage patients, improve care, improve patient and provider experience, and lower costs. This paper is a call to action that describes the current state of hospital-based addictions care, outlines key challenges to implementing SUD care in the hospital, debunks common misconceptions, and identifies actionable steps for hospitalists, hospital leaders, and hospitalist organizations.

Hospital-based addiction medicine consult services are emerging; they include a range of models, with variations in how patients are identified, team composition, service availability, and financing.¹⁰ Existing addiction medicine consult services commonly offer SUD assessments, psychological intervention, medical management of SUDs (eg, initiating methadone or buprenorphine), medical pain management, and linkage to SUD care after hospitalization. Some services also explicitly integrate harm reduction principles (eg, naloxone distribution, safe injection education, permitting patients to smoke).¹¹ Additional consult service activities include hospital-wide SUD education, and creation and implementation of hospital guidance documents (eg, methadone policies).¹⁰ Some consult services utilize only physicians, while others include interprofessional providers, such as nurses, social workers, and peers with lived experience of addiction. Whereas addiction medicine physicians staff some consult services, hospitalists with less formal addiction credentials staff others.

Broadly, hospital-based addictions care cannot depend solely on consult services. Just as not all hospitals have cardiology consult services, not all hospitals will have addiction consult services. As such, hospitalists can play an even greater role by implementing order sets and guidelines, supporting partnerships with community SUD treatment, and independently initiating evidence-based medications.

Pervasive individual and structural stigmas¹² are perhaps the most critical barriers to incorporating addiction medicine into routine hospital practice, and they are both cause and consequence of our system failures. Most medical schools and residencies lack SUD training, which means that the understanding of addiction as a moral deficiency or lack of willpower may remain unchallenged. Stigma surrounding SUDs contributes to hospitalists’ and hospital leaders’ aversion to treating patients with SUD, and to fears that providing quality SUD care will attract patients suffering from these conditions.

Recent national efforts have focused on the problem of opioid overprescribing. Without an equal emphasis on treatment, this focus can lead to undertreatment of pain and/or opioid use disorder in hospitalized patients, particularly since most hospitalists have little to no training in diagnosing SUD, prescribing life-saving medications for opioid use disorder, or managing acute pain in patients with SUD. The focus on overprescribing also diverts attention away from trends involving stimulants,² fentanyl contamination of the drug supply,¹³ and alcohol, all of which have important implications for the care of hospitalized adults.

Hospital policies are often not grounded in evidence (eg, recommending clonidine for first-line treatment of opioid withdrawal and not buprenorphine/methadone), and there are widespread misconceptions about perceived legal barriers to treating opioid use disorder in the hospital, which is both safe and legal.¹⁰ People with SUD may be unjustly viewed through a criminal justice lens. Policies focused on controlling visitors and conducting room searches disproportionately burden people with SUD, which may create further harms through reinforcing negative provider cognitive biases about SUDs. Finally, hospitals may lack inpatient social work and pharmacy supports, and they rarely have pathways to connect people to SUD care after discharge.

Funding remains a widespread challenge. While some hospital administrators support addiction medicine services because of the pressing medical need and public health crisis, most services depend on billing or demonstrated savings through reduced hospital days or readmissions.

Individual hospitalists, hospitalist leaders, and hospitalist organizations can engage by improving individual practice, driving systems change, and through advocacy and policy change (Table).

Individual Hospitalists

Providing basic addiction medicine care should be a core competency for all hospitalists, just as every hospitalist can initiate a goals-of-care conversation or prescribe insulin. For opioid use disorder, hospitalists should treat withdrawal and offer treatment initiation with opioid agonist therapy (ie, methadone, buprenorphine), which reduces mortality by over half. Commonly, hospitalized patients are subjected to harmful, nonevidence-based treatments, such as mandated rapid methadone tapers,²⁵ which can lead to undertreated withdrawal, increased pain, and opioid cravings. This increases patients’ risk for overdose after discharge and precludes them from receiving life-saving, evidence-based methadone maintenance, or buprenorphine treatment. Though widely misunderstood, prescribing methadone in the hospital is legal, and providers need no special waiver to prescribe buprenorphine during admission. Current laws require that hospitalists have a waiver to prescribe buprenorphine at discharge and prohibit hospitalists (or anyone outside of an opioid treatment program) from prescribing methadone for the treatment of opioid use disorder at discharge. Further, hospitalists should offer medication for alcohol use disorder (eg, naltrexone) and be good stewards of opioids during hospitalization, avoiding intravenous opioids where appropriate and curbing excessive prescribing at discharge. Given high rates of overdose and fentanyl contamination of stimulants, opioids, and benzodiazepines, hospitalists should prescribe naloxone at discharge to every patient with SUD, on chronic opioids, or who uses any nonmedical substances.

Resources exist for individual hospitalists seeking mentorship or additional training (Table). Though not necessary for in-hospital prescribing, hospitalists can obtain a waiver to prescribe buprenorphine at discharge (commonly called the X-waiver). To qualify, physicians must complete eight hours of accredited training (online and/or in-person), after which they must request a waiver from the Drug Enforcement Administration. Advanced-practice practitioners must complete 24 hours of training. Many have argued that policymakers should end this waiver requirement.²⁶ While we support efforts to “X the X” and urgently expand treatment access, additional training can enrich providers’ knowledge and confidence to prescribe buprenorphine, and is a relatively simple way that all hospitalists could act. Finally, by treating addiction and modeling patient-centered addictions care, hospitalists can legitimize and destigmatize the disease of addiction,⁸ and have the potential to mentor and train students, residents, nurses, and other staff.²⁷

Hospitalist Leaders

As leaders, hospitalists can play a key role in promoting hospital-based addictions care and tailoring solutions to meet local needs. Leaders can promote a cultural shift away from stigma, and promote evidence-based, life-saving care. Hospitalist leaders could require all hospitalists to obtain buprenorphine waivers. Leaders could initiate quality improvement projects related to SUD service delivery, develop policies that support inpatient SUD treatment, develop order sets for medication initiation, engage community substance use treatment partners, build pathways to timely addiction care after discharge, and champion development of addiction medicine consult services.

Hospitalist leaders can reference open-source guidelines, order sets, assessment and treatment tools, patient materials, pharmacy and therapeutics committee materials, and other resources for implementing services for hospitalized patients with SUD (Table).^21,22 Hospitalist leaders who understand financial and quality drivers can also champion the business and quality case for hospital-based addictions care, and help pursue local and national funding opportunities.

Hospitalist Organizations

Hospitalist societies could provide training at regional and national conferences to upskill hospitalists to care for people with SUD; support addiction medicine interest groups; and partner with addiction medicine societies, harm reduction organizations, and organizations focused on trauma-informed care. They could endorse practice guidelines and position statements describing the crucial role of hospitalists in addressing the overdose crisis and offering medication for addiction (Table). Hospitalist organizations can engage national and state hospital associations, lobby medical specialties to include addiction medicine competencies in board certification requirements, and advocate with governmental leaders to reduce barriers that restrict treatment access such as the X-waiver.

Regardless of whether a hospitalist is serving as an individual provider, a hospitalist leader, or as part of a hospitalist organization, hospitalists can take critical steps to advance the care of people with SUD. These steps shift the culture of hospitals from one where patients are afraid to discuss their substance use, to one that creates space for connection, treatment engagement, and healing. By starting medications, utilizing widely accessible resources, and collaborating with community treatment and harm reduction organizations, each one of us can play a part in addressing the epidemic.

Acknowledgments

The authors thank Alisa Patten for help preparing this manuscript. Dr. Englander would like to thank Dr. David Bangsberg and Dr. Christina Nicolaidis for their mentorship.

I stand in the hospital room of a little girl who was shot in her own home just two weeks ago. She was drawing in her sketchbook when a group of teenagers drove by her apartment and took aim. She was shot twice in the chest. Her life and her health will forever be altered. I am not part of her care team, but I am there because just hours after their arrival to the hospital her mother declared that she was going to do something, that gun violence must be stopped. She wants to speak out and she wants to give her daughter a voice. She does not want this to happen to other little girls. My colleagues know that I can help this woman by elevating her voice, by telling her daughter’s story. I have found a passion in gun violence prevention advocacy and I fight every day for little girls like this.

For almost 10 years, I studied asthma. I presented lectures. I conducted research. I published papers. It was my thing. In fact, it still is my thing. But one day shortly after the shooting at Marjory Stoneman Douglas High School in Parkland, Florida, I was dropping my oldest daughter off at Kindergarten and for the first time, I saw an armed police officer patrolling the drop-off line. It hit me like a ton of bricks. I went home and called my Senators and Representatives. As I was talking to an aide about evidence-based gun safety legislation, I lost it. I started crying. I finished the call and just sat there. I was momentarily frozen, uncertain of what to do next yet compelled to take action. I decided to attend a meeting of a local gun violence prevention group. Maybe this action of going to one meeting would quell the anxiety and fear that was building inside of me. I found my local Moms Demand Action chapter and I went. About halfway through the meeting, the chapter leader began describing their gun safety campaign, Be SMART for kids, and mentioned that they had been trying to make connections with the Children’s Hospital. That is the moment. That is when it clicked. I have a voice that this movement needs. I can help them. And I did.

Gun violence is the second leading cause of death in children.¹ Gun violence is a public health epidemic. Every day in America, approximately 100 people are shot and killed.² The rate of firearm deaths among children and teens in the United States is 36.5 times higher than that of 12 other high-income countries.¹ We know that states with stricter gun laws have lower rates of child firearm mortality.³ We also know that safe gun storage practices (storing guns locked, unloaded, and separate from ammunition) reduce the risk of suicide and firearm injuries,⁴ yet 4.6 million American children live in a home with a loaded, unlocked firearm.⁵ Promoting safe gun storage practices and advocating for common sense gun safety legislation are two effective ways to address this crisis.

Gun violence prevention is my passion, but it might not be yours. Regardless of your passion, the blueprint for becoming a physician advocate is the same.

Advocacy, in its most distilled form, is speaking out for something you believe in, often for someone who cannot speak out for themselves. This is at the core of what we, as healthcare providers, do every day. We help people through some of the hardest moments of their lives, when they are sick and vulnerable. Every day, we are faced with problems that need to be solved. Our experience at the bedside helps us understand how policies affect real people. We understand evidence, data, and science. We recognize that anecdotes are powerful but if not backed up with data will be unlikely to lead to meaningful change. Perhaps most importantly, as professional members of the community, we have agency. We can use our voice and our privilege as physicians to elevate the voices of others.

As you go through medical training, you may not even realize that what you are doing on a daily basis is advocacy. But there comes a moment when you realize that the problem is bigger than the individual patient in front of you. There are systems that are broken that, if fixed, could improve the health of patients everywhere and save lives. To create change on a population level, the status quo will need to be challenged and systems may need to be disrupted.

Hospitalists are particularly well positioned to be advocates because we interact with virtually all aspects of the healthcare system either directly or indirectly. We care for patients with a myriad of disease processes and medical needs using varying levels of resources and social support systems. We often see patients in their most dire moments and, unlike outpatient physicians, we have the luxury of time. Hospitalized patients are a captive audience. We have time to educate, assess what patients need, and connect patients with community resources.

Find your passion. Often, your passion will find you. When it does, listen to it. Initially, most of your advocacy will be done on your own time. If you are not passionate about your cause, you will struggle and you will be less likely to be an effective advocate. Keep in mind that sometimes the deeper you dig into an issue, the bigger problems you find and, as a result, your passion can grow.

Do your research. Read the literature. Do you really understand the issue? Identify local and national experts, read their work, and follow their careers. You do not need an advanced degree. Your experience as a physician, willingness to learn, and your voice are all you need.

Start small. Do something small every day. Read an article. Make a new contact. Talk to a colleague. Be thoughtful in your approach. Is this a problem that community advocacy can solve? Will legislation be an effective way to achieve my goal? Would state or federal legislation be more appropriate? In most cases, a combination of community advocacy and legislative advocacy is necessary.

Partner with community organizations. Find local organizations that have existing infrastructure and are engaged on the issue and create partnerships. Community organizations are fighting every day and are waiting for a powerful authoritative voice like yours. They want your voice and you need their support.

Find your allies and your challengers. Identify allies in your community, your institution, your field, and in government. Anticipate potential challengers. When you encounter them, work diligently to find common ground and be respectful. If you only talk to people who agree with you, you will not make progress. Tread carefully when necessary. Develop a thick skin. Read people and try to figure out what it is that they want, what is motivating their position. Make your first ask small and as noncontroversial as possible. Stick to the facts. If you keep your patients at the heart of what you are doing, it is hard to go wrong.

Stay focused and disciplined, but do not quiet the anger and frustration that you feel. That is your fuel. Build momentum and build your team. Passion is contagious; when people see that you are making progress, they will want to join you. Together, you can create a dialog that will change minds.

Align advocacy with your other work. Ideally, this work will not be done in isolation from your other professional duties. Advocacy initiatives make excellent quality improvement projects. When you identify holes in the evidence that could potentially inform the policy debate, apply health services research methods and publish. This approach builds the evidence base to affect change and contributes to your professional development. Consider developing an advocacy curriculum for trainees. Identify trainees interested in advocacy and mentor them. Look for opportunities to speak and write on the topic. Use your unique skillset to further your cause.

Work with your employer. Find common ground. Even if they fundamentally disagree with your point of view, you can still speak out as a private citizen. Recognize the difference between speaking as a physician and speaking as an employee of a specific institution. Unless you have explicit permission, you are speaking for yourself, not your institution. Do not be afraid to push leaders at your institution. Help them see why it is important for you to speak up on a particular issue. If your professional organization has a statement on the issue, use it to support your position.

Leverage social media. Social media is a powerful method to amplify your voice. Consider the impact of the #thisisourlane movement. It will connect you with people, across the world, who share similar passions. It will help you identify local allies. It will open opportunities for speaking engagements and publications. It can be a great way to bring positive attention to your institution. It will take time to find your voice. Try to use consistent messaging. Keep it professional. Tag people who you want to see the great work you are doing. It only takes one retweet by someone with hundreds of thousands of followers to get your message in the feed of exponentially more viewers. Tag your institution when you want them to know what you are up to or when you are doing something that you think they should be proud of. Tag the professional organizations that would be interested in your work. Tag community leaders. This can be a great way to elevate their voice with your platform. Include an “opinions my own” statement in your social media profiles. Beware of disinformation. Read articles before retweeting. Ignore the trolls. I repeat, ignore the trolls.

I did not start my career with a focus on advocacy and in becoming an advocate, I have not given up my previous focus on asthma research. I did not get an advanced degree or specialized training in advocacy. I let my passion drive me. I am now an active member and leader in our Moms Demand Action chapter. The safe storage campaign in our resident clinic has had significant success. We increased the frequency of discussion of gun safety during well-child visits from 2% to 50% and shared this success at local and national scientific meetings. We have worked with our local media to spread awareness about safe gun storage. We have spent time at the state capital to discuss child access prevention laws with legislators. We have collaborated with community leaders and elected officials for gun violence awareness events. We earned support from leaders at our institution. If you walk through our hospital units, clinics, resident areas, and faculty offices, you will see evidence of our success. Physicians and nurses are still wearing their ribbons from the Wear Orange day on their name badges. “We Can End Gun Violence” signs are hanging on faculty members’ doors. Thanks to local police departments, the clinic has a constant supply of gun locks that are provided to families free of charge. Our residents proudly walk the halls with Be SMART buttons on their badges. These physical reminders of our progress are incredibly motivating as we continue this work. However, it is the quiet moments alone with children and parents who are suffering because of the epidemic of gun violence that really move me. I will not give up this fight until children in our communities are safe.

Acknowledgments

Dr. Andrews wishes to thank Dr. Kelsey Gastineau for her efforts to increase the frequency of gun safety discussions in our Pediatric Primary Care clinic and for her support in all of this work.

I stand in the hospital room of a little girl who was shot in her own home just two weeks ago. She was drawing in her sketchbook when a group of teenagers drove by her apartment and took aim. She was shot twice in the chest. Her life and her health will forever be altered. I am not part of her care team, but I am there because just hours after their arrival to the hospital her mother declared that she was going to do something, that gun violence must be stopped. She wants to speak out and she wants to give her daughter a voice. She does not want this to happen to other little girls. My colleagues know that I can help this woman by elevating her voice, by telling her daughter’s story. I have found a passion in gun violence prevention advocacy and I fight every day for little girls like this.

For almost 10 years, I studied asthma. I presented lectures. I conducted research. I published papers. It was my thing. In fact, it still is my thing. But one day shortly after the shooting at Marjory Stoneman Douglas High School in Parkland, Florida, I was dropping my oldest daughter off at Kindergarten and for the first time, I saw an armed police officer patrolling the drop-off line. It hit me like a ton of bricks. I went home and called my Senators and Representatives. As I was talking to an aide about evidence-based gun safety legislation, I lost it. I started crying. I finished the call and just sat there. I was momentarily frozen, uncertain of what to do next yet compelled to take action. I decided to attend a meeting of a local gun violence prevention group. Maybe this action of going to one meeting would quell the anxiety and fear that was building inside of me. I found my local Moms Demand Action chapter and I went. About halfway through the meeting, the chapter leader began describing their gun safety campaign, Be SMART for kids, and mentioned that they had been trying to make connections with the Children’s Hospital. That is the moment. That is when it clicked. I have a voice that this movement needs. I can help them. And I did.

Gun violence is the second leading cause of death in children.¹ Gun violence is a public health epidemic. Every day in America, approximately 100 people are shot and killed.² The rate of firearm deaths among children and teens in the United States is 36.5 times higher than that of 12 other high-income countries.¹ We know that states with stricter gun laws have lower rates of child firearm mortality.³ We also know that safe gun storage practices (storing guns locked, unloaded, and separate from ammunition) reduce the risk of suicide and firearm injuries,⁴ yet 4.6 million American children live in a home with a loaded, unlocked firearm.⁵ Promoting safe gun storage practices and advocating for common sense gun safety legislation are two effective ways to address this crisis.

Gun violence prevention is my passion, but it might not be yours. Regardless of your passion, the blueprint for becoming a physician advocate is the same.

Advocacy, in its most distilled form, is speaking out for something you believe in, often for someone who cannot speak out for themselves. This is at the core of what we, as healthcare providers, do every day. We help people through some of the hardest moments of their lives, when they are sick and vulnerable. Every day, we are faced with problems that need to be solved. Our experience at the bedside helps us understand how policies affect real people. We understand evidence, data, and science. We recognize that anecdotes are powerful but if not backed up with data will be unlikely to lead to meaningful change. Perhaps most importantly, as professional members of the community, we have agency. We can use our voice and our privilege as physicians to elevate the voices of others.

As you go through medical training, you may not even realize that what you are doing on a daily basis is advocacy. But there comes a moment when you realize that the problem is bigger than the individual patient in front of you. There are systems that are broken that, if fixed, could improve the health of patients everywhere and save lives. To create change on a population level, the status quo will need to be challenged and systems may need to be disrupted.

Hospitalists are particularly well positioned to be advocates because we interact with virtually all aspects of the healthcare system either directly or indirectly. We care for patients with a myriad of disease processes and medical needs using varying levels of resources and social support systems. We often see patients in their most dire moments and, unlike outpatient physicians, we have the luxury of time. Hospitalized patients are a captive audience. We have time to educate, assess what patients need, and connect patients with community resources.

Find your passion. Often, your passion will find you. When it does, listen to it. Initially, most of your advocacy will be done on your own time. If you are not passionate about your cause, you will struggle and you will be less likely to be an effective advocate. Keep in mind that sometimes the deeper you dig into an issue, the bigger problems you find and, as a result, your passion can grow.

Do your research. Read the literature. Do you really understand the issue? Identify local and national experts, read their work, and follow their careers. You do not need an advanced degree. Your experience as a physician, willingness to learn, and your voice are all you need.

Start small. Do something small every day. Read an article. Make a new contact. Talk to a colleague. Be thoughtful in your approach. Is this a problem that community advocacy can solve? Will legislation be an effective way to achieve my goal? Would state or federal legislation be more appropriate? In most cases, a combination of community advocacy and legislative advocacy is necessary.

Partner with community organizations. Find local organizations that have existing infrastructure and are engaged on the issue and create partnerships. Community organizations are fighting every day and are waiting for a powerful authoritative voice like yours. They want your voice and you need their support.

Find your allies and your challengers. Identify allies in your community, your institution, your field, and in government. Anticipate potential challengers. When you encounter them, work diligently to find common ground and be respectful. If you only talk to people who agree with you, you will not make progress. Tread carefully when necessary. Develop a thick skin. Read people and try to figure out what it is that they want, what is motivating their position. Make your first ask small and as noncontroversial as possible. Stick to the facts. If you keep your patients at the heart of what you are doing, it is hard to go wrong.

Stay focused and disciplined, but do not quiet the anger and frustration that you feel. That is your fuel. Build momentum and build your team. Passion is contagious; when people see that you are making progress, they will want to join you. Together, you can create a dialog that will change minds.

Align advocacy with your other work. Ideally, this work will not be done in isolation from your other professional duties. Advocacy initiatives make excellent quality improvement projects. When you identify holes in the evidence that could potentially inform the policy debate, apply health services research methods and publish. This approach builds the evidence base to affect change and contributes to your professional development. Consider developing an advocacy curriculum for trainees. Identify trainees interested in advocacy and mentor them. Look for opportunities to speak and write on the topic. Use your unique skillset to further your cause.

Work with your employer. Find common ground. Even if they fundamentally disagree with your point of view, you can still speak out as a private citizen. Recognize the difference between speaking as a physician and speaking as an employee of a specific institution. Unless you have explicit permission, you are speaking for yourself, not your institution. Do not be afraid to push leaders at your institution. Help them see why it is important for you to speak up on a particular issue. If your professional organization has a statement on the issue, use it to support your position.

Leverage social media. Social media is a powerful method to amplify your voice. Consider the impact of the #thisisourlane movement. It will connect you with people, across the world, who share similar passions. It will help you identify local allies. It will open opportunities for speaking engagements and publications. It can be a great way to bring positive attention to your institution. It will take time to find your voice. Try to use consistent messaging. Keep it professional. Tag people who you want to see the great work you are doing. It only takes one retweet by someone with hundreds of thousands of followers to get your message in the feed of exponentially more viewers. Tag your institution when you want them to know what you are up to or when you are doing something that you think they should be proud of. Tag the professional organizations that would be interested in your work. Tag community leaders. This can be a great way to elevate their voice with your platform. Include an “opinions my own” statement in your social media profiles. Beware of disinformation. Read articles before retweeting. Ignore the trolls. I repeat, ignore the trolls.

I did not start my career with a focus on advocacy and in becoming an advocate, I have not given up my previous focus on asthma research. I did not get an advanced degree or specialized training in advocacy. I let my passion drive me. I am now an active member and leader in our Moms Demand Action chapter. The safe storage campaign in our resident clinic has had significant success. We increased the frequency of discussion of gun safety during well-child visits from 2% to 50% and shared this success at local and national scientific meetings. We have worked with our local media to spread awareness about safe gun storage. We have spent time at the state capital to discuss child access prevention laws with legislators. We have collaborated with community leaders and elected officials for gun violence awareness events. We earned support from leaders at our institution. If you walk through our hospital units, clinics, resident areas, and faculty offices, you will see evidence of our success. Physicians and nurses are still wearing their ribbons from the Wear Orange day on their name badges. “We Can End Gun Violence” signs are hanging on faculty members’ doors. Thanks to local police departments, the clinic has a constant supply of gun locks that are provided to families free of charge. Our residents proudly walk the halls with Be SMART buttons on their badges. These physical reminders of our progress are incredibly motivating as we continue this work. However, it is the quiet moments alone with children and parents who are suffering because of the epidemic of gun violence that really move me. I will not give up this fight until children in our communities are safe.

Acknowledgments

Dr. Andrews wishes to thank Dr. Kelsey Gastineau for her efforts to increase the frequency of gun safety discussions in our Pediatric Primary Care clinic and for her support in all of this work.

I stand in the hospital room of a little girl who was shot in her own home just two weeks ago. She was drawing in her sketchbook when a group of teenagers drove by her apartment and took aim. She was shot twice in the chest. Her life and her health will forever be altered. I am not part of her care team, but I am there because just hours after their arrival to the hospital her mother declared that she was going to do something, that gun violence must be stopped. She wants to speak out and she wants to give her daughter a voice. She does not want this to happen to other little girls. My colleagues know that I can help this woman by elevating her voice, by telling her daughter’s story. I have found a passion in gun violence prevention advocacy and I fight every day for little girls like this.

For almost 10 years, I studied asthma. I presented lectures. I conducted research. I published papers. It was my thing. In fact, it still is my thing. But one day shortly after the shooting at Marjory Stoneman Douglas High School in Parkland, Florida, I was dropping my oldest daughter off at Kindergarten and for the first time, I saw an armed police officer patrolling the drop-off line. It hit me like a ton of bricks. I went home and called my Senators and Representatives. As I was talking to an aide about evidence-based gun safety legislation, I lost it. I started crying. I finished the call and just sat there. I was momentarily frozen, uncertain of what to do next yet compelled to take action. I decided to attend a meeting of a local gun violence prevention group. Maybe this action of going to one meeting would quell the anxiety and fear that was building inside of me. I found my local Moms Demand Action chapter and I went. About halfway through the meeting, the chapter leader began describing their gun safety campaign, Be SMART for kids, and mentioned that they had been trying to make connections with the Children’s Hospital. That is the moment. That is when it clicked. I have a voice that this movement needs. I can help them. And I did.

Gun violence is the second leading cause of death in children.¹ Gun violence is a public health epidemic. Every day in America, approximately 100 people are shot and killed.² The rate of firearm deaths among children and teens in the United States is 36.5 times higher than that of 12 other high-income countries.¹ We know that states with stricter gun laws have lower rates of child firearm mortality.³ We also know that safe gun storage practices (storing guns locked, unloaded, and separate from ammunition) reduce the risk of suicide and firearm injuries,⁴ yet 4.6 million American children live in a home with a loaded, unlocked firearm.⁵ Promoting safe gun storage practices and advocating for common sense gun safety legislation are two effective ways to address this crisis.

Gun violence prevention is my passion, but it might not be yours. Regardless of your passion, the blueprint for becoming a physician advocate is the same.

Advocacy, in its most distilled form, is speaking out for something you believe in, often for someone who cannot speak out for themselves. This is at the core of what we, as healthcare providers, do every day. We help people through some of the hardest moments of their lives, when they are sick and vulnerable. Every day, we are faced with problems that need to be solved. Our experience at the bedside helps us understand how policies affect real people. We understand evidence, data, and science. We recognize that anecdotes are powerful but if not backed up with data will be unlikely to lead to meaningful change. Perhaps most importantly, as professional members of the community, we have agency. We can use our voice and our privilege as physicians to elevate the voices of others.

As you go through medical training, you may not even realize that what you are doing on a daily basis is advocacy. But there comes a moment when you realize that the problem is bigger than the individual patient in front of you. There are systems that are broken that, if fixed, could improve the health of patients everywhere and save lives. To create change on a population level, the status quo will need to be challenged and systems may need to be disrupted.

Hospitalists are particularly well positioned to be advocates because we interact with virtually all aspects of the healthcare system either directly or indirectly. We care for patients with a myriad of disease processes and medical needs using varying levels of resources and social support systems. We often see patients in their most dire moments and, unlike outpatient physicians, we have the luxury of time. Hospitalized patients are a captive audience. We have time to educate, assess what patients need, and connect patients with community resources.

Find your passion. Often, your passion will find you. When it does, listen to it. Initially, most of your advocacy will be done on your own time. If you are not passionate about your cause, you will struggle and you will be less likely to be an effective advocate. Keep in mind that sometimes the deeper you dig into an issue, the bigger problems you find and, as a result, your passion can grow.

Do your research. Read the literature. Do you really understand the issue? Identify local and national experts, read their work, and follow their careers. You do not need an advanced degree. Your experience as a physician, willingness to learn, and your voice are all you need.

Start small. Do something small every day. Read an article. Make a new contact. Talk to a colleague. Be thoughtful in your approach. Is this a problem that community advocacy can solve? Will legislation be an effective way to achieve my goal? Would state or federal legislation be more appropriate? In most cases, a combination of community advocacy and legislative advocacy is necessary.

Partner with community organizations. Find local organizations that have existing infrastructure and are engaged on the issue and create partnerships. Community organizations are fighting every day and are waiting for a powerful authoritative voice like yours. They want your voice and you need their support.

Find your allies and your challengers. Identify allies in your community, your institution, your field, and in government. Anticipate potential challengers. When you encounter them, work diligently to find common ground and be respectful. If you only talk to people who agree with you, you will not make progress. Tread carefully when necessary. Develop a thick skin. Read people and try to figure out what it is that they want, what is motivating their position. Make your first ask small and as noncontroversial as possible. Stick to the facts. If you keep your patients at the heart of what you are doing, it is hard to go wrong.

Stay focused and disciplined, but do not quiet the anger and frustration that you feel. That is your fuel. Build momentum and build your team. Passion is contagious; when people see that you are making progress, they will want to join you. Together, you can create a dialog that will change minds.

Align advocacy with your other work. Ideally, this work will not be done in isolation from your other professional duties. Advocacy initiatives make excellent quality improvement projects. When you identify holes in the evidence that could potentially inform the policy debate, apply health services research methods and publish. This approach builds the evidence base to affect change and contributes to your professional development. Consider developing an advocacy curriculum for trainees. Identify trainees interested in advocacy and mentor them. Look for opportunities to speak and write on the topic. Use your unique skillset to further your cause.

Work with your employer. Find common ground. Even if they fundamentally disagree with your point of view, you can still speak out as a private citizen. Recognize the difference between speaking as a physician and speaking as an employee of a specific institution. Unless you have explicit permission, you are speaking for yourself, not your institution. Do not be afraid to push leaders at your institution. Help them see why it is important for you to speak up on a particular issue. If your professional organization has a statement on the issue, use it to support your position.

Leverage social media. Social media is a powerful method to amplify your voice. Consider the impact of the #thisisourlane movement. It will connect you with people, across the world, who share similar passions. It will help you identify local allies. It will open opportunities for speaking engagements and publications. It can be a great way to bring positive attention to your institution. It will take time to find your voice. Try to use consistent messaging. Keep it professional. Tag people who you want to see the great work you are doing. It only takes one retweet by someone with hundreds of thousands of followers to get your message in the feed of exponentially more viewers. Tag your institution when you want them to know what you are up to or when you are doing something that you think they should be proud of. Tag the professional organizations that would be interested in your work. Tag community leaders. This can be a great way to elevate their voice with your platform. Include an “opinions my own” statement in your social media profiles. Beware of disinformation. Read articles before retweeting. Ignore the trolls. I repeat, ignore the trolls.

I did not start my career with a focus on advocacy and in becoming an advocate, I have not given up my previous focus on asthma research. I did not get an advanced degree or specialized training in advocacy. I let my passion drive me. I am now an active member and leader in our Moms Demand Action chapter. The safe storage campaign in our resident clinic has had significant success. We increased the frequency of discussion of gun safety during well-child visits from 2% to 50% and shared this success at local and national scientific meetings. We have worked with our local media to spread awareness about safe gun storage. We have spent time at the state capital to discuss child access prevention laws with legislators. We have collaborated with community leaders and elected officials for gun violence awareness events. We earned support from leaders at our institution. If you walk through our hospital units, clinics, resident areas, and faculty offices, you will see evidence of our success. Physicians and nurses are still wearing their ribbons from the Wear Orange day on their name badges. “We Can End Gun Violence” signs are hanging on faculty members’ doors. Thanks to local police departments, the clinic has a constant supply of gun locks that are provided to families free of charge. Our residents proudly walk the halls with Be SMART buttons on their badges. These physical reminders of our progress are incredibly motivating as we continue this work. However, it is the quiet moments alone with children and parents who are suffering because of the epidemic of gun violence that really move me. I will not give up this fight until children in our communities are safe.

Acknowledgments

Dr. Andrews wishes to thank Dr. Kelsey Gastineau for her efforts to increase the frequency of gun safety discussions in our Pediatric Primary Care clinic and for her support in all of this work.

A low percentage of mixed genotypes of hepatitis C virus (HCV) was found in a small study of recently infected HIV+ and HIV– men who have sex with men (MSM) according to a report by Thuy Nguyen, PhD, of the University of North Carolina, Chapel Hill, and colleagues published in the International Journal of Antimicrobial Agents.

SilverV/Thinkstock

The researchers assessed 58 HCV-infected individuals with a median age of 38.5 years, 50 of whom were HIV positive and 18 of whom were HIV negative. Most of the patients were MSM (85.3%), with the rest of unknown sexual orientation. HCV genotyping by Sanger found types GT1a, GT4d, GT3a, and GT2k infection in 47.1%, 41.2%, 8.8%, and 2.9% of the individuals.

After eliminating suspected contaminations, three patients (4.4%) were found with mixed GT infections All three patients were infected with HCV for the first time; two-thirds were coinfected with HIV. The mixed GTs comprised only GT4d and GT1a at different ratios. Mixed infections are potentially problematic when using direct-acting antiviral therapy without broad-spectrum activity, according to the researchers. In this case, however, all HCV patients achieved treatment success.

“From a public health perspective, the MSM population engaging in high-risk behaviors still requires special attention in terms of mixed infections compared with the general HCV-infected population with a regular monitoring of anti-HCV treatment response, particularly when pangenotypic treatment is not used,” the researchers concluded.

The study was funded by the French government; the authors reported having no conflicts.

mlesney@mdedge.com

SOURCE: Nguyen T et al. Int J Antimicrobial Agents. 2019. 54[4]:523-7.

A low percentage of mixed genotypes of hepatitis C virus (HCV) was found in a small study of recently infected HIV+ and HIV– men who have sex with men (MSM) according to a report by Thuy Nguyen, PhD, of the University of North Carolina, Chapel Hill, and colleagues published in the International Journal of Antimicrobial Agents.

SilverV/Thinkstock

The researchers assessed 58 HCV-infected individuals with a median age of 38.5 years, 50 of whom were HIV positive and 18 of whom were HIV negative. Most of the patients were MSM (85.3%), with the rest of unknown sexual orientation. HCV genotyping by Sanger found types GT1a, GT4d, GT3a, and GT2k infection in 47.1%, 41.2%, 8.8%, and 2.9% of the individuals.

After eliminating suspected contaminations, three patients (4.4%) were found with mixed GT infections All three patients were infected with HCV for the first time; two-thirds were coinfected with HIV. The mixed GTs comprised only GT4d and GT1a at different ratios. Mixed infections are potentially problematic when using direct-acting antiviral therapy without broad-spectrum activity, according to the researchers. In this case, however, all HCV patients achieved treatment success.

“From a public health perspective, the MSM population engaging in high-risk behaviors still requires special attention in terms of mixed infections compared with the general HCV-infected population with a regular monitoring of anti-HCV treatment response, particularly when pangenotypic treatment is not used,” the researchers concluded.

The study was funded by the French government; the authors reported having no conflicts.

mlesney@mdedge.com

SOURCE: Nguyen T et al. Int J Antimicrobial Agents. 2019. 54[4]:523-7.

A low percentage of mixed genotypes of hepatitis C virus (HCV) was found in a small study of recently infected HIV+ and HIV– men who have sex with men (MSM) according to a report by Thuy Nguyen, PhD, of the University of North Carolina, Chapel Hill, and colleagues published in the International Journal of Antimicrobial Agents.

SilverV/Thinkstock

The researchers assessed 58 HCV-infected individuals with a median age of 38.5 years, 50 of whom were HIV positive and 18 of whom were HIV negative. Most of the patients were MSM (85.3%), with the rest of unknown sexual orientation. HCV genotyping by Sanger found types GT1a, GT4d, GT3a, and GT2k infection in 47.1%, 41.2%, 8.8%, and 2.9% of the individuals.

After eliminating suspected contaminations, three patients (4.4%) were found with mixed GT infections All three patients were infected with HCV for the first time; two-thirds were coinfected with HIV. The mixed GTs comprised only GT4d and GT1a at different ratios. Mixed infections are potentially problematic when using direct-acting antiviral therapy without broad-spectrum activity, according to the researchers. In this case, however, all HCV patients achieved treatment success.

“From a public health perspective, the MSM population engaging in high-risk behaviors still requires special attention in terms of mixed infections compared with the general HCV-infected population with a regular monitoring of anti-HCV treatment response, particularly when pangenotypic treatment is not used,” the researchers concluded.

The study was funded by the French government; the authors reported having no conflicts.

mlesney@mdedge.com

SOURCE: Nguyen T et al. Int J Antimicrobial Agents. 2019. 54[4]:523-7.

Online resources are affecting most consumers’ selections of cosmetic providers, and social media are now a top-three influence on cosmetic procedure choices and skin care purchases, according to a new survey from the American Society for Dermatologic Surgery.

Almost 70% of respondents said that their use of rate and review websites had an impact on the choice of provider for cosmetic procedures: WebMD was the site most often visited, followed by Facebook, physician websites, and Yelp, the ASDS said based on its annual consumer survey.

For 43% of consumers, the decision to schedule an appointment was influenced by a provider’s social media presence, and 41% of patients said that they follow their current or potential provider on social media, the ASDS said.

“Online resources and social media platforms are clearly influencing consumers’ behavior and perception of skin health,” ASDS President Murad Alam, MD, MBA, chief of cutaneous and aesthetic surgery in the department of dermatology at Northwestern University, Chicago, said in a written statement.

Dermatologists, however, remain the leading influence on the decision to have a cosmetic procedure – named as a resource by 34% of respondents, who could select more than one possibility from a list of 15 – but social media moved ahead of primary care physicians into third place (24%), just behind friends (30%), the survey showed. Dermatologists, on the other hand, had polled at 50%-55% for the previous 5 years.

The dermatologists’ lead remained stronger as the top influencer for skin care purchases, selected by 45% of respondents, compared with 32% for friends and 28% for social media. In this category there were 14 factors from which respondents could choose. As for the cost of those skin care products, 48% of consumers spent $1-$50 a month, 31% said that they spent $51-$100 a month, and 12% reported spending $101-$150 a month, the ASDS said.

The society received 3,645 responses to the 2019 Consumer Survey on Cosmetic Dermatologic Procedures, which was conducted online from July 30 to Aug. 27 by Survata.

rfranki@mdedge.com

Online resources are affecting most consumers’ selections of cosmetic providers, and social media are now a top-three influence on cosmetic procedure choices and skin care purchases, according to a new survey from the American Society for Dermatologic Surgery.

Almost 70% of respondents said that their use of rate and review websites had an impact on the choice of provider for cosmetic procedures: WebMD was the site most often visited, followed by Facebook, physician websites, and Yelp, the ASDS said based on its annual consumer survey.

For 43% of consumers, the decision to schedule an appointment was influenced by a provider’s social media presence, and 41% of patients said that they follow their current or potential provider on social media, the ASDS said.

“Online resources and social media platforms are clearly influencing consumers’ behavior and perception of skin health,” ASDS President Murad Alam, MD, MBA, chief of cutaneous and aesthetic surgery in the department of dermatology at Northwestern University, Chicago, said in a written statement.

Dermatologists, however, remain the leading influence on the decision to have a cosmetic procedure – named as a resource by 34% of respondents, who could select more than one possibility from a list of 15 – but social media moved ahead of primary care physicians into third place (24%), just behind friends (30%), the survey showed. Dermatologists, on the other hand, had polled at 50%-55% for the previous 5 years.

The dermatologists’ lead remained stronger as the top influencer for skin care purchases, selected by 45% of respondents, compared with 32% for friends and 28% for social media. In this category there were 14 factors from which respondents could choose. As for the cost of those skin care products, 48% of consumers spent $1-$50 a month, 31% said that they spent $51-$100 a month, and 12% reported spending $101-$150 a month, the ASDS said.

The society received 3,645 responses to the 2019 Consumer Survey on Cosmetic Dermatologic Procedures, which was conducted online from July 30 to Aug. 27 by Survata.

rfranki@mdedge.com

Online resources are affecting most consumers’ selections of cosmetic providers, and social media are now a top-three influence on cosmetic procedure choices and skin care purchases, according to a new survey from the American Society for Dermatologic Surgery.

Almost 70% of respondents said that their use of rate and review websites had an impact on the choice of provider for cosmetic procedures: WebMD was the site most often visited, followed by Facebook, physician websites, and Yelp, the ASDS said based on its annual consumer survey.

For 43% of consumers, the decision to schedule an appointment was influenced by a provider’s social media presence, and 41% of patients said that they follow their current or potential provider on social media, the ASDS said.

“Online resources and social media platforms are clearly influencing consumers’ behavior and perception of skin health,” ASDS President Murad Alam, MD, MBA, chief of cutaneous and aesthetic surgery in the department of dermatology at Northwestern University, Chicago, said in a written statement.

Dermatologists, however, remain the leading influence on the decision to have a cosmetic procedure – named as a resource by 34% of respondents, who could select more than one possibility from a list of 15 – but social media moved ahead of primary care physicians into third place (24%), just behind friends (30%), the survey showed. Dermatologists, on the other hand, had polled at 50%-55% for the previous 5 years.

The dermatologists’ lead remained stronger as the top influencer for skin care purchases, selected by 45% of respondents, compared with 32% for friends and 28% for social media. In this category there were 14 factors from which respondents could choose. As for the cost of those skin care products, 48% of consumers spent $1-$50 a month, 31% said that they spent $51-$100 a month, and 12% reported spending $101-$150 a month, the ASDS said.

The society received 3,645 responses to the 2019 Consumer Survey on Cosmetic Dermatologic Procedures, which was conducted online from July 30 to Aug. 27 by Survata.

rfranki@mdedge.com

On Sept. 20, I had the opportunity to participate in AGA’s Advocacy Day for the second time, joining 40 of our gastroenterology colleagues from across the United States on Capitol Hill to advocate for our profession and our patients.

AGA Institute

The evening before Advocacy Day, we discussed strategies for having a successful meeting on Capitol Hill with AGA staff (including Kathleen Teixeira, AGA vice president of government affairs, and Jonathan Sollish, AGA senior coordinator, public policy). We discussed having our “asks” supported with evidence, and “getting personal” about how these policy issues directly affect us and our patients. We also had the chance to hear from Rep. Jim McGovern (D-Mass.) and Sen. Roy Blunt (R-Mo.) , both of whom invited our questions. Both congressmen are friends of AGA, with McGovern serving as chair of the House Rules Committee, and Blunt serving as chair of the Senate Labor-HHS Subcommittee on Appropriations.

Advocacy Day began with a group breakfast during which we reviewed some of the policy issues of central importance to gastroenterology:

• Removing Barriers to the Colorectal Cancer Screening Act (HR1570/S668), which enjoys strong bipartisan support, would correct the “cost-sharing” problem of screening colonoscopies turning therapeutic (with polypectomy) for our Medicare patients, by waiving the coinsurance for screening colonoscopies – regardless of whether we remove polyps during these colonoscopies.

• Safe Step Act, HR2279, legislation introduced in the House, facilitates a common-sense and timely (72 hours or 24 hours if life-threatening) appeals process when our patients are subjected to step therapy (“fail first”) by insurers.

• Improving Seniors’ Timely Access to Care Act of 2019, HR3107, legislation in the House, eases onerous prior authorization burdens by promoting an electronic prior authorization process, ensuring requests are approved by qualified medical professionals who have specialty-specific experience, and mandating that plans report their rates of delays and denials.

• NIH research funding facilitates innovative research and supports young investigators in our field.

Full of enthusiasm, our six-strong North Carolina contingent (pictured, L-R, Ziad Gellad, MD, MPH, AGAF; David Leiman, MD, MSPH; Animesh Jain, MD; Anne Finefrock Peery, MD; Lisa Gangarosa, MD, AGAF, chair of the AGA Government Affairs Committee; and Amit Patel, MD) met with the offices of Rep. David Price (D-N.C.), and both North Carolina Senators, Richard Burr (R) and Thom Tillis (R) on Capitol Hill to convey our “asks.”

AGA Institute

Dr. Patel is assistant professor, division of gastroenterology, Duke University, Cary, N.C.; member, AGA Clinical Guidelines Committee.

On Sept. 20, I had the opportunity to participate in AGA’s Advocacy Day for the second time, joining 40 of our gastroenterology colleagues from across the United States on Capitol Hill to advocate for our profession and our patients.

AGA Institute

The evening before Advocacy Day, we discussed strategies for having a successful meeting on Capitol Hill with AGA staff (including Kathleen Teixeira, AGA vice president of government affairs, and Jonathan Sollish, AGA senior coordinator, public policy). We discussed having our “asks” supported with evidence, and “getting personal” about how these policy issues directly affect us and our patients. We also had the chance to hear from Rep. Jim McGovern (D-Mass.) and Sen. Roy Blunt (R-Mo.) , both of whom invited our questions. Both congressmen are friends of AGA, with McGovern serving as chair of the House Rules Committee, and Blunt serving as chair of the Senate Labor-HHS Subcommittee on Appropriations.

Advocacy Day began with a group breakfast during which we reviewed some of the policy issues of central importance to gastroenterology:

• Removing Barriers to the Colorectal Cancer Screening Act (HR1570/S668), which enjoys strong bipartisan support, would correct the “cost-sharing” problem of screening colonoscopies turning therapeutic (with polypectomy) for our Medicare patients, by waiving the coinsurance for screening colonoscopies – regardless of whether we remove polyps during these colonoscopies.

• Safe Step Act, HR2279, legislation introduced in the House, facilitates a common-sense and timely (72 hours or 24 hours if life-threatening) appeals process when our patients are subjected to step therapy (“fail first”) by insurers.

• Improving Seniors’ Timely Access to Care Act of 2019, HR3107, legislation in the House, eases onerous prior authorization burdens by promoting an electronic prior authorization process, ensuring requests are approved by qualified medical professionals who have specialty-specific experience, and mandating that plans report their rates of delays and denials.

• NIH research funding facilitates innovative research and supports young investigators in our field.

Full of enthusiasm, our six-strong North Carolina contingent (pictured, L-R, Ziad Gellad, MD, MPH, AGAF; David Leiman, MD, MSPH; Animesh Jain, MD; Anne Finefrock Peery, MD; Lisa Gangarosa, MD, AGAF, chair of the AGA Government Affairs Committee; and Amit Patel, MD) met with the offices of Rep. David Price (D-N.C.), and both North Carolina Senators, Richard Burr (R) and Thom Tillis (R) on Capitol Hill to convey our “asks.”

AGA Institute

Dr. Patel is assistant professor, division of gastroenterology, Duke University, Cary, N.C.; member, AGA Clinical Guidelines Committee.

On Sept. 20, I had the opportunity to participate in AGA’s Advocacy Day for the second time, joining 40 of our gastroenterology colleagues from across the United States on Capitol Hill to advocate for our profession and our patients.

AGA Institute

The evening before Advocacy Day, we discussed strategies for having a successful meeting on Capitol Hill with AGA staff (including Kathleen Teixeira, AGA vice president of government affairs, and Jonathan Sollish, AGA senior coordinator, public policy). We discussed having our “asks” supported with evidence, and “getting personal” about how these policy issues directly affect us and our patients. We also had the chance to hear from Rep. Jim McGovern (D-Mass.) and Sen. Roy Blunt (R-Mo.) , both of whom invited our questions. Both congressmen are friends of AGA, with McGovern serving as chair of the House Rules Committee, and Blunt serving as chair of the Senate Labor-HHS Subcommittee on Appropriations.

Advocacy Day began with a group breakfast during which we reviewed some of the policy issues of central importance to gastroenterology:

• Removing Barriers to the Colorectal Cancer Screening Act (HR1570/S668), which enjoys strong bipartisan support, would correct the “cost-sharing” problem of screening colonoscopies turning therapeutic (with polypectomy) for our Medicare patients, by waiving the coinsurance for screening colonoscopies – regardless of whether we remove polyps during these colonoscopies.

• Safe Step Act, HR2279, legislation introduced in the House, facilitates a common-sense and timely (72 hours or 24 hours if life-threatening) appeals process when our patients are subjected to step therapy (“fail first”) by insurers.

• Improving Seniors’ Timely Access to Care Act of 2019, HR3107, legislation in the House, eases onerous prior authorization burdens by promoting an electronic prior authorization process, ensuring requests are approved by qualified medical professionals who have specialty-specific experience, and mandating that plans report their rates of delays and denials.

• NIH research funding facilitates innovative research and supports young investigators in our field.

Full of enthusiasm, our six-strong North Carolina contingent (pictured, L-R, Ziad Gellad, MD, MPH, AGAF; David Leiman, MD, MSPH; Animesh Jain, MD; Anne Finefrock Peery, MD; Lisa Gangarosa, MD, AGAF, chair of the AGA Government Affairs Committee; and Amit Patel, MD) met with the offices of Rep. David Price (D-N.C.), and both North Carolina Senators, Richard Burr (R) and Thom Tillis (R) on Capitol Hill to convey our “asks.”

AGA Institute

Dr. Patel is assistant professor, division of gastroenterology, Duke University, Cary, N.C.; member, AGA Clinical Guidelines Committee.

Dear Colleagues,

Join me in supporting talented investigators through a personal gift to the AGA Research Foundation.

As a member of the GI community, you understand the physical, emotional and financial costs of digestive diseases. And you understand the value of research to advance patient care. The gap in federal funding for research continues to grow. Many well-qualified young investigators cannot get government funding. Gifts to the AGA Research Foundation this year directly supported 52 talented investigators. Despite this success, over 200 other innovative and promising research ideas went unfunded.

That’s why I’m asking for your help.

Securing the future of the field is no small task. Every dollar is a step forward in helping to spark the scientific breakthroughs of today so clinicians will have the tools to improve care tomorrow.

Everyone benefits from GI research developed by dedicated investigators.

I invite you to help the AGA Research Foundation continue our efforts to fund and retain talented GI scientists whose research will impact the future care of patients. Donate today at www.gastro.org/donate.

Thank you for your generosity. Best wishes for a happy, healthy holiday season and successful New Year.

ginews@gastro.org

Dear Colleagues,

Join me in supporting talented investigators through a personal gift to the AGA Research Foundation.

As a member of the GI community, you understand the physical, emotional and financial costs of digestive diseases. And you understand the value of research to advance patient care. The gap in federal funding for research continues to grow. Many well-qualified young investigators cannot get government funding. Gifts to the AGA Research Foundation this year directly supported 52 talented investigators. Despite this success, over 200 other innovative and promising research ideas went unfunded.

That’s why I’m asking for your help.

Securing the future of the field is no small task. Every dollar is a step forward in helping to spark the scientific breakthroughs of today so clinicians will have the tools to improve care tomorrow.

Everyone benefits from GI research developed by dedicated investigators.

I invite you to help the AGA Research Foundation continue our efforts to fund and retain talented GI scientists whose research will impact the future care of patients. Donate today at www.gastro.org/donate.

Thank you for your generosity. Best wishes for a happy, healthy holiday season and successful New Year.

ginews@gastro.org

Dear Colleagues,

Join me in supporting talented investigators through a personal gift to the AGA Research Foundation.

As a member of the GI community, you understand the physical, emotional and financial costs of digestive diseases. And you understand the value of research to advance patient care. The gap in federal funding for research continues to grow. Many well-qualified young investigators cannot get government funding. Gifts to the AGA Research Foundation this year directly supported 52 talented investigators. Despite this success, over 200 other innovative and promising research ideas went unfunded.

That’s why I’m asking for your help.

Securing the future of the field is no small task. Every dollar is a step forward in helping to spark the scientific breakthroughs of today so clinicians will have the tools to improve care tomorrow.

Everyone benefits from GI research developed by dedicated investigators.

I invite you to help the AGA Research Foundation continue our efforts to fund and retain talented GI scientists whose research will impact the future care of patients. Donate today at www.gastro.org/donate.

Thank you for your generosity. Best wishes for a happy, healthy holiday season and successful New Year.

ginews@gastro.org

Physicians with difficult patient scenarios regularly bring their questions to the AGA Community to seek advice from colleagues about therapy and disease management options, best practices, and diagnoses. In case you missed it, here are the most popular clinical discussions shared in the forum recently:

1. Severe ulcerative colitis # IBD – A 41-year-old female patient with ulcerative colitis had a flare that didn’t improve with adalimumab and prednisone, and was admitted to the hospital with bloody stools and abdominal pain. The GI community discussed considerations for next steps and other tests to consider.

2. Unexplained diarrhea – Following the eQ&A with an AGA guideline coauthor on chronic diarrhea, this popular case follows a celiac disease patient on a gluten-free diet who continues to have significant diarrhea and fatigue.

3. Difficult ERCP – How would you handle an ERCP where the papilla is small and in a tricky location? View photos from your colleague’s scope and share your advice with the GI community.

Access these clinical cases and more discussions at https://community.gastro.org/discussions.
 

Physicians with difficult patient scenarios regularly bring their questions to the AGA Community to seek advice from colleagues about therapy and disease management options, best practices, and diagnoses. In case you missed it, here are the most popular clinical discussions shared in the forum recently:

1. Severe ulcerative colitis # IBD – A 41-year-old female patient with ulcerative colitis had a flare that didn’t improve with adalimumab and prednisone, and was admitted to the hospital with bloody stools and abdominal pain. The GI community discussed considerations for next steps and other tests to consider.

2. Unexplained diarrhea – Following the eQ&A with an AGA guideline coauthor on chronic diarrhea, this popular case follows a celiac disease patient on a gluten-free diet who continues to have significant diarrhea and fatigue.

3. Difficult ERCP – How would you handle an ERCP where the papilla is small and in a tricky location? View photos from your colleague’s scope and share your advice with the GI community.

Access these clinical cases and more discussions at https://community.gastro.org/discussions.
 

Physicians with difficult patient scenarios regularly bring their questions to the AGA Community to seek advice from colleagues about therapy and disease management options, best practices, and diagnoses. In case you missed it, here are the most popular clinical discussions shared in the forum recently:

1. Severe ulcerative colitis # IBD – A 41-year-old female patient with ulcerative colitis had a flare that didn’t improve with adalimumab and prednisone, and was admitted to the hospital with bloody stools and abdominal pain. The GI community discussed considerations for next steps and other tests to consider.

2. Unexplained diarrhea – Following the eQ&A with an AGA guideline coauthor on chronic diarrhea, this popular case follows a celiac disease patient on a gluten-free diet who continues to have significant diarrhea and fatigue.

3. Difficult ERCP – How would you handle an ERCP where the papilla is small and in a tricky location? View photos from your colleague’s scope and share your advice with the GI community.

Access these clinical cases and more discussions at https://community.gastro.org/discussions.