AGA Guideline: Use goal-directed fluid therapy, early oral feeding in acute pancreatitis

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Patients with acute pancreatitis should receive “goal-directed” fluid therapy with normal saline or Ringer’s lactate solution rather than hydroxyethyl starch (HES) fluids, states a new guideline from the AGA Institute.

In a single-center randomized trial, hydroxyethyl starch fluids conferred a 3.9-fold increase in the odds of multiorgan failure (95% confidence interval for odds ratio, 1.2-12.0) compared with normal saline in patients with acute pancreatitis, wrote guideline authors Seth D. Crockett, MD, MPH, of the University of North Carolina, Chapel Hill, and his associates. This trial and another randomized study found no mortality benefit for HES compared with fluid resuscitation. The evidence is “very low quality” but mirrors the critical care literature, according to the experts. So far, Ringer’s lactate solution and normal saline have shown similar effects on the risk of organ failure, necrosis, and mortality, but ongoing trials should better clarify this choice, they noted (Gastroenterology. doi: 10.1053/j.gastro.2018.01.032).

The guideline addresses the initial 2-week period of treating acute pancreatitis. It defines goal-directed fluid therapy as titration based on meaningful targets, such as heart rate, mean arterial pressure, central venous pressure, urine output, blood urea nitrogen concentration, and hematocrit. Studies of goal-directed fluid therapy in acute pancreatitis have been unblinded, have used inconsistent outcome measures, and have found no definite benefits over nontargeted fluid therapy, note the guideline authors. Nevertheless, they conditionally recommend goal-directed fluid therapy, partly because a randomized, blinded trial of patients with severe sepsis or septic shock (which physiologically resembles acute pancreatitis) had in-hospital mortality rates of 31% when they received goal-directed fluid therapy and 47% when they received standard fluid therapy (P = .0009).

The guideline recommends against routine use of two interventions: prophylactic antibiotics and urgent endoscopic retrograde cholangiopancreatography (ERCP) for patients with acute pancreatitis. The authors note that no evidence supports routine prophylactic antibiotics for acute pancreatitis patients without cholangitis, and that urgent ERCP did not significantly affect the risk of mortality, multiorgan failure, single-organ failure, infected pancreatic and peripancreatic necrosis, or necrotizing pancreatitis in eight randomized controlled trials of patients with acute gallstone pancreatitis.

 

 


The guideline strongly recommends early oral feeding and enteral rather than parenteral nutrition for all patients with acute pancreatitis. In 11 randomized controlled trials, early and delayed feeding led to similar rates of mortality, but delayed feeding produced a 2.5-fold higher risk of necrosis (95% CI for OR, 1.4-4.4) and tended to increase the risk of infected peripancreatic necrosis, multiorgan failure, and total necrotizing pancreatitis, the authors wrote. In another 12 trials, enteral nutrition significantly reduced the risk of infected peripancreatic necrosis, single-organ failure, and multiorgan failure compared with parenteral nutrition.

Clinicians continue to debate cholecystectomy timing in patients with biliary or gallstone pancreatitis. The guidelines strongly recommend same-admission cholecystectomy, citing a randomized controlled trial in which this approach markedly reduced the combined risk of mortality and gallstone-related complications (OR, 0.2, 95% CI, 0.1-0.6), readmission for recurrent pancreatitis (OR, 0.3, 95% CI, 0.1-0.9), and pancreaticobiliary complications (OR, 0.2, 95% CI, 0.1-0.6). “The AGA issued a strong recommendation due to the quality of available evidence and the high likelihood of benefit from early versus delayed cholecystectomy in this patient population,” the experts stated.

Patients with biliary pancreatitis should be evaluated for cholecystectomy during the same admission, while those with alcohol-induced pancreatitis should receive a brief alcohol intervention, according to the guidelines, which also call for better studies of how alcohol and tobacco cessation measures affect risk of recurrent acute pancreatitis, chronic pancreatitis, and pancreatic cancer, as well as quality of life, health care utilization, and mortality.

The authors also noted knowledge gaps concerning the relative benefits of risk stratification tools, the use of prophylactic antibiotics in patients with severe acute pancreatitis or necrotizing pancreatitis, and the timing of ERCP in patients with severe biliary pancreatitis with persistent biliary obstruction.
 

 


The guideline was developed with sole funding by the AGA Institute with no external funding. The authors disclosed no relevant conflicts of interest.
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Patients with acute pancreatitis should receive “goal-directed” fluid therapy with normal saline or Ringer’s lactate solution rather than hydroxyethyl starch (HES) fluids, states a new guideline from the AGA Institute.

In a single-center randomized trial, hydroxyethyl starch fluids conferred a 3.9-fold increase in the odds of multiorgan failure (95% confidence interval for odds ratio, 1.2-12.0) compared with normal saline in patients with acute pancreatitis, wrote guideline authors Seth D. Crockett, MD, MPH, of the University of North Carolina, Chapel Hill, and his associates. This trial and another randomized study found no mortality benefit for HES compared with fluid resuscitation. The evidence is “very low quality” but mirrors the critical care literature, according to the experts. So far, Ringer’s lactate solution and normal saline have shown similar effects on the risk of organ failure, necrosis, and mortality, but ongoing trials should better clarify this choice, they noted (Gastroenterology. doi: 10.1053/j.gastro.2018.01.032).

The guideline addresses the initial 2-week period of treating acute pancreatitis. It defines goal-directed fluid therapy as titration based on meaningful targets, such as heart rate, mean arterial pressure, central venous pressure, urine output, blood urea nitrogen concentration, and hematocrit. Studies of goal-directed fluid therapy in acute pancreatitis have been unblinded, have used inconsistent outcome measures, and have found no definite benefits over nontargeted fluid therapy, note the guideline authors. Nevertheless, they conditionally recommend goal-directed fluid therapy, partly because a randomized, blinded trial of patients with severe sepsis or septic shock (which physiologically resembles acute pancreatitis) had in-hospital mortality rates of 31% when they received goal-directed fluid therapy and 47% when they received standard fluid therapy (P = .0009).

The guideline recommends against routine use of two interventions: prophylactic antibiotics and urgent endoscopic retrograde cholangiopancreatography (ERCP) for patients with acute pancreatitis. The authors note that no evidence supports routine prophylactic antibiotics for acute pancreatitis patients without cholangitis, and that urgent ERCP did not significantly affect the risk of mortality, multiorgan failure, single-organ failure, infected pancreatic and peripancreatic necrosis, or necrotizing pancreatitis in eight randomized controlled trials of patients with acute gallstone pancreatitis.

 

 


The guideline strongly recommends early oral feeding and enteral rather than parenteral nutrition for all patients with acute pancreatitis. In 11 randomized controlled trials, early and delayed feeding led to similar rates of mortality, but delayed feeding produced a 2.5-fold higher risk of necrosis (95% CI for OR, 1.4-4.4) and tended to increase the risk of infected peripancreatic necrosis, multiorgan failure, and total necrotizing pancreatitis, the authors wrote. In another 12 trials, enteral nutrition significantly reduced the risk of infected peripancreatic necrosis, single-organ failure, and multiorgan failure compared with parenteral nutrition.

Clinicians continue to debate cholecystectomy timing in patients with biliary or gallstone pancreatitis. The guidelines strongly recommend same-admission cholecystectomy, citing a randomized controlled trial in which this approach markedly reduced the combined risk of mortality and gallstone-related complications (OR, 0.2, 95% CI, 0.1-0.6), readmission for recurrent pancreatitis (OR, 0.3, 95% CI, 0.1-0.9), and pancreaticobiliary complications (OR, 0.2, 95% CI, 0.1-0.6). “The AGA issued a strong recommendation due to the quality of available evidence and the high likelihood of benefit from early versus delayed cholecystectomy in this patient population,” the experts stated.

Patients with biliary pancreatitis should be evaluated for cholecystectomy during the same admission, while those with alcohol-induced pancreatitis should receive a brief alcohol intervention, according to the guidelines, which also call for better studies of how alcohol and tobacco cessation measures affect risk of recurrent acute pancreatitis, chronic pancreatitis, and pancreatic cancer, as well as quality of life, health care utilization, and mortality.

The authors also noted knowledge gaps concerning the relative benefits of risk stratification tools, the use of prophylactic antibiotics in patients with severe acute pancreatitis or necrotizing pancreatitis, and the timing of ERCP in patients with severe biliary pancreatitis with persistent biliary obstruction.
 

 


The guideline was developed with sole funding by the AGA Institute with no external funding. The authors disclosed no relevant conflicts of interest.

 

Patients with acute pancreatitis should receive “goal-directed” fluid therapy with normal saline or Ringer’s lactate solution rather than hydroxyethyl starch (HES) fluids, states a new guideline from the AGA Institute.

In a single-center randomized trial, hydroxyethyl starch fluids conferred a 3.9-fold increase in the odds of multiorgan failure (95% confidence interval for odds ratio, 1.2-12.0) compared with normal saline in patients with acute pancreatitis, wrote guideline authors Seth D. Crockett, MD, MPH, of the University of North Carolina, Chapel Hill, and his associates. This trial and another randomized study found no mortality benefit for HES compared with fluid resuscitation. The evidence is “very low quality” but mirrors the critical care literature, according to the experts. So far, Ringer’s lactate solution and normal saline have shown similar effects on the risk of organ failure, necrosis, and mortality, but ongoing trials should better clarify this choice, they noted (Gastroenterology. doi: 10.1053/j.gastro.2018.01.032).

The guideline addresses the initial 2-week period of treating acute pancreatitis. It defines goal-directed fluid therapy as titration based on meaningful targets, such as heart rate, mean arterial pressure, central venous pressure, urine output, blood urea nitrogen concentration, and hematocrit. Studies of goal-directed fluid therapy in acute pancreatitis have been unblinded, have used inconsistent outcome measures, and have found no definite benefits over nontargeted fluid therapy, note the guideline authors. Nevertheless, they conditionally recommend goal-directed fluid therapy, partly because a randomized, blinded trial of patients with severe sepsis or septic shock (which physiologically resembles acute pancreatitis) had in-hospital mortality rates of 31% when they received goal-directed fluid therapy and 47% when they received standard fluid therapy (P = .0009).

The guideline recommends against routine use of two interventions: prophylactic antibiotics and urgent endoscopic retrograde cholangiopancreatography (ERCP) for patients with acute pancreatitis. The authors note that no evidence supports routine prophylactic antibiotics for acute pancreatitis patients without cholangitis, and that urgent ERCP did not significantly affect the risk of mortality, multiorgan failure, single-organ failure, infected pancreatic and peripancreatic necrosis, or necrotizing pancreatitis in eight randomized controlled trials of patients with acute gallstone pancreatitis.

 

 


The guideline strongly recommends early oral feeding and enteral rather than parenteral nutrition for all patients with acute pancreatitis. In 11 randomized controlled trials, early and delayed feeding led to similar rates of mortality, but delayed feeding produced a 2.5-fold higher risk of necrosis (95% CI for OR, 1.4-4.4) and tended to increase the risk of infected peripancreatic necrosis, multiorgan failure, and total necrotizing pancreatitis, the authors wrote. In another 12 trials, enteral nutrition significantly reduced the risk of infected peripancreatic necrosis, single-organ failure, and multiorgan failure compared with parenteral nutrition.

Clinicians continue to debate cholecystectomy timing in patients with biliary or gallstone pancreatitis. The guidelines strongly recommend same-admission cholecystectomy, citing a randomized controlled trial in which this approach markedly reduced the combined risk of mortality and gallstone-related complications (OR, 0.2, 95% CI, 0.1-0.6), readmission for recurrent pancreatitis (OR, 0.3, 95% CI, 0.1-0.9), and pancreaticobiliary complications (OR, 0.2, 95% CI, 0.1-0.6). “The AGA issued a strong recommendation due to the quality of available evidence and the high likelihood of benefit from early versus delayed cholecystectomy in this patient population,” the experts stated.

Patients with biliary pancreatitis should be evaluated for cholecystectomy during the same admission, while those with alcohol-induced pancreatitis should receive a brief alcohol intervention, according to the guidelines, which also call for better studies of how alcohol and tobacco cessation measures affect risk of recurrent acute pancreatitis, chronic pancreatitis, and pancreatic cancer, as well as quality of life, health care utilization, and mortality.

The authors also noted knowledge gaps concerning the relative benefits of risk stratification tools, the use of prophylactic antibiotics in patients with severe acute pancreatitis or necrotizing pancreatitis, and the timing of ERCP in patients with severe biliary pancreatitis with persistent biliary obstruction.
 

 


The guideline was developed with sole funding by the AGA Institute with no external funding. The authors disclosed no relevant conflicts of interest.
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Hydrocortisone-fludrocortisone cuts deaths in septic shock

Corticosteroids: What’s their place in treating septic shock?
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Hydrocortisone in combination with fludrocortisone significantly reduced 90-day mortality in septic shock patients in a double-blind, randomized, controlled trial.

Prior to this study, two large trials had displayed that corticosteroids were beneficial in improving hemodynamic status and organ function, but little was known about corticosteroids’ ability to increase survival in sepsis patients.

DigitalVision/Thinkstock
“[Corticosteroids] improve cardiovascular function by restoring effective blood volume through increased mineralocorticoid activity and by increasing systemic vascular resistance, an effect that is partly related to endothelial glucocorticoid receptors,” wrote Djillali Annane, MD, of the University of Paris and his colleagues in the New England Journal of Medicine.“This might explain why in our trial there was less need for vasopressors with hydrocortisone plus fludrocortisone than with placebo.”

The study, named the Activated Protein C and Corticosteroids for Human Septic Shock (APROCCHSS) trial, was designed to assess the benefit/risk ratio of using activated protein C – drotrecogin alfa (activated) – and corticosteroids together or separately in septic shock patients. The original design of the study included Xigris (drotrecogin alfa) and was composed of four parallel groups, but Xigris was removed from the market in October of 2011, so the study continued with only two parallel groups.

A total of 1,241 patients experiencing chronic septic shock were recruited into the two double-blind, parallel groups, with patients in one group receiving hydrocortisone plus fludrocortisone and the other receiving placebos. The placebos used in this study were similar in appearance to the actual treatment drugs. The placebos for hydrocortisone and fludrocortisone were either parenteral mannitol (133.6 mg), disodium phosphate (8.73 mg), and sodium phosphate (0.92 mg) or tablets of microcrystalline cellulose (59.098 mg), respectively.

Hydrocortisone was given intravenously every 6 hours as a 50-mg intravenous bolus, and fludrocortisone was given once a day as a 50-mcg tablet through a nasogastric tube. Patients in ICUs who had septic shock for less than 24 hours were included in the study. Septic shock was identified by the presence of a clinically or microbiologically documented infection, a Sequential Organ Failure Assessment score of 3 or 4 for at least two organs and for at least 6 hours, and receipt of vasopressor therapy for at least 6 hours.

After 90 days, 264 of 614 of the patients (43%) in the hydrocortisone/fludrocortisone group and almost half (49.1%) of 627 patients in the placebo group had died (P = .03). The relative risk of death was 0.88 (95% confidence interval, 0.78-0.99), which favored the hydrocortisone/fludrocortisone group. The researchers also observed that death was significantly lower in the hydrocortisone/fludrocortisone group, compared with the placebo group, at time of ICU discharge (35.4% vs. 41.0%, respectively; P = .04).

While mortality was reduced, patients still experienced adverse events. 326 of 614 (53.1%) patients in the hydrocortisone/fludrocortisone group and 363 of 626 patients (58.0%) in the placebo group experienced at least one serious adverse event by day 180 (P = 0.08).

“Seven-day treatment with a 50-mg intravenous bolus of hydrocortisone every 6 hours and a daily dose of 50 mcg of oral fludrocortisone resulted in lower mortality at day 90 and at ICU and hospital discharge than placebo among adults with septic shock,” concluded Dr. Annane and his coauthors.

The majority of researchers had no relevant financial disclosures to report, while some doctors received grants and personal fees unrelated to this study. This study was funded in part by public grants from the French Ministry of Health.

SOURCE: Annana A et al. NEJM. 2018 Feb 28. doi: 10.1056/NEJMoa1705716.

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The results of the Activated Protein C and Corticosteroids for Human Septic Shock (APROCCHSS) trial and the Adjunctive Corticosteroid Treatment in Critically Ill Patients with Septic Shock (ADRENAL), both reported in the latest issue of NEJM, are landmark studies detailing the largest analyses of hydrocortisone use in patients with septic shock.

Both of these trials were massive, with over 5,000 patients combined, which is much larger than all previous studies according to Anthony Suffredini, MD, of the National Institutes of Health. An additional useful feature of these trials was that they had clear criteria for entry into the study. These criteria included: “vasopressor-dependent shock and respiratory failure leading to the use of mechanical ventilation, details of antimicrobial therapy, assessment of survival at 90 days, and well-defined secondary outcomes and analyses of adverse events.”

The ADRENAL and APROCCHSS had vastly different 90-day mortality rates: ADRENAL had mortality rates of 27.9% with hydrocortisone and 28.8% with placebo (P = .50), while APROACCHSS had mortality rates of 43.0% with hydrocortisone plus fludrocortisone and 49.1% with placebo (P = .03). Despite this, they both display the beneficial effect anti-inflammatory therapies, such as hydrocortisone, have on secondary outcomes of shock reversal and the reduction in duration of mechanical ventilation. “It is unlikely that in the near future sufficiently powered trials will provide us with better data” than the ADRENAL and APROCCHSS trials, Dr. Suffredini wrote.

Dr. Suffredini made these comments in an editorial accompanying this study in the New England Journal of Medicine. He is the deputy chief of the critical care medicine department at the National Institutes of Health Clinical Center, and he has served on the executive committee of the Department of Veteran Affairs Cooperative Studies Program. He has no other relevant financial disclosures to report.

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The results of the Activated Protein C and Corticosteroids for Human Septic Shock (APROCCHSS) trial and the Adjunctive Corticosteroid Treatment in Critically Ill Patients with Septic Shock (ADRENAL), both reported in the latest issue of NEJM, are landmark studies detailing the largest analyses of hydrocortisone use in patients with septic shock.

Both of these trials were massive, with over 5,000 patients combined, which is much larger than all previous studies according to Anthony Suffredini, MD, of the National Institutes of Health. An additional useful feature of these trials was that they had clear criteria for entry into the study. These criteria included: “vasopressor-dependent shock and respiratory failure leading to the use of mechanical ventilation, details of antimicrobial therapy, assessment of survival at 90 days, and well-defined secondary outcomes and analyses of adverse events.”

The ADRENAL and APROCCHSS had vastly different 90-day mortality rates: ADRENAL had mortality rates of 27.9% with hydrocortisone and 28.8% with placebo (P = .50), while APROACCHSS had mortality rates of 43.0% with hydrocortisone plus fludrocortisone and 49.1% with placebo (P = .03). Despite this, they both display the beneficial effect anti-inflammatory therapies, such as hydrocortisone, have on secondary outcomes of shock reversal and the reduction in duration of mechanical ventilation. “It is unlikely that in the near future sufficiently powered trials will provide us with better data” than the ADRENAL and APROCCHSS trials, Dr. Suffredini wrote.

Dr. Suffredini made these comments in an editorial accompanying this study in the New England Journal of Medicine. He is the deputy chief of the critical care medicine department at the National Institutes of Health Clinical Center, and he has served on the executive committee of the Department of Veteran Affairs Cooperative Studies Program. He has no other relevant financial disclosures to report.

Body

 

The results of the Activated Protein C and Corticosteroids for Human Septic Shock (APROCCHSS) trial and the Adjunctive Corticosteroid Treatment in Critically Ill Patients with Septic Shock (ADRENAL), both reported in the latest issue of NEJM, are landmark studies detailing the largest analyses of hydrocortisone use in patients with septic shock.

Both of these trials were massive, with over 5,000 patients combined, which is much larger than all previous studies according to Anthony Suffredini, MD, of the National Institutes of Health. An additional useful feature of these trials was that they had clear criteria for entry into the study. These criteria included: “vasopressor-dependent shock and respiratory failure leading to the use of mechanical ventilation, details of antimicrobial therapy, assessment of survival at 90 days, and well-defined secondary outcomes and analyses of adverse events.”

The ADRENAL and APROCCHSS had vastly different 90-day mortality rates: ADRENAL had mortality rates of 27.9% with hydrocortisone and 28.8% with placebo (P = .50), while APROACCHSS had mortality rates of 43.0% with hydrocortisone plus fludrocortisone and 49.1% with placebo (P = .03). Despite this, they both display the beneficial effect anti-inflammatory therapies, such as hydrocortisone, have on secondary outcomes of shock reversal and the reduction in duration of mechanical ventilation. “It is unlikely that in the near future sufficiently powered trials will provide us with better data” than the ADRENAL and APROCCHSS trials, Dr. Suffredini wrote.

Dr. Suffredini made these comments in an editorial accompanying this study in the New England Journal of Medicine. He is the deputy chief of the critical care medicine department at the National Institutes of Health Clinical Center, and he has served on the executive committee of the Department of Veteran Affairs Cooperative Studies Program. He has no other relevant financial disclosures to report.

Title
Corticosteroids: What’s their place in treating septic shock?
Corticosteroids: What’s their place in treating septic shock?

 

Hydrocortisone in combination with fludrocortisone significantly reduced 90-day mortality in septic shock patients in a double-blind, randomized, controlled trial.

Prior to this study, two large trials had displayed that corticosteroids were beneficial in improving hemodynamic status and organ function, but little was known about corticosteroids’ ability to increase survival in sepsis patients.

DigitalVision/Thinkstock
“[Corticosteroids] improve cardiovascular function by restoring effective blood volume through increased mineralocorticoid activity and by increasing systemic vascular resistance, an effect that is partly related to endothelial glucocorticoid receptors,” wrote Djillali Annane, MD, of the University of Paris and his colleagues in the New England Journal of Medicine.“This might explain why in our trial there was less need for vasopressors with hydrocortisone plus fludrocortisone than with placebo.”

The study, named the Activated Protein C and Corticosteroids for Human Septic Shock (APROCCHSS) trial, was designed to assess the benefit/risk ratio of using activated protein C – drotrecogin alfa (activated) – and corticosteroids together or separately in septic shock patients. The original design of the study included Xigris (drotrecogin alfa) and was composed of four parallel groups, but Xigris was removed from the market in October of 2011, so the study continued with only two parallel groups.

A total of 1,241 patients experiencing chronic septic shock were recruited into the two double-blind, parallel groups, with patients in one group receiving hydrocortisone plus fludrocortisone and the other receiving placebos. The placebos used in this study were similar in appearance to the actual treatment drugs. The placebos for hydrocortisone and fludrocortisone were either parenteral mannitol (133.6 mg), disodium phosphate (8.73 mg), and sodium phosphate (0.92 mg) or tablets of microcrystalline cellulose (59.098 mg), respectively.

Hydrocortisone was given intravenously every 6 hours as a 50-mg intravenous bolus, and fludrocortisone was given once a day as a 50-mcg tablet through a nasogastric tube. Patients in ICUs who had septic shock for less than 24 hours were included in the study. Septic shock was identified by the presence of a clinically or microbiologically documented infection, a Sequential Organ Failure Assessment score of 3 or 4 for at least two organs and for at least 6 hours, and receipt of vasopressor therapy for at least 6 hours.

After 90 days, 264 of 614 of the patients (43%) in the hydrocortisone/fludrocortisone group and almost half (49.1%) of 627 patients in the placebo group had died (P = .03). The relative risk of death was 0.88 (95% confidence interval, 0.78-0.99), which favored the hydrocortisone/fludrocortisone group. The researchers also observed that death was significantly lower in the hydrocortisone/fludrocortisone group, compared with the placebo group, at time of ICU discharge (35.4% vs. 41.0%, respectively; P = .04).

While mortality was reduced, patients still experienced adverse events. 326 of 614 (53.1%) patients in the hydrocortisone/fludrocortisone group and 363 of 626 patients (58.0%) in the placebo group experienced at least one serious adverse event by day 180 (P = 0.08).

“Seven-day treatment with a 50-mg intravenous bolus of hydrocortisone every 6 hours and a daily dose of 50 mcg of oral fludrocortisone resulted in lower mortality at day 90 and at ICU and hospital discharge than placebo among adults with septic shock,” concluded Dr. Annane and his coauthors.

The majority of researchers had no relevant financial disclosures to report, while some doctors received grants and personal fees unrelated to this study. This study was funded in part by public grants from the French Ministry of Health.

SOURCE: Annana A et al. NEJM. 2018 Feb 28. doi: 10.1056/NEJMoa1705716.

 

Hydrocortisone in combination with fludrocortisone significantly reduced 90-day mortality in septic shock patients in a double-blind, randomized, controlled trial.

Prior to this study, two large trials had displayed that corticosteroids were beneficial in improving hemodynamic status and organ function, but little was known about corticosteroids’ ability to increase survival in sepsis patients.

DigitalVision/Thinkstock
“[Corticosteroids] improve cardiovascular function by restoring effective blood volume through increased mineralocorticoid activity and by increasing systemic vascular resistance, an effect that is partly related to endothelial glucocorticoid receptors,” wrote Djillali Annane, MD, of the University of Paris and his colleagues in the New England Journal of Medicine.“This might explain why in our trial there was less need for vasopressors with hydrocortisone plus fludrocortisone than with placebo.”

The study, named the Activated Protein C and Corticosteroids for Human Septic Shock (APROCCHSS) trial, was designed to assess the benefit/risk ratio of using activated protein C – drotrecogin alfa (activated) – and corticosteroids together or separately in septic shock patients. The original design of the study included Xigris (drotrecogin alfa) and was composed of four parallel groups, but Xigris was removed from the market in October of 2011, so the study continued with only two parallel groups.

A total of 1,241 patients experiencing chronic septic shock were recruited into the two double-blind, parallel groups, with patients in one group receiving hydrocortisone plus fludrocortisone and the other receiving placebos. The placebos used in this study were similar in appearance to the actual treatment drugs. The placebos for hydrocortisone and fludrocortisone were either parenteral mannitol (133.6 mg), disodium phosphate (8.73 mg), and sodium phosphate (0.92 mg) or tablets of microcrystalline cellulose (59.098 mg), respectively.

Hydrocortisone was given intravenously every 6 hours as a 50-mg intravenous bolus, and fludrocortisone was given once a day as a 50-mcg tablet through a nasogastric tube. Patients in ICUs who had septic shock for less than 24 hours were included in the study. Septic shock was identified by the presence of a clinically or microbiologically documented infection, a Sequential Organ Failure Assessment score of 3 or 4 for at least two organs and for at least 6 hours, and receipt of vasopressor therapy for at least 6 hours.

After 90 days, 264 of 614 of the patients (43%) in the hydrocortisone/fludrocortisone group and almost half (49.1%) of 627 patients in the placebo group had died (P = .03). The relative risk of death was 0.88 (95% confidence interval, 0.78-0.99), which favored the hydrocortisone/fludrocortisone group. The researchers also observed that death was significantly lower in the hydrocortisone/fludrocortisone group, compared with the placebo group, at time of ICU discharge (35.4% vs. 41.0%, respectively; P = .04).

While mortality was reduced, patients still experienced adverse events. 326 of 614 (53.1%) patients in the hydrocortisone/fludrocortisone group and 363 of 626 patients (58.0%) in the placebo group experienced at least one serious adverse event by day 180 (P = 0.08).

“Seven-day treatment with a 50-mg intravenous bolus of hydrocortisone every 6 hours and a daily dose of 50 mcg of oral fludrocortisone resulted in lower mortality at day 90 and at ICU and hospital discharge than placebo among adults with septic shock,” concluded Dr. Annane and his coauthors.

The majority of researchers had no relevant financial disclosures to report, while some doctors received grants and personal fees unrelated to this study. This study was funded in part by public grants from the French Ministry of Health.

SOURCE: Annana A et al. NEJM. 2018 Feb 28. doi: 10.1056/NEJMoa1705716.

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Key clinical point: Hydrocortisone in combination with fludrocortisone significantly reduced 90-day mortality in septic shock patients.

Major finding: Mortality rates were lower in patients treated with hydrocortisone plus fludrocortisone, compared with patients treated with placebos (43% vs. 49.1%, respectively; P = .03).

Study details: A randomized, double-blind study of 1,241 patients with septic shock.

Disclosures: The majority of researchers had no relevant financial disclosures to report, while some doctors received grants and personal fees unrelated to this study. This study was funded in part by public grants from the French Ministry of Health.

Source: Annane A et al. NEJM. 2018 Feb 28. doi: 10.1056/NEJMoa1705716.

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On-demand nebulization in ICU equivalent to standard

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Among ICU patients receiving invasive ventilation, on-demand nebulization of acetylcysteine or salbutamol was noninferior to routine nebulization with both medications, according to the results of a randomized clinical trial presented by Frederique Paulus, RN, PhD.

In this study, adverse events such as tachyarrhythmia and agitation were less frequent with the on-demand approach, in which patients receive nebulization based on strict clinical indications, Dr. Paulus reported at the Critical Care Congress sponsored by the Society for Critical Care Medicine. The study was published simultaneously in JAMA.

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Dr. Frederique Paulus
“On-demand nebulization was noninferior to routine nebulization, but routine nebulization is associated with more side effects, so we think on-demand nebulization may be a reasonable alternative to routine nebulization,” said Dr. Paulus of the department of intensive care at the Academic Medical Center, University of Amsterdam, during her presentation.

The on-demand approach may also be cost saving, she noted, citing an economic analysis underway that is not yet ready for publication.

“In our ICU, it will save us 350,000 Euros a year,” she said. “In the Netherlands, 40,000 patients will be mechanically ventilated in a year, so it will save us millions in the Netherlands alone.”

The study included adult ICU patients who were expected not to be extubated for at least 24 hours. Dr. Paulus presented the primary analysis of the study, which included data for 922 patients who were randomized either to the on-demand group (n = 455) or the routine nebulization group (n = 467) and completed follow-up.

Patients assigned to the on-demand group received acetylcysteine-containing solutions if they had thick or tenacious secretions, or salbutamol-containing solutions if wheezing was observed or suspected or when findings were suggestive of lower-airway obstruction, according to the paper, published in JAMA.

 

 

SOURCE: Paulus F et al. (van Meenen DMP et al.) JAMA. 2018 Feb. doi: 10.1001/jama.2018.0949.

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Dr. Eric J. Gartman
Eric Gartman, MD, FCCP, comments: I would not say there is necessarily a standard way people do this, and practice patterns likely vary widely. There are some places where respiratory therapy has wide control of vented patients and often implements protocols, while at other places every vented patient has to have specific orders for things by the providers. I would find it very likely that more patients receive standing bronchodilator therapy than should (thus the reason for the study). Our practice pattern locally mirrors the idea of the study (where a patient's therapy is tailored to the reason for their intubation).

I would suspect local practice patterns with nebulized acytylcysteine to vary even more widely than bronchodilator administration strategies. 

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Dr. Eric J. Gartman
Eric Gartman, MD, FCCP, comments: I would not say there is necessarily a standard way people do this, and practice patterns likely vary widely. There are some places where respiratory therapy has wide control of vented patients and often implements protocols, while at other places every vented patient has to have specific orders for things by the providers. I would find it very likely that more patients receive standing bronchodilator therapy than should (thus the reason for the study). Our practice pattern locally mirrors the idea of the study (where a patient's therapy is tailored to the reason for their intubation).

I would suspect local practice patterns with nebulized acytylcysteine to vary even more widely than bronchodilator administration strategies. 

Body

Dr. Eric J. Gartman
Eric Gartman, MD, FCCP, comments: I would not say there is necessarily a standard way people do this, and practice patterns likely vary widely. There are some places where respiratory therapy has wide control of vented patients and often implements protocols, while at other places every vented patient has to have specific orders for things by the providers. I would find it very likely that more patients receive standing bronchodilator therapy than should (thus the reason for the study). Our practice pattern locally mirrors the idea of the study (where a patient's therapy is tailored to the reason for their intubation).

I would suspect local practice patterns with nebulized acytylcysteine to vary even more widely than bronchodilator administration strategies. 

 

Among ICU patients receiving invasive ventilation, on-demand nebulization of acetylcysteine or salbutamol was noninferior to routine nebulization with both medications, according to the results of a randomized clinical trial presented by Frederique Paulus, RN, PhD.

In this study, adverse events such as tachyarrhythmia and agitation were less frequent with the on-demand approach, in which patients receive nebulization based on strict clinical indications, Dr. Paulus reported at the Critical Care Congress sponsored by the Society for Critical Care Medicine. The study was published simultaneously in JAMA.

Andrew Bowser/Frontline Medical News
Dr. Frederique Paulus
“On-demand nebulization was noninferior to routine nebulization, but routine nebulization is associated with more side effects, so we think on-demand nebulization may be a reasonable alternative to routine nebulization,” said Dr. Paulus of the department of intensive care at the Academic Medical Center, University of Amsterdam, during her presentation.

The on-demand approach may also be cost saving, she noted, citing an economic analysis underway that is not yet ready for publication.

“In our ICU, it will save us 350,000 Euros a year,” she said. “In the Netherlands, 40,000 patients will be mechanically ventilated in a year, so it will save us millions in the Netherlands alone.”

The study included adult ICU patients who were expected not to be extubated for at least 24 hours. Dr. Paulus presented the primary analysis of the study, which included data for 922 patients who were randomized either to the on-demand group (n = 455) or the routine nebulization group (n = 467) and completed follow-up.

Patients assigned to the on-demand group received acetylcysteine-containing solutions if they had thick or tenacious secretions, or salbutamol-containing solutions if wheezing was observed or suspected or when findings were suggestive of lower-airway obstruction, according to the paper, published in JAMA.

 

 

SOURCE: Paulus F et al. (van Meenen DMP et al.) JAMA. 2018 Feb. doi: 10.1001/jama.2018.0949.

 

Among ICU patients receiving invasive ventilation, on-demand nebulization of acetylcysteine or salbutamol was noninferior to routine nebulization with both medications, according to the results of a randomized clinical trial presented by Frederique Paulus, RN, PhD.

In this study, adverse events such as tachyarrhythmia and agitation were less frequent with the on-demand approach, in which patients receive nebulization based on strict clinical indications, Dr. Paulus reported at the Critical Care Congress sponsored by the Society for Critical Care Medicine. The study was published simultaneously in JAMA.

Andrew Bowser/Frontline Medical News
Dr. Frederique Paulus
“On-demand nebulization was noninferior to routine nebulization, but routine nebulization is associated with more side effects, so we think on-demand nebulization may be a reasonable alternative to routine nebulization,” said Dr. Paulus of the department of intensive care at the Academic Medical Center, University of Amsterdam, during her presentation.

The on-demand approach may also be cost saving, she noted, citing an economic analysis underway that is not yet ready for publication.

“In our ICU, it will save us 350,000 Euros a year,” she said. “In the Netherlands, 40,000 patients will be mechanically ventilated in a year, so it will save us millions in the Netherlands alone.”

The study included adult ICU patients who were expected not to be extubated for at least 24 hours. Dr. Paulus presented the primary analysis of the study, which included data for 922 patients who were randomized either to the on-demand group (n = 455) or the routine nebulization group (n = 467) and completed follow-up.

Patients assigned to the on-demand group received acetylcysteine-containing solutions if they had thick or tenacious secretions, or salbutamol-containing solutions if wheezing was observed or suspected or when findings were suggestive of lower-airway obstruction, according to the paper, published in JAMA.

 

 

SOURCE: Paulus F et al. (van Meenen DMP et al.) JAMA. 2018 Feb. doi: 10.1001/jama.2018.0949.

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Key clinical point: Compared with routine nebulization with acetylcysteine or salbutamol, on-demand nebulization with acetylcysteine or salbutamol was noninferior among patients receiving invasive ventilation in the ICU.

Major finding: At day 28, the median number of ventilator-free days was 21 in the on-demand group and 20 in the routine care group.

Data source: Primary analysis of a randomized clinical trial including 922 adult patients who were expected to need at least 24 hours of invasive ventilation at one of seven ICUs in the Netherlands.

Disclosures: Authors reported no conflicts of interest related to the study.

Source: Paulus F et al. (van Meenen DMP et al.) JAMA. 2018 Feb. doi: 10.1001/jama.2018.0949.

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NIAID proposes 3-pronged plan for universal influenza vaccine

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Three specific research areas were proposed by the National Institute of Allergy and Infectious Diseases (NIAID) in its development plan for a universal influenza vaccine, as detailed in a report published online in the Journal of Infectious Diseases.

Anthony S. Fauci, MD, director of the NIAID, spoke with Frontline Medical News in an interview regarding the plan and noted that he and his colleagues felt that it was important to accelerate the effort for a universal vaccine.

Dr. Anthony Fauci
The plan will focus on: transmission, natural history, and pathogenesis studies utilizing prospective cohorts; influenza immunity and correlates of immune protection; and strategies in rational vaccine design to elicit broad, protective immune responses, according to Emily J. Erbelding, MD, MPH, director of microbiology and infectious diseases at the NIAID, and her associates in their report. They noted that the three research areas are not prioritized and that advances in each are expected to be interdependent.

“The strategic plan also includes a description of research resources essential to advancing these three research areas that [the] NIAID will develop, support, and provide for the scientific community,” wrote Dr. Erbelding and her coauthors.

The development plan comes 8 months after scientists from academia, industry, and government convened for the NIAID Pathway to a Universal Influenza Vaccine workshop to address knowledge gaps and strategy, which was summarized last year in the journal Immunity (2017;47: 599-603). The scientists at the workshop developed criteria that would define a universal vaccine and decided that a universal vaccine for influenza should do three things: be at least 75% effective against symptomatic influenza infection; protect against group I and II influenza A viruses; and have durable protections that lasts at least 1 year and preferably through multiple seasons.

“Clearly, a vaccine that would cover most or all seasonal strains of influenza and also provide protection during a pandemic is highly desirable,” wrote Catharine I. Paules, MD, of the University of Maryland, Baltimore, and her coauthors in the workshop summary.

Dr. Fauci told Frontline Medical News how “experts from all over the country addressed their thoughts and concerns with us last year [at the workshop], and now we have a development plan,” he said. “But the next step will be doing the research and finding more resources. ... The work is yet to be done.”

The development plan was published amid an ongoing historic flu season.

Dr. Fauci noted that this season had particular circumstances that made it worse than normal. “I don’t think that, had we had this plan in place a year ago, it would have had an impact on this flu season,” he said.

The authors reported no relevant financial conflicts and that the National Institutes of Health produced this plan.
 

SOURCE: Erbelding E et al. J Infect Dis. 2018 Feb 28. doi: 10.1093/infdis/jiy103.

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Three specific research areas were proposed by the National Institute of Allergy and Infectious Diseases (NIAID) in its development plan for a universal influenza vaccine, as detailed in a report published online in the Journal of Infectious Diseases.

Anthony S. Fauci, MD, director of the NIAID, spoke with Frontline Medical News in an interview regarding the plan and noted that he and his colleagues felt that it was important to accelerate the effort for a universal vaccine.

Dr. Anthony Fauci
The plan will focus on: transmission, natural history, and pathogenesis studies utilizing prospective cohorts; influenza immunity and correlates of immune protection; and strategies in rational vaccine design to elicit broad, protective immune responses, according to Emily J. Erbelding, MD, MPH, director of microbiology and infectious diseases at the NIAID, and her associates in their report. They noted that the three research areas are not prioritized and that advances in each are expected to be interdependent.

“The strategic plan also includes a description of research resources essential to advancing these three research areas that [the] NIAID will develop, support, and provide for the scientific community,” wrote Dr. Erbelding and her coauthors.

The development plan comes 8 months after scientists from academia, industry, and government convened for the NIAID Pathway to a Universal Influenza Vaccine workshop to address knowledge gaps and strategy, which was summarized last year in the journal Immunity (2017;47: 599-603). The scientists at the workshop developed criteria that would define a universal vaccine and decided that a universal vaccine for influenza should do three things: be at least 75% effective against symptomatic influenza infection; protect against group I and II influenza A viruses; and have durable protections that lasts at least 1 year and preferably through multiple seasons.

“Clearly, a vaccine that would cover most or all seasonal strains of influenza and also provide protection during a pandemic is highly desirable,” wrote Catharine I. Paules, MD, of the University of Maryland, Baltimore, and her coauthors in the workshop summary.

Dr. Fauci told Frontline Medical News how “experts from all over the country addressed their thoughts and concerns with us last year [at the workshop], and now we have a development plan,” he said. “But the next step will be doing the research and finding more resources. ... The work is yet to be done.”

The development plan was published amid an ongoing historic flu season.

Dr. Fauci noted that this season had particular circumstances that made it worse than normal. “I don’t think that, had we had this plan in place a year ago, it would have had an impact on this flu season,” he said.

The authors reported no relevant financial conflicts and that the National Institutes of Health produced this plan.
 

SOURCE: Erbelding E et al. J Infect Dis. 2018 Feb 28. doi: 10.1093/infdis/jiy103.

 

Three specific research areas were proposed by the National Institute of Allergy and Infectious Diseases (NIAID) in its development plan for a universal influenza vaccine, as detailed in a report published online in the Journal of Infectious Diseases.

Anthony S. Fauci, MD, director of the NIAID, spoke with Frontline Medical News in an interview regarding the plan and noted that he and his colleagues felt that it was important to accelerate the effort for a universal vaccine.

Dr. Anthony Fauci
The plan will focus on: transmission, natural history, and pathogenesis studies utilizing prospective cohorts; influenza immunity and correlates of immune protection; and strategies in rational vaccine design to elicit broad, protective immune responses, according to Emily J. Erbelding, MD, MPH, director of microbiology and infectious diseases at the NIAID, and her associates in their report. They noted that the three research areas are not prioritized and that advances in each are expected to be interdependent.

“The strategic plan also includes a description of research resources essential to advancing these three research areas that [the] NIAID will develop, support, and provide for the scientific community,” wrote Dr. Erbelding and her coauthors.

The development plan comes 8 months after scientists from academia, industry, and government convened for the NIAID Pathway to a Universal Influenza Vaccine workshop to address knowledge gaps and strategy, which was summarized last year in the journal Immunity (2017;47: 599-603). The scientists at the workshop developed criteria that would define a universal vaccine and decided that a universal vaccine for influenza should do three things: be at least 75% effective against symptomatic influenza infection; protect against group I and II influenza A viruses; and have durable protections that lasts at least 1 year and preferably through multiple seasons.

“Clearly, a vaccine that would cover most or all seasonal strains of influenza and also provide protection during a pandemic is highly desirable,” wrote Catharine I. Paules, MD, of the University of Maryland, Baltimore, and her coauthors in the workshop summary.

Dr. Fauci told Frontline Medical News how “experts from all over the country addressed their thoughts and concerns with us last year [at the workshop], and now we have a development plan,” he said. “But the next step will be doing the research and finding more resources. ... The work is yet to be done.”

The development plan was published amid an ongoing historic flu season.

Dr. Fauci noted that this season had particular circumstances that made it worse than normal. “I don’t think that, had we had this plan in place a year ago, it would have had an impact on this flu season,” he said.

The authors reported no relevant financial conflicts and that the National Institutes of Health produced this plan.
 

SOURCE: Erbelding E et al. J Infect Dis. 2018 Feb 28. doi: 10.1093/infdis/jiy103.

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Abruptio placenta brings increased cardiovascular risk – and soon

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ANAHEIM, CALIF.– Women who experience placental abruption are at significantly increased risk for multiple forms of cardiovascular disease beginning within the first few years after their pregnancy complication, according to a study of more than 1.6 million California women.

While gestational hypertension, preeclampsia, and fetal growth restriction have previously all been shown to be associated with increased risk of incident cardiovascular disease, this huge California study provides the first strong epidemiologic evidence that placental abruption is as well. Prior studies looking at the issue have been underpowered, Michael J. Healey, MD, said at the American Heart Association scientific sessions.

Bruce Jancin/Frontline Medical News
Dr. Michael J. Healy
Like preeclampsia and fetal growth restriction, placental abruption is a placental ischemic syndrome.

“Our hypothesis is that there might be some type of shared mechanism, probably involving microvascular dysfunction, that explains the relationships we see between these pregnancy complications and increased near-term risk of cardiovascular disease,” he explained in an interview.

Dr. Healy, a hospitalist attached to the heart failure service at the University of California, San Francisco, presented a retrospective study of a multiethnic cohort comprising 1,614,950 parous women aged 15-50 years who participated in the California Healthcare Cost and Utility Project during 2005-2009. Placental abruption occurred in 15,057 of them at a mean age of 29.2 years.

During a median 4.9 years of follow-up, women who experienced abruptio placenta were at 6% increased risk for heart failure, 11% greater risk for MI, 8% increased risk for hypertensive urgency, and 2% greater risk for myocardial infarction with no obstructive atherosclerosis (MINOCA) in an age- and race-adjusted analysis. All of these were statistically significant differences.

Of note, however, in a multivariate analysis fully adjusted for standard cardiovascular risk factors, as well as hypercoagulability, preterm birth, grand multiparity, and insurance status, placental abruption was independently associated with a 2.14-fold risk of MINOCA, but it was no longer linked to significantly increased risks of the other cardiovascular events.

The implication is that the increased risk of these other forms of cardiovascular disease is mediated through the women’s increased prevalence of the traditional cardiovascular risk factors, whereas a novel mechanism – most likely microvascular dysfunction – underlies the association between placental abruption and MINOCA, according to Dr. Healy.

He plans to extend this research by taking a look at the relationship between placental abruption and the various subtypes of MINOCA, including coronary dissection, vasospasm, thrombophilia disorders, and stress cardiomyopathy, in order to examine whether the increased risk posed by placental abruption is concentrated in certain forms of MINOCA. Data on MINOCA subtypes were recorded as part of the California project.

He reported having no financial conflicts of interest regarding his study.

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ANAHEIM, CALIF.– Women who experience placental abruption are at significantly increased risk for multiple forms of cardiovascular disease beginning within the first few years after their pregnancy complication, according to a study of more than 1.6 million California women.

While gestational hypertension, preeclampsia, and fetal growth restriction have previously all been shown to be associated with increased risk of incident cardiovascular disease, this huge California study provides the first strong epidemiologic evidence that placental abruption is as well. Prior studies looking at the issue have been underpowered, Michael J. Healey, MD, said at the American Heart Association scientific sessions.

Bruce Jancin/Frontline Medical News
Dr. Michael J. Healy
Like preeclampsia and fetal growth restriction, placental abruption is a placental ischemic syndrome.

“Our hypothesis is that there might be some type of shared mechanism, probably involving microvascular dysfunction, that explains the relationships we see between these pregnancy complications and increased near-term risk of cardiovascular disease,” he explained in an interview.

Dr. Healy, a hospitalist attached to the heart failure service at the University of California, San Francisco, presented a retrospective study of a multiethnic cohort comprising 1,614,950 parous women aged 15-50 years who participated in the California Healthcare Cost and Utility Project during 2005-2009. Placental abruption occurred in 15,057 of them at a mean age of 29.2 years.

During a median 4.9 years of follow-up, women who experienced abruptio placenta were at 6% increased risk for heart failure, 11% greater risk for MI, 8% increased risk for hypertensive urgency, and 2% greater risk for myocardial infarction with no obstructive atherosclerosis (MINOCA) in an age- and race-adjusted analysis. All of these were statistically significant differences.

Of note, however, in a multivariate analysis fully adjusted for standard cardiovascular risk factors, as well as hypercoagulability, preterm birth, grand multiparity, and insurance status, placental abruption was independently associated with a 2.14-fold risk of MINOCA, but it was no longer linked to significantly increased risks of the other cardiovascular events.

The implication is that the increased risk of these other forms of cardiovascular disease is mediated through the women’s increased prevalence of the traditional cardiovascular risk factors, whereas a novel mechanism – most likely microvascular dysfunction – underlies the association between placental abruption and MINOCA, according to Dr. Healy.

He plans to extend this research by taking a look at the relationship between placental abruption and the various subtypes of MINOCA, including coronary dissection, vasospasm, thrombophilia disorders, and stress cardiomyopathy, in order to examine whether the increased risk posed by placental abruption is concentrated in certain forms of MINOCA. Data on MINOCA subtypes were recorded as part of the California project.

He reported having no financial conflicts of interest regarding his study.

 

ANAHEIM, CALIF.– Women who experience placental abruption are at significantly increased risk for multiple forms of cardiovascular disease beginning within the first few years after their pregnancy complication, according to a study of more than 1.6 million California women.

While gestational hypertension, preeclampsia, and fetal growth restriction have previously all been shown to be associated with increased risk of incident cardiovascular disease, this huge California study provides the first strong epidemiologic evidence that placental abruption is as well. Prior studies looking at the issue have been underpowered, Michael J. Healey, MD, said at the American Heart Association scientific sessions.

Bruce Jancin/Frontline Medical News
Dr. Michael J. Healy
Like preeclampsia and fetal growth restriction, placental abruption is a placental ischemic syndrome.

“Our hypothesis is that there might be some type of shared mechanism, probably involving microvascular dysfunction, that explains the relationships we see between these pregnancy complications and increased near-term risk of cardiovascular disease,” he explained in an interview.

Dr. Healy, a hospitalist attached to the heart failure service at the University of California, San Francisco, presented a retrospective study of a multiethnic cohort comprising 1,614,950 parous women aged 15-50 years who participated in the California Healthcare Cost and Utility Project during 2005-2009. Placental abruption occurred in 15,057 of them at a mean age of 29.2 years.

During a median 4.9 years of follow-up, women who experienced abruptio placenta were at 6% increased risk for heart failure, 11% greater risk for MI, 8% increased risk for hypertensive urgency, and 2% greater risk for myocardial infarction with no obstructive atherosclerosis (MINOCA) in an age- and race-adjusted analysis. All of these were statistically significant differences.

Of note, however, in a multivariate analysis fully adjusted for standard cardiovascular risk factors, as well as hypercoagulability, preterm birth, grand multiparity, and insurance status, placental abruption was independently associated with a 2.14-fold risk of MINOCA, but it was no longer linked to significantly increased risks of the other cardiovascular events.

The implication is that the increased risk of these other forms of cardiovascular disease is mediated through the women’s increased prevalence of the traditional cardiovascular risk factors, whereas a novel mechanism – most likely microvascular dysfunction – underlies the association between placental abruption and MINOCA, according to Dr. Healy.

He plans to extend this research by taking a look at the relationship between placental abruption and the various subtypes of MINOCA, including coronary dissection, vasospasm, thrombophilia disorders, and stress cardiomyopathy, in order to examine whether the increased risk posed by placental abruption is concentrated in certain forms of MINOCA. Data on MINOCA subtypes were recorded as part of the California project.

He reported having no financial conflicts of interest regarding his study.

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Key clinical point: Placental abruption is associated with increased risk of maternal cardiovascular events within a few years after delivery.

Major finding: Placental abruption was independently associated with a 2.14-fold increased risk of myocardial infarction with no obstructive atherosclerosis during a median 4.9 years of follow-up.

Study details: This was a retrospective study of more than 1.6 million parous women enrolled in the California Healthcare Cost and Utilization Project, including 15,057 with placental abruption.

Disclosures: The study presenter reported having no financial conflicts of interest.

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Expert argues for improving MACRA, not scrapping it

Dr. Michael E. Nelson argues for improving MACRA, not scrapping it
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Even given the notable problems and challenges associated with Medicare’s Merit-based Incentive Payment System (MIPS), the program should be improved via pilot programs and demonstration projects, according to Gail R. Wilensky, PhD, economist and senior fellow at Project Hope and a former top health aide to President George H.W. Bush.

Dr. Gail Wilensky
The Medicare Payment Advisory Committee (MedPAC) is set to recommend to Congress that the MIPS portion of the value-based reforms enacted under the Medicare Access and CHIP Reauthorization Act (MACRA) be eliminated and replaced with a Voluntary Value Program. MedPAC’s report is due to Congress in March.



“Although I agree with MedPAC about the problems it has identified, I am also concerned about the commission’s proposal,” Dr. Wilensky wrote in an editorial published in the New England Journal of Medicine (doi: 10.1056/NEJMp1801673). She noted that a lack of support from major medical associations, combined with the impending midterm elections, means that it would be challenging to get a legislative fix through Congress.

Read her suggestions on how to improve MIPS in the New England Journal of Medicine.

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Michael E. Nelson, MD, FCCP, comments: Dr. Wilensky made some cogent arguments as to why scrapping MIPS may not be such a good idea. In my mind, however, the final paragraph of the editorial was the most important. “Practicing physicians need make their views about the MIPS and its alternatives known to their representative medical groups and, if necessary, to their representatives in Congress as well. In the past, practicing clinicians have been woefully bad at making their voices heard. Now is a good time for that to change.” Your future is being decided without you. The squeaky wheel gets the grease.

Dr. Michael E. Nelson

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Michael E. Nelson, MD, FCCP, comments: Dr. Wilensky made some cogent arguments as to why scrapping MIPS may not be such a good idea. In my mind, however, the final paragraph of the editorial was the most important. “Practicing physicians need make their views about the MIPS and its alternatives known to their representative medical groups and, if necessary, to their representatives in Congress as well. In the past, practicing clinicians have been woefully bad at making their voices heard. Now is a good time for that to change.” Your future is being decided without you. The squeaky wheel gets the grease.

Dr. Michael E. Nelson

Body

Michael E. Nelson, MD, FCCP, comments: Dr. Wilensky made some cogent arguments as to why scrapping MIPS may not be such a good idea. In my mind, however, the final paragraph of the editorial was the most important. “Practicing physicians need make their views about the MIPS and its alternatives known to their representative medical groups and, if necessary, to their representatives in Congress as well. In the past, practicing clinicians have been woefully bad at making their voices heard. Now is a good time for that to change.” Your future is being decided without you. The squeaky wheel gets the grease.

Dr. Michael E. Nelson

Title
Dr. Michael E. Nelson argues for improving MACRA, not scrapping it
Dr. Michael E. Nelson argues for improving MACRA, not scrapping it

 

Even given the notable problems and challenges associated with Medicare’s Merit-based Incentive Payment System (MIPS), the program should be improved via pilot programs and demonstration projects, according to Gail R. Wilensky, PhD, economist and senior fellow at Project Hope and a former top health aide to President George H.W. Bush.

Dr. Gail Wilensky
The Medicare Payment Advisory Committee (MedPAC) is set to recommend to Congress that the MIPS portion of the value-based reforms enacted under the Medicare Access and CHIP Reauthorization Act (MACRA) be eliminated and replaced with a Voluntary Value Program. MedPAC’s report is due to Congress in March.



“Although I agree with MedPAC about the problems it has identified, I am also concerned about the commission’s proposal,” Dr. Wilensky wrote in an editorial published in the New England Journal of Medicine (doi: 10.1056/NEJMp1801673). She noted that a lack of support from major medical associations, combined with the impending midterm elections, means that it would be challenging to get a legislative fix through Congress.

Read her suggestions on how to improve MIPS in the New England Journal of Medicine.

 

Even given the notable problems and challenges associated with Medicare’s Merit-based Incentive Payment System (MIPS), the program should be improved via pilot programs and demonstration projects, according to Gail R. Wilensky, PhD, economist and senior fellow at Project Hope and a former top health aide to President George H.W. Bush.

Dr. Gail Wilensky
The Medicare Payment Advisory Committee (MedPAC) is set to recommend to Congress that the MIPS portion of the value-based reforms enacted under the Medicare Access and CHIP Reauthorization Act (MACRA) be eliminated and replaced with a Voluntary Value Program. MedPAC’s report is due to Congress in March.



“Although I agree with MedPAC about the problems it has identified, I am also concerned about the commission’s proposal,” Dr. Wilensky wrote in an editorial published in the New England Journal of Medicine (doi: 10.1056/NEJMp1801673). She noted that a lack of support from major medical associations, combined with the impending midterm elections, means that it would be challenging to get a legislative fix through Congress.

Read her suggestions on how to improve MIPS in the New England Journal of Medicine.

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Mycosis fungoides increases risk for second cancers

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– Patients with mycosis fungoides are at increased risk for developing other cancers and should be screened for second primary and hematologic malignancies, results of a cancer registry survey suggest.

A study of data on 6,196 patients included in 18 population-based cancer registries comprising the SEER-18 (Surveillance, Epidemiology, and End Results 18) database who were diagnosed and followed from 2000 to 2014 showed that 514 (8.3%) developed second cancers, compared with the 70.8 secondary malignancies that would be expected in the general population. This difference translated into a standardized incidence ratio (SIR) of 7.3, reported Amrita Goyal, MD, and Aleksandr Lazaryan, MD, PhD, of the University of Minnesota, Minneapolis.

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Dr. Amrita Goyal
“If you compare the rate of the development of these malignancies to a population of gender-matched controls, the rates of second malignancy are substantially higher in patients with MF [mycosis fungoides] than you would expect,” Dr. Goyal said in an interview at the annual T-cell Lymphoma Forum.

Patients with MF have a 500% greater risk for developing a second solid malignancy and a 2700% greater likelihood of developing a second hematologic malignancy, she said.

The investigators hypothesized that MF predisposes patients to second malignancies because of its immunocompromising effects.

Dr. Goyal said that, although the SEER data set does not include information on disease stage for all patients, when they looked at a separate cohort of 173 University of Minnesota patients with MF, they saw that patients with higher-stage MF were significantly more likely to develop secondary malignancies than patients with lower-stage disease.

The investigators looked at the actual and expected cancer incidence rates for the SEER-18 population sample, and used data on age, sex, race, and calendar year to generate incidence estimates for the general population.

They found that 514 patients in the SEER-18 population developed a total of 170 second primary hematologic malignancies, for a SIR of 27.4, compared with the general population. The most common hematologic cancers were Hodgkin lymphoma (SIR 69.8) and non-Hodgkin lymphoma (SIR 46.5), and other second hematologic malignancies included multiple myeloma (SIR 4.5), chronic lymphocytic leukemia (SIR 9.1). and acute leukemias (SIR 8.1).

The most frequently occurring second solid tumors included cancers of the nose, nasal cavity, and middle ear (SIR 30.4); thyroid (SIR 16.1); brain (SIR 15.1); and breast (SIR 8.0).

Other solid tumors with an approximately 400%-500% higher incidence included cancers of the prostate, bladder, colon, and kidneys.

Dr. Goyal and Dr. Lazaryan recommend development of targeted cancer screening strategies for patients with MF.

The study was funded in part by an American Society of Hematology HONORS grant. The researchers reported having no conflicts of interest. The T-Cell Lymphoma Forum is held by Jonathan Wood & Associates, which is owned by the same company as this news organization.

SOURCE: Goyal A et al. TCLF 2018 Abstract EP18_2.

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– Patients with mycosis fungoides are at increased risk for developing other cancers and should be screened for second primary and hematologic malignancies, results of a cancer registry survey suggest.

A study of data on 6,196 patients included in 18 population-based cancer registries comprising the SEER-18 (Surveillance, Epidemiology, and End Results 18) database who were diagnosed and followed from 2000 to 2014 showed that 514 (8.3%) developed second cancers, compared with the 70.8 secondary malignancies that would be expected in the general population. This difference translated into a standardized incidence ratio (SIR) of 7.3, reported Amrita Goyal, MD, and Aleksandr Lazaryan, MD, PhD, of the University of Minnesota, Minneapolis.

Neil Osterweil/Frontline Medical News
Dr. Amrita Goyal
“If you compare the rate of the development of these malignancies to a population of gender-matched controls, the rates of second malignancy are substantially higher in patients with MF [mycosis fungoides] than you would expect,” Dr. Goyal said in an interview at the annual T-cell Lymphoma Forum.

Patients with MF have a 500% greater risk for developing a second solid malignancy and a 2700% greater likelihood of developing a second hematologic malignancy, she said.

The investigators hypothesized that MF predisposes patients to second malignancies because of its immunocompromising effects.

Dr. Goyal said that, although the SEER data set does not include information on disease stage for all patients, when they looked at a separate cohort of 173 University of Minnesota patients with MF, they saw that patients with higher-stage MF were significantly more likely to develop secondary malignancies than patients with lower-stage disease.

The investigators looked at the actual and expected cancer incidence rates for the SEER-18 population sample, and used data on age, sex, race, and calendar year to generate incidence estimates for the general population.

They found that 514 patients in the SEER-18 population developed a total of 170 second primary hematologic malignancies, for a SIR of 27.4, compared with the general population. The most common hematologic cancers were Hodgkin lymphoma (SIR 69.8) and non-Hodgkin lymphoma (SIR 46.5), and other second hematologic malignancies included multiple myeloma (SIR 4.5), chronic lymphocytic leukemia (SIR 9.1). and acute leukemias (SIR 8.1).

The most frequently occurring second solid tumors included cancers of the nose, nasal cavity, and middle ear (SIR 30.4); thyroid (SIR 16.1); brain (SIR 15.1); and breast (SIR 8.0).

Other solid tumors with an approximately 400%-500% higher incidence included cancers of the prostate, bladder, colon, and kidneys.

Dr. Goyal and Dr. Lazaryan recommend development of targeted cancer screening strategies for patients with MF.

The study was funded in part by an American Society of Hematology HONORS grant. The researchers reported having no conflicts of interest. The T-Cell Lymphoma Forum is held by Jonathan Wood & Associates, which is owned by the same company as this news organization.

SOURCE: Goyal A et al. TCLF 2018 Abstract EP18_2.

 

– Patients with mycosis fungoides are at increased risk for developing other cancers and should be screened for second primary and hematologic malignancies, results of a cancer registry survey suggest.

A study of data on 6,196 patients included in 18 population-based cancer registries comprising the SEER-18 (Surveillance, Epidemiology, and End Results 18) database who were diagnosed and followed from 2000 to 2014 showed that 514 (8.3%) developed second cancers, compared with the 70.8 secondary malignancies that would be expected in the general population. This difference translated into a standardized incidence ratio (SIR) of 7.3, reported Amrita Goyal, MD, and Aleksandr Lazaryan, MD, PhD, of the University of Minnesota, Minneapolis.

Neil Osterweil/Frontline Medical News
Dr. Amrita Goyal
“If you compare the rate of the development of these malignancies to a population of gender-matched controls, the rates of second malignancy are substantially higher in patients with MF [mycosis fungoides] than you would expect,” Dr. Goyal said in an interview at the annual T-cell Lymphoma Forum.

Patients with MF have a 500% greater risk for developing a second solid malignancy and a 2700% greater likelihood of developing a second hematologic malignancy, she said.

The investigators hypothesized that MF predisposes patients to second malignancies because of its immunocompromising effects.

Dr. Goyal said that, although the SEER data set does not include information on disease stage for all patients, when they looked at a separate cohort of 173 University of Minnesota patients with MF, they saw that patients with higher-stage MF were significantly more likely to develop secondary malignancies than patients with lower-stage disease.

The investigators looked at the actual and expected cancer incidence rates for the SEER-18 population sample, and used data on age, sex, race, and calendar year to generate incidence estimates for the general population.

They found that 514 patients in the SEER-18 population developed a total of 170 second primary hematologic malignancies, for a SIR of 27.4, compared with the general population. The most common hematologic cancers were Hodgkin lymphoma (SIR 69.8) and non-Hodgkin lymphoma (SIR 46.5), and other second hematologic malignancies included multiple myeloma (SIR 4.5), chronic lymphocytic leukemia (SIR 9.1). and acute leukemias (SIR 8.1).

The most frequently occurring second solid tumors included cancers of the nose, nasal cavity, and middle ear (SIR 30.4); thyroid (SIR 16.1); brain (SIR 15.1); and breast (SIR 8.0).

Other solid tumors with an approximately 400%-500% higher incidence included cancers of the prostate, bladder, colon, and kidneys.

Dr. Goyal and Dr. Lazaryan recommend development of targeted cancer screening strategies for patients with MF.

The study was funded in part by an American Society of Hematology HONORS grant. The researchers reported having no conflicts of interest. The T-Cell Lymphoma Forum is held by Jonathan Wood & Associates, which is owned by the same company as this news organization.

SOURCE: Goyal A et al. TCLF 2018 Abstract EP18_2.

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Key clinical point: Mycosis fungoides (MF) predisposes patients to second primary malignancies.

Major finding: Patients with MF have a 730% greater likelihood of developing a second primary hematologic malignancy.

Study details: A retrospective review of data on 6,196 patients in the SEER-18 database.

Disclosures: The study was funded in part by an American Society of Hematology HONORS grant. The researchers reported having no conflicts of interest.

Source: Goyal A et al. TCLF 2018 Abstract EP18_2.

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Characteristics, Frequency, and Disposition of Patients With a HeartMate II Left Ventricular Assist Device Presenting to the ED

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This article is adapted from preliminary data presented at the 2012 American College of Emergency Physicians’ Research Forum.

Introduction

Approximately 6.5 million adults in the United States have heart failure, accounting for nearly 1 million ED visits annually.1 Advanced heart failure is particularly difficult to treat, and is associated with significant morbidity and mortality. While medical therapy is the initial treatment for patients with advanced heart failure, it has limited effectiveness; therefore, at the present time, heart transplant is the most effective treatment for heart failure refractory to medical management.

According to the 2013 Registry of the International Society for Heart and Lung Transplantation, 4,096 cardiac transplants were performed worldwide in 2011, approximately 2,000 of which were done in the United States.2

The average age of a heart transplant recipient in the United States is 55 years.2 In 2017, there were nearly 4,000 patients on the United Network for Organ Sharing, the organization that manages the national transplant waiting list in the United States and matches donors to recipients.3 Unfortunately, the number of patients requiring a heart transplant far exceeds the number of registered donors, and a large number of patients must wait years for transplantation. In addition to those awaiting a heart transplant, there are many patients with advanced heart failure who are not suitable candidates for transplant (usually due to age).

Left Ventricular Assist Devices

As of December 31, 2016, a total of 22,866 US Food and Drug Administration (FDA)-approved devices were listed in the Interagency Registry for Mechanically Assisted Circulatory Support, 17,016 of which were continuous-flow (CF) left ventricular assist devices (LVADs), including the HeartMate II (HMII) (Abbott Laboratories) and the HeartWare Ventricular Assist Device (HVAD) (Medtronic).4 Left ventricular assist devices, which have been in use for over 30 years, have evolved into smaller, quieter, and more durable devices. The current generation of LVADs has a CF design (as opposed to the older pulsatile-flow [PF] design). More importantly, CF LVADs are associated with higher survival rates and increased quality of life than the earlier PF models.5 For these reasons, CF LVADs are being used much more frequently today. As previously noted, LVADs serve as a temporizing measure for patients awaiting a heart transplant (ie, bridge-to-transplant therapy [BTT]) or as the primary treatment for patients who are not suitable candidates for transplant (ie, destination therapy [DT]).

The percentage of patients receiving an LVAD as a DT has increased from around 15% between 2006 to 2007 to nearly 46% in 2014.6Recently, several reports following LVAD patients demonstrated a reverse remodeling of the heart and recovery of native cardiac function that was sufficient enough in some patients as to permit LVAD removal (ie, bridge to recovery).7 In the United States, the number of patients undergoing LVAD removal due to recovery remains fewer than 3%.6With the increase in the number of patients receiving LVADs, there is an increased likelihood of LVAD patients presenting to an ED due to device-related complications. Recognized complications associated with LVADs include thrombosis, infection, bleeding, and issues with volume status.5,7 However, the frequency of LVAD-associated complications and the final disposition of these patients is less well known.

HeartMate II Patient ED Presentation Study

Purpose

The purpose of our study was to identify the reasons for LVAD patient presentation to the ED, the frequency of these presentations, and the final disposition of these patients. Our institution, Sentara Norfolk General Hospital (SNGH), is a level I trauma and a tertiary care referral center, and it is the only hospital in a large area of Virginia to perform LVAD implantation.

Our study involved only patients implanted with the HMII LVAD.

Methods

Patients and Study Design

This was a retrospective study of patients with an HMII LVAD who presented to the SNGH ED between April 1, 2009 and September 9, 2012. All patients implanted with an HMII LVAD during the study period were assigned a study number linking the patient to their medical record number and social security number. Study numbers were assigned at the time of LVAD implantation by one of the investigators. This document was kept in a secure and locked location in the department of emergency medicine and was not accessible to anyone other than study investigators.

The electronic medical records were retrospectively reviewed to identify any HMII LVAD patient presenting to the SNGH ED during the study period. Information abstracted from the ED medical records included patient age, sex, initial complaint, final diagnosis, and disposition. Only the patient’s assigned study number was used on the data collection form, and no personal identifying information was present.

This study was granted approval for human subject research by the Eastern Virginia Medical School Institutional Review Board. Eligible patients included all patients with an HMII LVAD implanted during the study period. Study patients who presented to the SNGH ED between April 1, 2009 and September 9, 2012 were identified by a retrospective chart review. These patients were instructed to specifically seek care at the SNGH ED in the event of an emergency. There were no exclusion criteria.

Data were collected and reported in real numbers and percentages. No formal statistical analysis was used in evaluating the results.

Results

Between April 1, 2009 and September 9, 2012, there were a total of 98 patients with an HMII LVAD that had been implanted during the study period at SNGH. The average patient age was 53.6 years, with a range from age 20 years to 78 years. Sixty-seven (68%) of the patients enrolled in the study required at least one ED visit. The HMII LVAD patients who presented to the ED ranged in age from 20 years to 78 years, with an average age of 53.1 years. The average number of ED visits by these 67 patients was 3.7, with a range of 1 to 12. Approximately 56% of the ED visits were directly LVAD-related. In all, 67 patients were responsible for a total of 248 ED visits.

The two most common reasons for presentation to the ED involved bleeding and volume overload. A total of 37 ED visits (14.9%), were related to bleeding, which included gastrointestinal (GI) bleeding (18/37 or 49%), epistaxis, hematuria, gingival bleeding, and postoperative bleeding following tooth extraction.

Volume overload accounted for 37 ED visits (14.9%), and the most common presenting symptom in these patients was shortness of breath. Other reasons patients presented to the ED were weakness/lightheadedness/dizziness/syncope (24/9.6%), device malfunction (20/8.1%), infection (7/2.8%), and transient ischemic attack/cerebrovascular accident (6/2.4%). For infection-related ED visits, two presentations (2.9%) involved a driveline infection. Common causes for ED visits related to device malfunction included battery failure and device-alarm activation. Overall, 142 of the 248 total ED visits (57.3%) resulted in hospital admission. One patient in the study presented in cardiac arrest and could not be resuscitated.

The remaining 108 LVAD patient ED visits (44%), did not appear to be related to the presence of the LVAD, but rather represented common reasons for presentation to an ED. These other non-LVAD-related reasons for presentation to the ED were due to motor vehicle incidents (3); assault (2); dental pain (3); mechanical fall (5); and upper respiratory tract infection (4), and represented small groupings of patient reasons for an ED visit.

Examples of singular reasons for presentation to the ED included one patient who presented with suicidal ideation, and another patient who presented for evaluation of symptoms suspicious for a sexually transmitted infection.

Discussion

As the number of patients with advanced heart failure continues to increase, the number of those with an LVAD also increases. Between 2006 and June 2013, nearly 9,000 adult patients in the United States received a durable LVAD.6 In the early years of LVAD implantation, patients were restricted to remain in proximity of geographical areas surrounding academic health care centers. An increased comfort level by both physicians and patients now allows LVAD patients to reside in more distant communities. This increase in LVAD implantation, coupled with the widening patient distribution, make it important for every emergency physician (EP) to have a working knowledge of the device and its associated complications. To date, the characteristics and frequency of LVAD patient presentations to the ED have not been well characterized.

Left ventricular assist devices are considered in patients who have significant symptoms associated with poor LV function or who cannot maintain normal hemodynamics and vital organ function. Continuous-flow LVADs account for almost all devices currently implanted. During our data-collection period, there were two FDA-approved implantable LVADs—the HMII, approved for BTT in 2008 and for DT in 2010; and the HVAD approved for BTT in 2012. In August 2017, HeartMate III (Abbott Laboratories) was approved by the FDA. All patients enrolled in our study were recipients of the HMII device, as this was the only type of LVAD implant performed at our hospital. Current survival with the HMII LVAD is 80% at 1 year and 69% at 2 years, and there has not been shown to be a significant difference when stratified by era of implant.6

Device Designs and Structures

The pump of the HMII is inserted into the abdominal cavity, whereas the HVAD is implanted in the chest cavity, with the inflow cannula in the apex of the LV and the outflow cannula connecting to the proximal aorta. Blood is continuously pumped through the system.8,9 The pump is connected to a driveline that exits the body and connects to a controller. Continuous-flow devices have either an axial or centrifugal blood pump. Axial devices have an impeller that is connected to ball-and-cup bearings that accelerate blood along its axis. Newer axial flow pumps incorporate magnetic levitation of the rotor and do not require the use of bearings. Centrifugal devices accelerate blood circumferentially with a rotor that is suspended within in the blood pool by electromagnetic or hydrodynamic forces.10 The controller is powered by two external batteries or connected to a power base unit where the pump can be interrogated. The controller is usually housed in a garment worn by the patient, one that also includes the batteries. The controller can also be powered by a base unit that can be plugged into an electrical outlet.11

 

 

There are, and continue to be, advances in both LVAD design and function. Since the time period of our study, changes have been made in the outflow bend relief (the tube at the junction of the outflow cannula and the pump housing designed to prevent kinking of the outflow cannula) and the LVAD controller. Older controllers have been replaced with newer models, but many of the LVAD pumps in this article remain in service.

Anticoagulation Therapy

Patients who have a CF LVAD require anticoagulation therapy with warfarin to a target international normalized ratio (INR) of 2 to 3, in addition to aspirin therapy of 325 mg daily.8,9Newer oral anticoagulant drugs are not routinely given to patients who have a CF LVAD.

Cardiopulmonary Evaluation

With CF LVADs, blood is pumped continuously, and a constant, machine-like murmur can be heard on auscultation rather than the typical heart sounds. Patients who have an LVAD may not have palpable arterial pulses. Doppler evaluation of the brachial artery and a manual blood pressure (BP) cuff are used to listen for the start of Korotkoff sounds as the cuff is released. The pressure at which the first sound is heard is used to estimate the patient’s mean arterial pressure (MAP) at the time when there is no pulse; and the systolic BP (SBP) is heard at the time when there is pulse. Patients with a CF LVAD with nonpulsatile flow should have a MAP between 70 mm Hg and 90 mm Hg (HMII), or 70 mm Hg and 80 mm Hg (HVAD). Patients who have a CF LVAD with a palpable pulse should have an SBP less than 120 mm Hg (HMII) or 105 mm Hg (HVAD). Readings outside of these ranges require an adjustment in the patient’s antihypertensive therapy, since high BP increases the risk of stroke and can impair the cardiac support provided by the LVAD.8Low BP may be the result of inadequate pump speed, dehydration, inflow cannula obstruction, or pump thrombus.

Bleeding

In our study, bleeding and volume overload were the two most common reasons LVAD patients presented to the ED. Interestingly, in a systematic review of clinical outcomes following CF LVAD implantation, bleeding was the most commonly recorded adverse event.12In fact, the majority of patients in all of the studies reviewed experienced at least one bleeding event. In one study of 139 HMII LVAD patients, the risk of bleeding was greatest within the first two weeks, and early bleeding was associated with increased mortality.13The most common source of bleeding complications in patients with a CF LVAD are GI, similar to our study.14

In a review and meta-analysis by Draper et al,15of GI bleeding in 1,697 patients with CF LVADs, the pooled prevalence was 23%.Subgroup analysis demonstrated an increased risk of bleeding in older patients and in those who had an elevated serum creatinine level.15 Upper GI bleeding occurred in 48% of patients, lower GI bleeding in 22%, small-bowel bleeding in 15%, and bleeding at an unknown site in 19%. The most common cause of the bleeding was from arteriovenous malformations (AVMs).15 In their review, Draper et al15 found a 9.3% prevalence of recurrent GI bleeding and a pooled event rate for an all-cause mortality rate of 23%.

They also noted that the increased risk of GI bleeding in CF LVAD patients is multifactorial. For example, there was decreased activity of type 2 von Willebrand factor multimers in patients with CF LVADs, leading to an acquired von Willebrand syndrome.15

Another finding seen in this review was that CF devices lead to a low pulse-pressure system, which is thought to cause some degree of intestinal hypoperfusion, potentially leading to vascular dilation and AVM formation.15 Based on findings, a neurovascular etiology involving increased sympathetic tone resulting in smooth muscle relaxation and AVM formation has been proposed. Lastly, the anticoagulation required with the CF LVADs to prevent pump thrombosis also increases the risk of GI bleeding, especially when combined with aspirin or other antiplatelet agents which are routinely prescribed.15

Volume Overload

Interestingly, in our study, volume overload as a cause for ED presentation was the same as for bleeding complications. In the systematic review of clinical outcomes in CF LVAD patients, volume overload or ongoing heart failure occurred in 18% of patients 1 year after device implantation.12

The clinical presentation of patients experiencing volume overload is typically dyspnea and fatigue; on physical examination they will frequently demonstrate evidence of fluid retention, such as dependent edema and pulmonary congestion.16Causes of volume overload in the LVAD patient includes medication noncompliance, inadequate pump speed, device malfunction, right ventricular failure, impaired renal function, and cardiac tamponade.16 These patients will frequently have MAPs greater than 90 mm Hg, and may require treatment with diuretics, calcium channel blockers, beta-blockers, or angiotensin-converting enzyme inhibitors.8

Weakness, Lightheadedness, Dizziness, Syncope

In our study, some combination of weakness, lightheadedness, dizziness, and syncope accounted for the third most common cause of ED presentation (9.6%). In the majority of cases, this was due to dehydration. Usually, these patients will have a MAP less than 60 mm Hg. Unfortunately, patients with pump thrombosis, sepsis, or cannula malposition can also present with a low MAP. It is important to differentiate the cause, as the management is quite different, depending on the etiology. Bedside ultrasound can play an important role in evaluating the volume status and cannula position.8 In addition, emergent consult with the patients ventricular assist device (VAD) treatment team is critical.8 Pump thrombus is a medical emergency and is usually associated with hematuria without red blood cells in the urine, acute kidney injury, and marked elevations in lactate dehydrogenase and serum free hemoglobin.8 If not treated promptly, renal failure and death may result. If dehydration is the cause, gentle rehydration with intravenous normal saline and electrolyte replacement may be all that is required.

Device Malfunction

Device malfunction was the next most common reason for ED presentation in our study, at 8.1%. This category included a number of different events, including battery failure, driveline fracture, and pump thrombosis. According to McIlvennan et al,12 causes of device malfunction include thrombus formation with hemolysis, mechanical failure of the impeller, and driveline lead fractures with electrical failure.Again, the VAD team should be consulted immediately, and the EP should plug the LVAD into a hospital power base, if available, to conserve battery life. If power is interrupted, the pump will stop working. The EP should examine all of the connections from the percutaneous lead to the controller and from the controller to the batteries to ensure they are intact. The exit site for the percutaneous lead should be examined for evidence of trauma or signs of infection. The patient should also be asked about recent trauma to the driveline.

Neurological Events

Interestingly, in other reviews, neurological events, including ischemic stroke, hemorrhagic stroke, and transient ischemic attack occur with higher frequency than was the case in the study, and are relatively common complications that can result in severe morbidity and mortality.12In the Interagency Registry for Mechanically Assisted Circulatory Support report, there was a 3% risk of stroke at 1 month, 5% at 3 months, 7% at 6 months, 11% at 12 months, 17% at 24 months, and 19% at 36 months post-implant.6,12Similarly, the HMII DT Trial demonstrated rates of ischemic and hemorrhagic stroke as high as 8% and 11% respectively, within the first 2 years following LVAD placement.5,6In our study, neurological events accounted for only six (2.4%) of ED visits. It is unclear why our numbers were less than those reported by others.

Cardiac Events and Management

During the study period, one LVAD patient presented to the ED in cardiac arrest. Patients who have an LVAD and are in cardiac arrest have unique considerations that deserve discussion. If the LVAD pump has stopped functioning, connections between the system controller and the pump and power source must be checked, as loose connections need to be refitted and the pump restarted. It is important to note that when an LVAD ceases operation, blood becomes stagnant in the pump and conduits. Delays of even several minutes pose a significant risk for pump thrombosis, stroke, and thromboembolism when the device is restarted. If the pump does not restart and the patient is connected to batteries, the batteries should be replaced with a new, fully charged pair, or the device should be connected to a base unit.17

Due to the location of the outflow graft on the aorta and the inflow conduit in the LV apex, external chest compressions pose a risk of dislodging the device and causing fatal hemorrhage. Clinical judgment should be used when deciding to perform external chest compressions. A recent American Heart Association scientific statement concluded that withholding chest compression in a patient with an LVAD who is truly in circulatory failure that is not attributable to a device failure would cause more harm to the patient than the potential to dislodge the device.18

Direct cardiac massage, performed by a skilled surgeon may be effective in patients that have had recent device implantation, especially if prior to mediastinal healing.16 If external defibrillation/cardioversion is required, the percutaneous lead should not be disconnected from the system controller and the pump should not be stopped prior to the delivery of a shock.17

Study Limitations

This was a retrospective study and has the limitations common to all such studies. It is possible that some of the patients in our study sought care at a hospital ED outside of our system, and therefore were not included in our study. This, however, is exceedingly unlikely as the cardiologists and care team continually emphasized and instructed all patients in our study only to present to the study hospital ED for any complaint. Similarly, the various emergency medical services agencies for our region were also instructed to bring all LVAD patients to the study hospital.

 

 

Another limitation of our study is the relatively small total number of patients (98) and that our findings may not apply to other patient populations. This limitation, however, would be true for any hospital system that limits the type of LVAD implant procedure to one manufacturer (HMII in this instance).

Conclusion

Emergency physicians must be prepared to evaluate the LVAD patient presenting to the ED. A little over 55% of the time, the visit will be directly related to the LVAD; in the remainder of cases, patient presentation will be due to a non-LVAD-related cause. At initial presentation, however, the EP should assume that the ED visit is related to the LVAD, until a thorough history and physical examination can exclude otherwise.

Because of the high incidence of GI bleeding in LVAD patients, a rectal examination for blood in the stool should be performed for any complaint that may be related, such as generalized weakness, syncope, or shortness of breath. In the majority of cases, a complete blood count; complete metabolic profile, including lactic acid dehydrogenase; and coagulation studies, including prothrombin time and INRs, are indicated. Most patients with an LVAD will require a member of the VAD team (typically the perfusionist or biomedical engineer) to interrogate the controller if there is any concern about its function, including alarm sounding or lights flashing.

References

1. Benjamin EJ, Blaha MJ, Chiuve SE, et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics-2017 update: a report from the American Heart Association. Circulation. 2017;135(10):e146-e603. doi:10.1161/CIR.0000000000000485. Erratum in: Circulation. 2017;135(1):e646. doi:10.1161/CIR.0000000000000491.

2. Lund LH, Edwards LB, Kucheryavaya AY, et al. The Registry of the International Society for Heart and Lung Transplantation: thirtieth official adult heart transplant report—2013; focus theme: age. J Heart Lung Transplant. 2013;32(10):951-964. doi:10.1016/j.healun.2013.08.006.

3. UNOS (United Network for Organ Sharing) Web site. https://unos.org/data/transplant-trends/waiting-list-candidates-by-organ-type/. Accessed February 8, 2018.

4. Kirklin JK, Pagani FD, Kormos RL, et al. Eighth annual INTERMACS report: Special focus on framing the impact of adverse events. J Heart Lung Transplant. 2017;36(10):1080-1086. doi:10.1016/j.healun.2017.07.005.

5. Slaughter MS, Rogers JG, Milano CA, et al. Advanced heart failure treated with continuous flow left ventricular assist device. N Engl J Med. 2009;361(23):2241-2251. doi:10.1056/NEJMoa0909938.

6. Kirklin JK, Naftel DC, Pagani FD, et al. Seventh INTERMACS annual report: 15,000 patients and counting. J Heart Lung Transplant. 2015;34(12):1495-1504. doi:10.1016/j.healun.2015.10.003.

7. Ambardekar AV, Buttrick PM. Reverse remodeling with left ventricular assist devices: a review of clinical, cellular and molecular effects. Circ Heart Fail. 2011;4(2):224-233. doi:10.1161/CIRCHEARTFAILURE.110.959684.

8. Slaughter MS, Pagani FD, Rogers JG, et al. Clinical management of continuous-flow left ventricular assist devices in advanced heart failure. J Heart Lung Transplant. 2010;29 (suppl 4):1-39. doi:10.1016/j.healun.2010.01.011.

9. Lo BM, Devine AS. Patients with left ventricular assist devices. Critical Decisions in Emergency Medicine. 2014;28(7):2-9.

10. Feldman D, Pamboukian SV, Teuteberg JJ, et al. The 2013 International Society for Heart and Lung Transplantation guidelines for mechanical circulatory support: executive summary. J Heart Lung Transplant. 2013;32(2):157-187. doi:10.1016/j.healun.2012.09.013.

11. Miller LW, Pagani FD, Russell SD, et al. Use of a continuous-flow device in patients awaiting heart transplantation. N Engl J Med. 2007;357(9):885-896. doi:10.1056/NEJMoa067758.

12. McIlvennan CK, Magid KH, Ambardekar AV, et al. Clinical outcomes following continuous-flow left ventricular assist device: a systematic review. Circ Heart Fail. 2014;7(6):1003-1013. doi:10.1161/Circheartfailure.114.001391.

13. Mulloy DP, Bhamidipati CM, Stone ML, et al. Cryoablation during left ventricular assist device implantation reduces postoperative ventricular tachyarrhythmias. J Thorac Cardiovasc Surg. 2013;145(5):1207-1213. doi:10.1016/j.jtcvs.2012.03.061.

14. Stern DR, Kazam J, Edwards P, et al. Increased incidence of gastrointestinal bleeding following implantation of the Heartmate II LVAD. J Card Surg. 2010;25(3):352-356. doi:10.1111/j.1540-8191.2010.01025.x.

15. Draper KV, Huang RJ, Gerson LB. GI bleeding in patients with continuous-flow left ventricular assist devices: a systematic review and meta-analysis. Gastrointest Endosc. 2014;80(3):435-446. doi:10.1016/j.gie.2014.03.040.

16. Aissaoui N, Morshuis M, Diebold B, et al. Heart failure while on ventricular assist device support: a true clinical entity? Arch Cardiovasc Dis. 2013:106(1):44-51. doi:10.1016/j.acvd.2012.09.006.

17. Thoratec HeartMate II Left Ventricular Assist System (LVAS) Information and Emergency Assistance Guide. Thoratec Corporation Web site. http://www.thoratec.com/_assets/download-tracker/HM_II_Info_Emergency_Assist_Guide_US_103873B_ENGLISH.pdf. Accessed July 5, 2017.

18. Peberdy MA, Gluck JA, Ornato JP, et al; American Heart Association Emergency Cardiovascular Care Committee; Council on Cardiopulmonary, Critical Care, Perioperative, and Resuscitation; Council on Cardiovascular Diseases in the Young; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular and Stroke Nursing; and Council on Clinical Cardiology. Cardiopulmonary resuscitation in adults and children with mechanical circulatory support a scientific statement from the American Heart Association. Circulation. 2017;135(24):e1115-e1134. doi:10.1161/CIR.0000000000000504.

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Authors’ Disclosure Statement: Dr Herre reports that he is a coinvestigator for the Multicenter Study of MagLev Technology in Patients Undergoing Mechanical Circulatory Support Therapy With HeartMate 3 (MOMENTUM 3) trial. The other authors report no actual or potential conflict of interest in relation to this article.

Dr Devine is an assistant professor in the department of emergency medicine, Eastern Virginia Medical School; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Knapp is a professor and residency program director, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Lo is an associate professor, emergency medicine residency program, Eastern Virginia Medical School, Norfolk; medical director, Sentara Norfolk General Hospital, Virginia; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Bono is a professor and vice chairman, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Harbin is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Jennings is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Gogel is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk. Dr Johnson is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk. Dr Bernstein is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia. Dr Alimard is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia. Dr Old is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia. Ms Hoedt Sentara Cardiology Specialists, Norfolk, Virginia. Dr Herre is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia.

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Authors’ Disclosure Statement: Dr Herre reports that he is a coinvestigator for the Multicenter Study of MagLev Technology in Patients Undergoing Mechanical Circulatory Support Therapy With HeartMate 3 (MOMENTUM 3) trial. The other authors report no actual or potential conflict of interest in relation to this article.

Dr Devine is an assistant professor in the department of emergency medicine, Eastern Virginia Medical School; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Knapp is a professor and residency program director, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Lo is an associate professor, emergency medicine residency program, Eastern Virginia Medical School, Norfolk; medical director, Sentara Norfolk General Hospital, Virginia; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Bono is a professor and vice chairman, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Harbin is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Jennings is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Gogel is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk. Dr Johnson is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk. Dr Bernstein is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia. Dr Alimard is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia. Dr Old is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia. Ms Hoedt Sentara Cardiology Specialists, Norfolk, Virginia. Dr Herre is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia.

Author and Disclosure Information

Authors’ Disclosure Statement: Dr Herre reports that he is a coinvestigator for the Multicenter Study of MagLev Technology in Patients Undergoing Mechanical Circulatory Support Therapy With HeartMate 3 (MOMENTUM 3) trial. The other authors report no actual or potential conflict of interest in relation to this article.

Dr Devine is an assistant professor in the department of emergency medicine, Eastern Virginia Medical School; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Knapp is a professor and residency program director, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Lo is an associate professor, emergency medicine residency program, Eastern Virginia Medical School, Norfolk; medical director, Sentara Norfolk General Hospital, Virginia; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Bono is a professor and vice chairman, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Harbin is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Jennings is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk; and a member of Emergency Physicians of Tidewater, Norfolk. Dr Gogel is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk. Dr Johnson is an emergency physician, department of emergency medicine, Eastern Virginia Medical School, Norfolk. Dr Bernstein is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia. Dr Alimard is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia. Dr Old is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia. Ms Hoedt Sentara Cardiology Specialists, Norfolk, Virginia. Dr Herre is a cardiologist, Sentara Cardiology Specialists, Norfolk, Virginia.

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This article is adapted from preliminary data presented at the 2012 American College of Emergency Physicians’ Research Forum.
This article is adapted from preliminary data presented at the 2012 American College of Emergency Physicians’ Research Forum.

Introduction

Approximately 6.5 million adults in the United States have heart failure, accounting for nearly 1 million ED visits annually.1 Advanced heart failure is particularly difficult to treat, and is associated with significant morbidity and mortality. While medical therapy is the initial treatment for patients with advanced heart failure, it has limited effectiveness; therefore, at the present time, heart transplant is the most effective treatment for heart failure refractory to medical management.

According to the 2013 Registry of the International Society for Heart and Lung Transplantation, 4,096 cardiac transplants were performed worldwide in 2011, approximately 2,000 of which were done in the United States.2

The average age of a heart transplant recipient in the United States is 55 years.2 In 2017, there were nearly 4,000 patients on the United Network for Organ Sharing, the organization that manages the national transplant waiting list in the United States and matches donors to recipients.3 Unfortunately, the number of patients requiring a heart transplant far exceeds the number of registered donors, and a large number of patients must wait years for transplantation. In addition to those awaiting a heart transplant, there are many patients with advanced heart failure who are not suitable candidates for transplant (usually due to age).

Left Ventricular Assist Devices

As of December 31, 2016, a total of 22,866 US Food and Drug Administration (FDA)-approved devices were listed in the Interagency Registry for Mechanically Assisted Circulatory Support, 17,016 of which were continuous-flow (CF) left ventricular assist devices (LVADs), including the HeartMate II (HMII) (Abbott Laboratories) and the HeartWare Ventricular Assist Device (HVAD) (Medtronic).4 Left ventricular assist devices, which have been in use for over 30 years, have evolved into smaller, quieter, and more durable devices. The current generation of LVADs has a CF design (as opposed to the older pulsatile-flow [PF] design). More importantly, CF LVADs are associated with higher survival rates and increased quality of life than the earlier PF models.5 For these reasons, CF LVADs are being used much more frequently today. As previously noted, LVADs serve as a temporizing measure for patients awaiting a heart transplant (ie, bridge-to-transplant therapy [BTT]) or as the primary treatment for patients who are not suitable candidates for transplant (ie, destination therapy [DT]).

The percentage of patients receiving an LVAD as a DT has increased from around 15% between 2006 to 2007 to nearly 46% in 2014.6Recently, several reports following LVAD patients demonstrated a reverse remodeling of the heart and recovery of native cardiac function that was sufficient enough in some patients as to permit LVAD removal (ie, bridge to recovery).7 In the United States, the number of patients undergoing LVAD removal due to recovery remains fewer than 3%.6With the increase in the number of patients receiving LVADs, there is an increased likelihood of LVAD patients presenting to an ED due to device-related complications. Recognized complications associated with LVADs include thrombosis, infection, bleeding, and issues with volume status.5,7 However, the frequency of LVAD-associated complications and the final disposition of these patients is less well known.

HeartMate II Patient ED Presentation Study

Purpose

The purpose of our study was to identify the reasons for LVAD patient presentation to the ED, the frequency of these presentations, and the final disposition of these patients. Our institution, Sentara Norfolk General Hospital (SNGH), is a level I trauma and a tertiary care referral center, and it is the only hospital in a large area of Virginia to perform LVAD implantation.

Our study involved only patients implanted with the HMII LVAD.

Methods

Patients and Study Design

This was a retrospective study of patients with an HMII LVAD who presented to the SNGH ED between April 1, 2009 and September 9, 2012. All patients implanted with an HMII LVAD during the study period were assigned a study number linking the patient to their medical record number and social security number. Study numbers were assigned at the time of LVAD implantation by one of the investigators. This document was kept in a secure and locked location in the department of emergency medicine and was not accessible to anyone other than study investigators.

The electronic medical records were retrospectively reviewed to identify any HMII LVAD patient presenting to the SNGH ED during the study period. Information abstracted from the ED medical records included patient age, sex, initial complaint, final diagnosis, and disposition. Only the patient’s assigned study number was used on the data collection form, and no personal identifying information was present.

This study was granted approval for human subject research by the Eastern Virginia Medical School Institutional Review Board. Eligible patients included all patients with an HMII LVAD implanted during the study period. Study patients who presented to the SNGH ED between April 1, 2009 and September 9, 2012 were identified by a retrospective chart review. These patients were instructed to specifically seek care at the SNGH ED in the event of an emergency. There were no exclusion criteria.

Data were collected and reported in real numbers and percentages. No formal statistical analysis was used in evaluating the results.

Results

Between April 1, 2009 and September 9, 2012, there were a total of 98 patients with an HMII LVAD that had been implanted during the study period at SNGH. The average patient age was 53.6 years, with a range from age 20 years to 78 years. Sixty-seven (68%) of the patients enrolled in the study required at least one ED visit. The HMII LVAD patients who presented to the ED ranged in age from 20 years to 78 years, with an average age of 53.1 years. The average number of ED visits by these 67 patients was 3.7, with a range of 1 to 12. Approximately 56% of the ED visits were directly LVAD-related. In all, 67 patients were responsible for a total of 248 ED visits.

The two most common reasons for presentation to the ED involved bleeding and volume overload. A total of 37 ED visits (14.9%), were related to bleeding, which included gastrointestinal (GI) bleeding (18/37 or 49%), epistaxis, hematuria, gingival bleeding, and postoperative bleeding following tooth extraction.

Volume overload accounted for 37 ED visits (14.9%), and the most common presenting symptom in these patients was shortness of breath. Other reasons patients presented to the ED were weakness/lightheadedness/dizziness/syncope (24/9.6%), device malfunction (20/8.1%), infection (7/2.8%), and transient ischemic attack/cerebrovascular accident (6/2.4%). For infection-related ED visits, two presentations (2.9%) involved a driveline infection. Common causes for ED visits related to device malfunction included battery failure and device-alarm activation. Overall, 142 of the 248 total ED visits (57.3%) resulted in hospital admission. One patient in the study presented in cardiac arrest and could not be resuscitated.

The remaining 108 LVAD patient ED visits (44%), did not appear to be related to the presence of the LVAD, but rather represented common reasons for presentation to an ED. These other non-LVAD-related reasons for presentation to the ED were due to motor vehicle incidents (3); assault (2); dental pain (3); mechanical fall (5); and upper respiratory tract infection (4), and represented small groupings of patient reasons for an ED visit.

Examples of singular reasons for presentation to the ED included one patient who presented with suicidal ideation, and another patient who presented for evaluation of symptoms suspicious for a sexually transmitted infection.

Discussion

As the number of patients with advanced heart failure continues to increase, the number of those with an LVAD also increases. Between 2006 and June 2013, nearly 9,000 adult patients in the United States received a durable LVAD.6 In the early years of LVAD implantation, patients were restricted to remain in proximity of geographical areas surrounding academic health care centers. An increased comfort level by both physicians and patients now allows LVAD patients to reside in more distant communities. This increase in LVAD implantation, coupled with the widening patient distribution, make it important for every emergency physician (EP) to have a working knowledge of the device and its associated complications. To date, the characteristics and frequency of LVAD patient presentations to the ED have not been well characterized.

Left ventricular assist devices are considered in patients who have significant symptoms associated with poor LV function or who cannot maintain normal hemodynamics and vital organ function. Continuous-flow LVADs account for almost all devices currently implanted. During our data-collection period, there were two FDA-approved implantable LVADs—the HMII, approved for BTT in 2008 and for DT in 2010; and the HVAD approved for BTT in 2012. In August 2017, HeartMate III (Abbott Laboratories) was approved by the FDA. All patients enrolled in our study were recipients of the HMII device, as this was the only type of LVAD implant performed at our hospital. Current survival with the HMII LVAD is 80% at 1 year and 69% at 2 years, and there has not been shown to be a significant difference when stratified by era of implant.6

Device Designs and Structures

The pump of the HMII is inserted into the abdominal cavity, whereas the HVAD is implanted in the chest cavity, with the inflow cannula in the apex of the LV and the outflow cannula connecting to the proximal aorta. Blood is continuously pumped through the system.8,9 The pump is connected to a driveline that exits the body and connects to a controller. Continuous-flow devices have either an axial or centrifugal blood pump. Axial devices have an impeller that is connected to ball-and-cup bearings that accelerate blood along its axis. Newer axial flow pumps incorporate magnetic levitation of the rotor and do not require the use of bearings. Centrifugal devices accelerate blood circumferentially with a rotor that is suspended within in the blood pool by electromagnetic or hydrodynamic forces.10 The controller is powered by two external batteries or connected to a power base unit where the pump can be interrogated. The controller is usually housed in a garment worn by the patient, one that also includes the batteries. The controller can also be powered by a base unit that can be plugged into an electrical outlet.11

 

 

There are, and continue to be, advances in both LVAD design and function. Since the time period of our study, changes have been made in the outflow bend relief (the tube at the junction of the outflow cannula and the pump housing designed to prevent kinking of the outflow cannula) and the LVAD controller. Older controllers have been replaced with newer models, but many of the LVAD pumps in this article remain in service.

Anticoagulation Therapy

Patients who have a CF LVAD require anticoagulation therapy with warfarin to a target international normalized ratio (INR) of 2 to 3, in addition to aspirin therapy of 325 mg daily.8,9Newer oral anticoagulant drugs are not routinely given to patients who have a CF LVAD.

Cardiopulmonary Evaluation

With CF LVADs, blood is pumped continuously, and a constant, machine-like murmur can be heard on auscultation rather than the typical heart sounds. Patients who have an LVAD may not have palpable arterial pulses. Doppler evaluation of the brachial artery and a manual blood pressure (BP) cuff are used to listen for the start of Korotkoff sounds as the cuff is released. The pressure at which the first sound is heard is used to estimate the patient’s mean arterial pressure (MAP) at the time when there is no pulse; and the systolic BP (SBP) is heard at the time when there is pulse. Patients with a CF LVAD with nonpulsatile flow should have a MAP between 70 mm Hg and 90 mm Hg (HMII), or 70 mm Hg and 80 mm Hg (HVAD). Patients who have a CF LVAD with a palpable pulse should have an SBP less than 120 mm Hg (HMII) or 105 mm Hg (HVAD). Readings outside of these ranges require an adjustment in the patient’s antihypertensive therapy, since high BP increases the risk of stroke and can impair the cardiac support provided by the LVAD.8Low BP may be the result of inadequate pump speed, dehydration, inflow cannula obstruction, or pump thrombus.

Bleeding

In our study, bleeding and volume overload were the two most common reasons LVAD patients presented to the ED. Interestingly, in a systematic review of clinical outcomes following CF LVAD implantation, bleeding was the most commonly recorded adverse event.12In fact, the majority of patients in all of the studies reviewed experienced at least one bleeding event. In one study of 139 HMII LVAD patients, the risk of bleeding was greatest within the first two weeks, and early bleeding was associated with increased mortality.13The most common source of bleeding complications in patients with a CF LVAD are GI, similar to our study.14

In a review and meta-analysis by Draper et al,15of GI bleeding in 1,697 patients with CF LVADs, the pooled prevalence was 23%.Subgroup analysis demonstrated an increased risk of bleeding in older patients and in those who had an elevated serum creatinine level.15 Upper GI bleeding occurred in 48% of patients, lower GI bleeding in 22%, small-bowel bleeding in 15%, and bleeding at an unknown site in 19%. The most common cause of the bleeding was from arteriovenous malformations (AVMs).15 In their review, Draper et al15 found a 9.3% prevalence of recurrent GI bleeding and a pooled event rate for an all-cause mortality rate of 23%.

They also noted that the increased risk of GI bleeding in CF LVAD patients is multifactorial. For example, there was decreased activity of type 2 von Willebrand factor multimers in patients with CF LVADs, leading to an acquired von Willebrand syndrome.15

Another finding seen in this review was that CF devices lead to a low pulse-pressure system, which is thought to cause some degree of intestinal hypoperfusion, potentially leading to vascular dilation and AVM formation.15 Based on findings, a neurovascular etiology involving increased sympathetic tone resulting in smooth muscle relaxation and AVM formation has been proposed. Lastly, the anticoagulation required with the CF LVADs to prevent pump thrombosis also increases the risk of GI bleeding, especially when combined with aspirin or other antiplatelet agents which are routinely prescribed.15

Volume Overload

Interestingly, in our study, volume overload as a cause for ED presentation was the same as for bleeding complications. In the systematic review of clinical outcomes in CF LVAD patients, volume overload or ongoing heart failure occurred in 18% of patients 1 year after device implantation.12

The clinical presentation of patients experiencing volume overload is typically dyspnea and fatigue; on physical examination they will frequently demonstrate evidence of fluid retention, such as dependent edema and pulmonary congestion.16Causes of volume overload in the LVAD patient includes medication noncompliance, inadequate pump speed, device malfunction, right ventricular failure, impaired renal function, and cardiac tamponade.16 These patients will frequently have MAPs greater than 90 mm Hg, and may require treatment with diuretics, calcium channel blockers, beta-blockers, or angiotensin-converting enzyme inhibitors.8

Weakness, Lightheadedness, Dizziness, Syncope

In our study, some combination of weakness, lightheadedness, dizziness, and syncope accounted for the third most common cause of ED presentation (9.6%). In the majority of cases, this was due to dehydration. Usually, these patients will have a MAP less than 60 mm Hg. Unfortunately, patients with pump thrombosis, sepsis, or cannula malposition can also present with a low MAP. It is important to differentiate the cause, as the management is quite different, depending on the etiology. Bedside ultrasound can play an important role in evaluating the volume status and cannula position.8 In addition, emergent consult with the patients ventricular assist device (VAD) treatment team is critical.8 Pump thrombus is a medical emergency and is usually associated with hematuria without red blood cells in the urine, acute kidney injury, and marked elevations in lactate dehydrogenase and serum free hemoglobin.8 If not treated promptly, renal failure and death may result. If dehydration is the cause, gentle rehydration with intravenous normal saline and electrolyte replacement may be all that is required.

Device Malfunction

Device malfunction was the next most common reason for ED presentation in our study, at 8.1%. This category included a number of different events, including battery failure, driveline fracture, and pump thrombosis. According to McIlvennan et al,12 causes of device malfunction include thrombus formation with hemolysis, mechanical failure of the impeller, and driveline lead fractures with electrical failure.Again, the VAD team should be consulted immediately, and the EP should plug the LVAD into a hospital power base, if available, to conserve battery life. If power is interrupted, the pump will stop working. The EP should examine all of the connections from the percutaneous lead to the controller and from the controller to the batteries to ensure they are intact. The exit site for the percutaneous lead should be examined for evidence of trauma or signs of infection. The patient should also be asked about recent trauma to the driveline.

Neurological Events

Interestingly, in other reviews, neurological events, including ischemic stroke, hemorrhagic stroke, and transient ischemic attack occur with higher frequency than was the case in the study, and are relatively common complications that can result in severe morbidity and mortality.12In the Interagency Registry for Mechanically Assisted Circulatory Support report, there was a 3% risk of stroke at 1 month, 5% at 3 months, 7% at 6 months, 11% at 12 months, 17% at 24 months, and 19% at 36 months post-implant.6,12Similarly, the HMII DT Trial demonstrated rates of ischemic and hemorrhagic stroke as high as 8% and 11% respectively, within the first 2 years following LVAD placement.5,6In our study, neurological events accounted for only six (2.4%) of ED visits. It is unclear why our numbers were less than those reported by others.

Cardiac Events and Management

During the study period, one LVAD patient presented to the ED in cardiac arrest. Patients who have an LVAD and are in cardiac arrest have unique considerations that deserve discussion. If the LVAD pump has stopped functioning, connections between the system controller and the pump and power source must be checked, as loose connections need to be refitted and the pump restarted. It is important to note that when an LVAD ceases operation, blood becomes stagnant in the pump and conduits. Delays of even several minutes pose a significant risk for pump thrombosis, stroke, and thromboembolism when the device is restarted. If the pump does not restart and the patient is connected to batteries, the batteries should be replaced with a new, fully charged pair, or the device should be connected to a base unit.17

Due to the location of the outflow graft on the aorta and the inflow conduit in the LV apex, external chest compressions pose a risk of dislodging the device and causing fatal hemorrhage. Clinical judgment should be used when deciding to perform external chest compressions. A recent American Heart Association scientific statement concluded that withholding chest compression in a patient with an LVAD who is truly in circulatory failure that is not attributable to a device failure would cause more harm to the patient than the potential to dislodge the device.18

Direct cardiac massage, performed by a skilled surgeon may be effective in patients that have had recent device implantation, especially if prior to mediastinal healing.16 If external defibrillation/cardioversion is required, the percutaneous lead should not be disconnected from the system controller and the pump should not be stopped prior to the delivery of a shock.17

Study Limitations

This was a retrospective study and has the limitations common to all such studies. It is possible that some of the patients in our study sought care at a hospital ED outside of our system, and therefore were not included in our study. This, however, is exceedingly unlikely as the cardiologists and care team continually emphasized and instructed all patients in our study only to present to the study hospital ED for any complaint. Similarly, the various emergency medical services agencies for our region were also instructed to bring all LVAD patients to the study hospital.

 

 

Another limitation of our study is the relatively small total number of patients (98) and that our findings may not apply to other patient populations. This limitation, however, would be true for any hospital system that limits the type of LVAD implant procedure to one manufacturer (HMII in this instance).

Conclusion

Emergency physicians must be prepared to evaluate the LVAD patient presenting to the ED. A little over 55% of the time, the visit will be directly related to the LVAD; in the remainder of cases, patient presentation will be due to a non-LVAD-related cause. At initial presentation, however, the EP should assume that the ED visit is related to the LVAD, until a thorough history and physical examination can exclude otherwise.

Because of the high incidence of GI bleeding in LVAD patients, a rectal examination for blood in the stool should be performed for any complaint that may be related, such as generalized weakness, syncope, or shortness of breath. In the majority of cases, a complete blood count; complete metabolic profile, including lactic acid dehydrogenase; and coagulation studies, including prothrombin time and INRs, are indicated. Most patients with an LVAD will require a member of the VAD team (typically the perfusionist or biomedical engineer) to interrogate the controller if there is any concern about its function, including alarm sounding or lights flashing.

Introduction

Approximately 6.5 million adults in the United States have heart failure, accounting for nearly 1 million ED visits annually.1 Advanced heart failure is particularly difficult to treat, and is associated with significant morbidity and mortality. While medical therapy is the initial treatment for patients with advanced heart failure, it has limited effectiveness; therefore, at the present time, heart transplant is the most effective treatment for heart failure refractory to medical management.

According to the 2013 Registry of the International Society for Heart and Lung Transplantation, 4,096 cardiac transplants were performed worldwide in 2011, approximately 2,000 of which were done in the United States.2

The average age of a heart transplant recipient in the United States is 55 years.2 In 2017, there were nearly 4,000 patients on the United Network for Organ Sharing, the organization that manages the national transplant waiting list in the United States and matches donors to recipients.3 Unfortunately, the number of patients requiring a heart transplant far exceeds the number of registered donors, and a large number of patients must wait years for transplantation. In addition to those awaiting a heart transplant, there are many patients with advanced heart failure who are not suitable candidates for transplant (usually due to age).

Left Ventricular Assist Devices

As of December 31, 2016, a total of 22,866 US Food and Drug Administration (FDA)-approved devices were listed in the Interagency Registry for Mechanically Assisted Circulatory Support, 17,016 of which were continuous-flow (CF) left ventricular assist devices (LVADs), including the HeartMate II (HMII) (Abbott Laboratories) and the HeartWare Ventricular Assist Device (HVAD) (Medtronic).4 Left ventricular assist devices, which have been in use for over 30 years, have evolved into smaller, quieter, and more durable devices. The current generation of LVADs has a CF design (as opposed to the older pulsatile-flow [PF] design). More importantly, CF LVADs are associated with higher survival rates and increased quality of life than the earlier PF models.5 For these reasons, CF LVADs are being used much more frequently today. As previously noted, LVADs serve as a temporizing measure for patients awaiting a heart transplant (ie, bridge-to-transplant therapy [BTT]) or as the primary treatment for patients who are not suitable candidates for transplant (ie, destination therapy [DT]).

The percentage of patients receiving an LVAD as a DT has increased from around 15% between 2006 to 2007 to nearly 46% in 2014.6Recently, several reports following LVAD patients demonstrated a reverse remodeling of the heart and recovery of native cardiac function that was sufficient enough in some patients as to permit LVAD removal (ie, bridge to recovery).7 In the United States, the number of patients undergoing LVAD removal due to recovery remains fewer than 3%.6With the increase in the number of patients receiving LVADs, there is an increased likelihood of LVAD patients presenting to an ED due to device-related complications. Recognized complications associated with LVADs include thrombosis, infection, bleeding, and issues with volume status.5,7 However, the frequency of LVAD-associated complications and the final disposition of these patients is less well known.

HeartMate II Patient ED Presentation Study

Purpose

The purpose of our study was to identify the reasons for LVAD patient presentation to the ED, the frequency of these presentations, and the final disposition of these patients. Our institution, Sentara Norfolk General Hospital (SNGH), is a level I trauma and a tertiary care referral center, and it is the only hospital in a large area of Virginia to perform LVAD implantation.

Our study involved only patients implanted with the HMII LVAD.

Methods

Patients and Study Design

This was a retrospective study of patients with an HMII LVAD who presented to the SNGH ED between April 1, 2009 and September 9, 2012. All patients implanted with an HMII LVAD during the study period were assigned a study number linking the patient to their medical record number and social security number. Study numbers were assigned at the time of LVAD implantation by one of the investigators. This document was kept in a secure and locked location in the department of emergency medicine and was not accessible to anyone other than study investigators.

The electronic medical records were retrospectively reviewed to identify any HMII LVAD patient presenting to the SNGH ED during the study period. Information abstracted from the ED medical records included patient age, sex, initial complaint, final diagnosis, and disposition. Only the patient’s assigned study number was used on the data collection form, and no personal identifying information was present.

This study was granted approval for human subject research by the Eastern Virginia Medical School Institutional Review Board. Eligible patients included all patients with an HMII LVAD implanted during the study period. Study patients who presented to the SNGH ED between April 1, 2009 and September 9, 2012 were identified by a retrospective chart review. These patients were instructed to specifically seek care at the SNGH ED in the event of an emergency. There were no exclusion criteria.

Data were collected and reported in real numbers and percentages. No formal statistical analysis was used in evaluating the results.

Results

Between April 1, 2009 and September 9, 2012, there were a total of 98 patients with an HMII LVAD that had been implanted during the study period at SNGH. The average patient age was 53.6 years, with a range from age 20 years to 78 years. Sixty-seven (68%) of the patients enrolled in the study required at least one ED visit. The HMII LVAD patients who presented to the ED ranged in age from 20 years to 78 years, with an average age of 53.1 years. The average number of ED visits by these 67 patients was 3.7, with a range of 1 to 12. Approximately 56% of the ED visits were directly LVAD-related. In all, 67 patients were responsible for a total of 248 ED visits.

The two most common reasons for presentation to the ED involved bleeding and volume overload. A total of 37 ED visits (14.9%), were related to bleeding, which included gastrointestinal (GI) bleeding (18/37 or 49%), epistaxis, hematuria, gingival bleeding, and postoperative bleeding following tooth extraction.

Volume overload accounted for 37 ED visits (14.9%), and the most common presenting symptom in these patients was shortness of breath. Other reasons patients presented to the ED were weakness/lightheadedness/dizziness/syncope (24/9.6%), device malfunction (20/8.1%), infection (7/2.8%), and transient ischemic attack/cerebrovascular accident (6/2.4%). For infection-related ED visits, two presentations (2.9%) involved a driveline infection. Common causes for ED visits related to device malfunction included battery failure and device-alarm activation. Overall, 142 of the 248 total ED visits (57.3%) resulted in hospital admission. One patient in the study presented in cardiac arrest and could not be resuscitated.

The remaining 108 LVAD patient ED visits (44%), did not appear to be related to the presence of the LVAD, but rather represented common reasons for presentation to an ED. These other non-LVAD-related reasons for presentation to the ED were due to motor vehicle incidents (3); assault (2); dental pain (3); mechanical fall (5); and upper respiratory tract infection (4), and represented small groupings of patient reasons for an ED visit.

Examples of singular reasons for presentation to the ED included one patient who presented with suicidal ideation, and another patient who presented for evaluation of symptoms suspicious for a sexually transmitted infection.

Discussion

As the number of patients with advanced heart failure continues to increase, the number of those with an LVAD also increases. Between 2006 and June 2013, nearly 9,000 adult patients in the United States received a durable LVAD.6 In the early years of LVAD implantation, patients were restricted to remain in proximity of geographical areas surrounding academic health care centers. An increased comfort level by both physicians and patients now allows LVAD patients to reside in more distant communities. This increase in LVAD implantation, coupled with the widening patient distribution, make it important for every emergency physician (EP) to have a working knowledge of the device and its associated complications. To date, the characteristics and frequency of LVAD patient presentations to the ED have not been well characterized.

Left ventricular assist devices are considered in patients who have significant symptoms associated with poor LV function or who cannot maintain normal hemodynamics and vital organ function. Continuous-flow LVADs account for almost all devices currently implanted. During our data-collection period, there were two FDA-approved implantable LVADs—the HMII, approved for BTT in 2008 and for DT in 2010; and the HVAD approved for BTT in 2012. In August 2017, HeartMate III (Abbott Laboratories) was approved by the FDA. All patients enrolled in our study were recipients of the HMII device, as this was the only type of LVAD implant performed at our hospital. Current survival with the HMII LVAD is 80% at 1 year and 69% at 2 years, and there has not been shown to be a significant difference when stratified by era of implant.6

Device Designs and Structures

The pump of the HMII is inserted into the abdominal cavity, whereas the HVAD is implanted in the chest cavity, with the inflow cannula in the apex of the LV and the outflow cannula connecting to the proximal aorta. Blood is continuously pumped through the system.8,9 The pump is connected to a driveline that exits the body and connects to a controller. Continuous-flow devices have either an axial or centrifugal blood pump. Axial devices have an impeller that is connected to ball-and-cup bearings that accelerate blood along its axis. Newer axial flow pumps incorporate magnetic levitation of the rotor and do not require the use of bearings. Centrifugal devices accelerate blood circumferentially with a rotor that is suspended within in the blood pool by electromagnetic or hydrodynamic forces.10 The controller is powered by two external batteries or connected to a power base unit where the pump can be interrogated. The controller is usually housed in a garment worn by the patient, one that also includes the batteries. The controller can also be powered by a base unit that can be plugged into an electrical outlet.11

 

 

There are, and continue to be, advances in both LVAD design and function. Since the time period of our study, changes have been made in the outflow bend relief (the tube at the junction of the outflow cannula and the pump housing designed to prevent kinking of the outflow cannula) and the LVAD controller. Older controllers have been replaced with newer models, but many of the LVAD pumps in this article remain in service.

Anticoagulation Therapy

Patients who have a CF LVAD require anticoagulation therapy with warfarin to a target international normalized ratio (INR) of 2 to 3, in addition to aspirin therapy of 325 mg daily.8,9Newer oral anticoagulant drugs are not routinely given to patients who have a CF LVAD.

Cardiopulmonary Evaluation

With CF LVADs, blood is pumped continuously, and a constant, machine-like murmur can be heard on auscultation rather than the typical heart sounds. Patients who have an LVAD may not have palpable arterial pulses. Doppler evaluation of the brachial artery and a manual blood pressure (BP) cuff are used to listen for the start of Korotkoff sounds as the cuff is released. The pressure at which the first sound is heard is used to estimate the patient’s mean arterial pressure (MAP) at the time when there is no pulse; and the systolic BP (SBP) is heard at the time when there is pulse. Patients with a CF LVAD with nonpulsatile flow should have a MAP between 70 mm Hg and 90 mm Hg (HMII), or 70 mm Hg and 80 mm Hg (HVAD). Patients who have a CF LVAD with a palpable pulse should have an SBP less than 120 mm Hg (HMII) or 105 mm Hg (HVAD). Readings outside of these ranges require an adjustment in the patient’s antihypertensive therapy, since high BP increases the risk of stroke and can impair the cardiac support provided by the LVAD.8Low BP may be the result of inadequate pump speed, dehydration, inflow cannula obstruction, or pump thrombus.

Bleeding

In our study, bleeding and volume overload were the two most common reasons LVAD patients presented to the ED. Interestingly, in a systematic review of clinical outcomes following CF LVAD implantation, bleeding was the most commonly recorded adverse event.12In fact, the majority of patients in all of the studies reviewed experienced at least one bleeding event. In one study of 139 HMII LVAD patients, the risk of bleeding was greatest within the first two weeks, and early bleeding was associated with increased mortality.13The most common source of bleeding complications in patients with a CF LVAD are GI, similar to our study.14

In a review and meta-analysis by Draper et al,15of GI bleeding in 1,697 patients with CF LVADs, the pooled prevalence was 23%.Subgroup analysis demonstrated an increased risk of bleeding in older patients and in those who had an elevated serum creatinine level.15 Upper GI bleeding occurred in 48% of patients, lower GI bleeding in 22%, small-bowel bleeding in 15%, and bleeding at an unknown site in 19%. The most common cause of the bleeding was from arteriovenous malformations (AVMs).15 In their review, Draper et al15 found a 9.3% prevalence of recurrent GI bleeding and a pooled event rate for an all-cause mortality rate of 23%.

They also noted that the increased risk of GI bleeding in CF LVAD patients is multifactorial. For example, there was decreased activity of type 2 von Willebrand factor multimers in patients with CF LVADs, leading to an acquired von Willebrand syndrome.15

Another finding seen in this review was that CF devices lead to a low pulse-pressure system, which is thought to cause some degree of intestinal hypoperfusion, potentially leading to vascular dilation and AVM formation.15 Based on findings, a neurovascular etiology involving increased sympathetic tone resulting in smooth muscle relaxation and AVM formation has been proposed. Lastly, the anticoagulation required with the CF LVADs to prevent pump thrombosis also increases the risk of GI bleeding, especially when combined with aspirin or other antiplatelet agents which are routinely prescribed.15

Volume Overload

Interestingly, in our study, volume overload as a cause for ED presentation was the same as for bleeding complications. In the systematic review of clinical outcomes in CF LVAD patients, volume overload or ongoing heart failure occurred in 18% of patients 1 year after device implantation.12

The clinical presentation of patients experiencing volume overload is typically dyspnea and fatigue; on physical examination they will frequently demonstrate evidence of fluid retention, such as dependent edema and pulmonary congestion.16Causes of volume overload in the LVAD patient includes medication noncompliance, inadequate pump speed, device malfunction, right ventricular failure, impaired renal function, and cardiac tamponade.16 These patients will frequently have MAPs greater than 90 mm Hg, and may require treatment with diuretics, calcium channel blockers, beta-blockers, or angiotensin-converting enzyme inhibitors.8

Weakness, Lightheadedness, Dizziness, Syncope

In our study, some combination of weakness, lightheadedness, dizziness, and syncope accounted for the third most common cause of ED presentation (9.6%). In the majority of cases, this was due to dehydration. Usually, these patients will have a MAP less than 60 mm Hg. Unfortunately, patients with pump thrombosis, sepsis, or cannula malposition can also present with a low MAP. It is important to differentiate the cause, as the management is quite different, depending on the etiology. Bedside ultrasound can play an important role in evaluating the volume status and cannula position.8 In addition, emergent consult with the patients ventricular assist device (VAD) treatment team is critical.8 Pump thrombus is a medical emergency and is usually associated with hematuria without red blood cells in the urine, acute kidney injury, and marked elevations in lactate dehydrogenase and serum free hemoglobin.8 If not treated promptly, renal failure and death may result. If dehydration is the cause, gentle rehydration with intravenous normal saline and electrolyte replacement may be all that is required.

Device Malfunction

Device malfunction was the next most common reason for ED presentation in our study, at 8.1%. This category included a number of different events, including battery failure, driveline fracture, and pump thrombosis. According to McIlvennan et al,12 causes of device malfunction include thrombus formation with hemolysis, mechanical failure of the impeller, and driveline lead fractures with electrical failure.Again, the VAD team should be consulted immediately, and the EP should plug the LVAD into a hospital power base, if available, to conserve battery life. If power is interrupted, the pump will stop working. The EP should examine all of the connections from the percutaneous lead to the controller and from the controller to the batteries to ensure they are intact. The exit site for the percutaneous lead should be examined for evidence of trauma or signs of infection. The patient should also be asked about recent trauma to the driveline.

Neurological Events

Interestingly, in other reviews, neurological events, including ischemic stroke, hemorrhagic stroke, and transient ischemic attack occur with higher frequency than was the case in the study, and are relatively common complications that can result in severe morbidity and mortality.12In the Interagency Registry for Mechanically Assisted Circulatory Support report, there was a 3% risk of stroke at 1 month, 5% at 3 months, 7% at 6 months, 11% at 12 months, 17% at 24 months, and 19% at 36 months post-implant.6,12Similarly, the HMII DT Trial demonstrated rates of ischemic and hemorrhagic stroke as high as 8% and 11% respectively, within the first 2 years following LVAD placement.5,6In our study, neurological events accounted for only six (2.4%) of ED visits. It is unclear why our numbers were less than those reported by others.

Cardiac Events and Management

During the study period, one LVAD patient presented to the ED in cardiac arrest. Patients who have an LVAD and are in cardiac arrest have unique considerations that deserve discussion. If the LVAD pump has stopped functioning, connections between the system controller and the pump and power source must be checked, as loose connections need to be refitted and the pump restarted. It is important to note that when an LVAD ceases operation, blood becomes stagnant in the pump and conduits. Delays of even several minutes pose a significant risk for pump thrombosis, stroke, and thromboembolism when the device is restarted. If the pump does not restart and the patient is connected to batteries, the batteries should be replaced with a new, fully charged pair, or the device should be connected to a base unit.17

Due to the location of the outflow graft on the aorta and the inflow conduit in the LV apex, external chest compressions pose a risk of dislodging the device and causing fatal hemorrhage. Clinical judgment should be used when deciding to perform external chest compressions. A recent American Heart Association scientific statement concluded that withholding chest compression in a patient with an LVAD who is truly in circulatory failure that is not attributable to a device failure would cause more harm to the patient than the potential to dislodge the device.18

Direct cardiac massage, performed by a skilled surgeon may be effective in patients that have had recent device implantation, especially if prior to mediastinal healing.16 If external defibrillation/cardioversion is required, the percutaneous lead should not be disconnected from the system controller and the pump should not be stopped prior to the delivery of a shock.17

Study Limitations

This was a retrospective study and has the limitations common to all such studies. It is possible that some of the patients in our study sought care at a hospital ED outside of our system, and therefore were not included in our study. This, however, is exceedingly unlikely as the cardiologists and care team continually emphasized and instructed all patients in our study only to present to the study hospital ED for any complaint. Similarly, the various emergency medical services agencies for our region were also instructed to bring all LVAD patients to the study hospital.

 

 

Another limitation of our study is the relatively small total number of patients (98) and that our findings may not apply to other patient populations. This limitation, however, would be true for any hospital system that limits the type of LVAD implant procedure to one manufacturer (HMII in this instance).

Conclusion

Emergency physicians must be prepared to evaluate the LVAD patient presenting to the ED. A little over 55% of the time, the visit will be directly related to the LVAD; in the remainder of cases, patient presentation will be due to a non-LVAD-related cause. At initial presentation, however, the EP should assume that the ED visit is related to the LVAD, until a thorough history and physical examination can exclude otherwise.

Because of the high incidence of GI bleeding in LVAD patients, a rectal examination for blood in the stool should be performed for any complaint that may be related, such as generalized weakness, syncope, or shortness of breath. In the majority of cases, a complete blood count; complete metabolic profile, including lactic acid dehydrogenase; and coagulation studies, including prothrombin time and INRs, are indicated. Most patients with an LVAD will require a member of the VAD team (typically the perfusionist or biomedical engineer) to interrogate the controller if there is any concern about its function, including alarm sounding or lights flashing.

References

1. Benjamin EJ, Blaha MJ, Chiuve SE, et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics-2017 update: a report from the American Heart Association. Circulation. 2017;135(10):e146-e603. doi:10.1161/CIR.0000000000000485. Erratum in: Circulation. 2017;135(1):e646. doi:10.1161/CIR.0000000000000491.

2. Lund LH, Edwards LB, Kucheryavaya AY, et al. The Registry of the International Society for Heart and Lung Transplantation: thirtieth official adult heart transplant report—2013; focus theme: age. J Heart Lung Transplant. 2013;32(10):951-964. doi:10.1016/j.healun.2013.08.006.

3. UNOS (United Network for Organ Sharing) Web site. https://unos.org/data/transplant-trends/waiting-list-candidates-by-organ-type/. Accessed February 8, 2018.

4. Kirklin JK, Pagani FD, Kormos RL, et al. Eighth annual INTERMACS report: Special focus on framing the impact of adverse events. J Heart Lung Transplant. 2017;36(10):1080-1086. doi:10.1016/j.healun.2017.07.005.

5. Slaughter MS, Rogers JG, Milano CA, et al. Advanced heart failure treated with continuous flow left ventricular assist device. N Engl J Med. 2009;361(23):2241-2251. doi:10.1056/NEJMoa0909938.

6. Kirklin JK, Naftel DC, Pagani FD, et al. Seventh INTERMACS annual report: 15,000 patients and counting. J Heart Lung Transplant. 2015;34(12):1495-1504. doi:10.1016/j.healun.2015.10.003.

7. Ambardekar AV, Buttrick PM. Reverse remodeling with left ventricular assist devices: a review of clinical, cellular and molecular effects. Circ Heart Fail. 2011;4(2):224-233. doi:10.1161/CIRCHEARTFAILURE.110.959684.

8. Slaughter MS, Pagani FD, Rogers JG, et al. Clinical management of continuous-flow left ventricular assist devices in advanced heart failure. J Heart Lung Transplant. 2010;29 (suppl 4):1-39. doi:10.1016/j.healun.2010.01.011.

9. Lo BM, Devine AS. Patients with left ventricular assist devices. Critical Decisions in Emergency Medicine. 2014;28(7):2-9.

10. Feldman D, Pamboukian SV, Teuteberg JJ, et al. The 2013 International Society for Heart and Lung Transplantation guidelines for mechanical circulatory support: executive summary. J Heart Lung Transplant. 2013;32(2):157-187. doi:10.1016/j.healun.2012.09.013.

11. Miller LW, Pagani FD, Russell SD, et al. Use of a continuous-flow device in patients awaiting heart transplantation. N Engl J Med. 2007;357(9):885-896. doi:10.1056/NEJMoa067758.

12. McIlvennan CK, Magid KH, Ambardekar AV, et al. Clinical outcomes following continuous-flow left ventricular assist device: a systematic review. Circ Heart Fail. 2014;7(6):1003-1013. doi:10.1161/Circheartfailure.114.001391.

13. Mulloy DP, Bhamidipati CM, Stone ML, et al. Cryoablation during left ventricular assist device implantation reduces postoperative ventricular tachyarrhythmias. J Thorac Cardiovasc Surg. 2013;145(5):1207-1213. doi:10.1016/j.jtcvs.2012.03.061.

14. Stern DR, Kazam J, Edwards P, et al. Increased incidence of gastrointestinal bleeding following implantation of the Heartmate II LVAD. J Card Surg. 2010;25(3):352-356. doi:10.1111/j.1540-8191.2010.01025.x.

15. Draper KV, Huang RJ, Gerson LB. GI bleeding in patients with continuous-flow left ventricular assist devices: a systematic review and meta-analysis. Gastrointest Endosc. 2014;80(3):435-446. doi:10.1016/j.gie.2014.03.040.

16. Aissaoui N, Morshuis M, Diebold B, et al. Heart failure while on ventricular assist device support: a true clinical entity? Arch Cardiovasc Dis. 2013:106(1):44-51. doi:10.1016/j.acvd.2012.09.006.

17. Thoratec HeartMate II Left Ventricular Assist System (LVAS) Information and Emergency Assistance Guide. Thoratec Corporation Web site. http://www.thoratec.com/_assets/download-tracker/HM_II_Info_Emergency_Assist_Guide_US_103873B_ENGLISH.pdf. Accessed July 5, 2017.

18. Peberdy MA, Gluck JA, Ornato JP, et al; American Heart Association Emergency Cardiovascular Care Committee; Council on Cardiopulmonary, Critical Care, Perioperative, and Resuscitation; Council on Cardiovascular Diseases in the Young; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular and Stroke Nursing; and Council on Clinical Cardiology. Cardiopulmonary resuscitation in adults and children with mechanical circulatory support a scientific statement from the American Heart Association. Circulation. 2017;135(24):e1115-e1134. doi:10.1161/CIR.0000000000000504.

References

1. Benjamin EJ, Blaha MJ, Chiuve SE, et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics-2017 update: a report from the American Heart Association. Circulation. 2017;135(10):e146-e603. doi:10.1161/CIR.0000000000000485. Erratum in: Circulation. 2017;135(1):e646. doi:10.1161/CIR.0000000000000491.

2. Lund LH, Edwards LB, Kucheryavaya AY, et al. The Registry of the International Society for Heart and Lung Transplantation: thirtieth official adult heart transplant report—2013; focus theme: age. J Heart Lung Transplant. 2013;32(10):951-964. doi:10.1016/j.healun.2013.08.006.

3. UNOS (United Network for Organ Sharing) Web site. https://unos.org/data/transplant-trends/waiting-list-candidates-by-organ-type/. Accessed February 8, 2018.

4. Kirklin JK, Pagani FD, Kormos RL, et al. Eighth annual INTERMACS report: Special focus on framing the impact of adverse events. J Heart Lung Transplant. 2017;36(10):1080-1086. doi:10.1016/j.healun.2017.07.005.

5. Slaughter MS, Rogers JG, Milano CA, et al. Advanced heart failure treated with continuous flow left ventricular assist device. N Engl J Med. 2009;361(23):2241-2251. doi:10.1056/NEJMoa0909938.

6. Kirklin JK, Naftel DC, Pagani FD, et al. Seventh INTERMACS annual report: 15,000 patients and counting. J Heart Lung Transplant. 2015;34(12):1495-1504. doi:10.1016/j.healun.2015.10.003.

7. Ambardekar AV, Buttrick PM. Reverse remodeling with left ventricular assist devices: a review of clinical, cellular and molecular effects. Circ Heart Fail. 2011;4(2):224-233. doi:10.1161/CIRCHEARTFAILURE.110.959684.

8. Slaughter MS, Pagani FD, Rogers JG, et al. Clinical management of continuous-flow left ventricular assist devices in advanced heart failure. J Heart Lung Transplant. 2010;29 (suppl 4):1-39. doi:10.1016/j.healun.2010.01.011.

9. Lo BM, Devine AS. Patients with left ventricular assist devices. Critical Decisions in Emergency Medicine. 2014;28(7):2-9.

10. Feldman D, Pamboukian SV, Teuteberg JJ, et al. The 2013 International Society for Heart and Lung Transplantation guidelines for mechanical circulatory support: executive summary. J Heart Lung Transplant. 2013;32(2):157-187. doi:10.1016/j.healun.2012.09.013.

11. Miller LW, Pagani FD, Russell SD, et al. Use of a continuous-flow device in patients awaiting heart transplantation. N Engl J Med. 2007;357(9):885-896. doi:10.1056/NEJMoa067758.

12. McIlvennan CK, Magid KH, Ambardekar AV, et al. Clinical outcomes following continuous-flow left ventricular assist device: a systematic review. Circ Heart Fail. 2014;7(6):1003-1013. doi:10.1161/Circheartfailure.114.001391.

13. Mulloy DP, Bhamidipati CM, Stone ML, et al. Cryoablation during left ventricular assist device implantation reduces postoperative ventricular tachyarrhythmias. J Thorac Cardiovasc Surg. 2013;145(5):1207-1213. doi:10.1016/j.jtcvs.2012.03.061.

14. Stern DR, Kazam J, Edwards P, et al. Increased incidence of gastrointestinal bleeding following implantation of the Heartmate II LVAD. J Card Surg. 2010;25(3):352-356. doi:10.1111/j.1540-8191.2010.01025.x.

15. Draper KV, Huang RJ, Gerson LB. GI bleeding in patients with continuous-flow left ventricular assist devices: a systematic review and meta-analysis. Gastrointest Endosc. 2014;80(3):435-446. doi:10.1016/j.gie.2014.03.040.

16. Aissaoui N, Morshuis M, Diebold B, et al. Heart failure while on ventricular assist device support: a true clinical entity? Arch Cardiovasc Dis. 2013:106(1):44-51. doi:10.1016/j.acvd.2012.09.006.

17. Thoratec HeartMate II Left Ventricular Assist System (LVAS) Information and Emergency Assistance Guide. Thoratec Corporation Web site. http://www.thoratec.com/_assets/download-tracker/HM_II_Info_Emergency_Assist_Guide_US_103873B_ENGLISH.pdf. Accessed July 5, 2017.

18. Peberdy MA, Gluck JA, Ornato JP, et al; American Heart Association Emergency Cardiovascular Care Committee; Council on Cardiopulmonary, Critical Care, Perioperative, and Resuscitation; Council on Cardiovascular Diseases in the Young; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular and Stroke Nursing; and Council on Clinical Cardiology. Cardiopulmonary resuscitation in adults and children with mechanical circulatory support a scientific statement from the American Heart Association. Circulation. 2017;135(24):e1115-e1134. doi:10.1161/CIR.0000000000000504.

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Disruptive Physician Behavior: The Importance of Recognition and Intervention and Its Impact on Patient Safety

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Dramatic stories of disruptive physician behavior (DPB) appear occasionally in the news, such as the physician who shot and killed a colleague within hospital confines or the gynecologist who secretly took photographs using a camera disguised as a pen during pelvic examinations. More common in hospitals, however, are incidents of inappropriate behavior that may generate complaints from patients or other providers and at times snowball into administrative or legal challenges.

“Professionalism” is one of the six competencies listed by the Accreditation Council for Graduate Medical Education (ACGME)1 and the American Board of Medical Specialties. Unfortunately, incidents of disruptive behavior can result in violation of the tenets of professionalism in the healthcare environment. These behaviors fall along a continuum ranging from outwardly aggressive and uncivil to overly passive and insidious. Although these behaviors can occur across all healthcare disciplines and settings and are not just limited to physicians, the behaviors of physicians often have a much greater impact on the healthcare system as a whole because of their positions of relative “power” within the system.2 Hence, this problem requires greater awareness and education. In this context, the aim of this article is to discuss disruptive behaviors in physicians.

The AMA defines DPB as “personal conduct, verbal or physical that has the potential to negatively affect patient care or the ability to work with other members of the healthcare team.”3 The definition of DPB by the Joint Commission includes “all behaviors that undermine a culture of safety.”4 Both the Joint Commission and the AMA recognize the significance and patient safety implications of such behavior. Policy statements by both these organizations underscore the importance of confronting and remedying these potentially dangerous interpersonal behaviors.

Data regarding the prevalence of DPB have been inconsistent. One study estimated that 3%–5% of physicians demonstrate this behavior,5 whereas another study reported a DPB prevalence of 97% among physicians and nurses in the workplace.6 According to a 2004 survey of physician executives, more than 95% of them reported regular encounters of DPB.7

The etiology of such disruptive behaviors is multifactorial and complex. Explanations associated with ‘nature versus nurture’ have ranged from physician psychopathology to unhealthy modeling during training. Both extrinsic and intrinsic factors may also contribute to DPB. External stressors and negative experiences–professional and/or personal–can provoke disruptive behaviors. Overwork, fatigue, strife, and a dysfunctional environment that can arise in both work and home environments can contribute to the development of mental health problems. Stress, burnout, and depression have increasingly become prevalent among physicians and can play a significant role in causing impaired patterns of professional conduct.8, 9 These mental health problems can cause physicians to acquire maladaptive coping strategies such as substance abuse and drug or alcohol dependence. However, it is important to note that physician impairment and substance abuse are not the most frequent causes of DPB. In fact, fewer than 10% of physician behavior issues have been related to substance abuse.2, 5

Intrinsic factors that contribute to DPB include personality traits and disorders, psychiatric diagnoses, and even medical conditions (eg, age and disease-related cognitive impairment).5 Personality disorders have been implicated in causing DPB and constitute varying levels of pathology that may exist in several shades along a continuum. A single individual may fit into multiple different personality disorders (eg, narcissistic, borderline, and antisocial).10 As a result, making a clear diagnosis is often difficult for mental health professionals. Occasionally, it is simpler to conceptualize DPB in the context of subclinical personality traits, rather than diagnosable personality disorders. Not all these personality traits are pathologic—in fact, some are desirable (Table 1).10

Psychiatric disorders such as major depression and bipolar and anxiety disorders may also contribute to DPB.10 Most of these disorders (except for schizophrenia) are likely as common among physicians as among the general public.9 An essential clarification is that although DPB can be a manifestation of personality disorders or psychiatric disorders, it does not always stem from underlying psychopathology. Clarifying these distinctions is important for managing the problem and calls for expert professional evaluation in some cases.10

A person’s behavior is shaped by character, values, perceptions, and attitudes. Individuals who engage in DPB typically lack insight and justify their behaviors as a means to achieve a goal. Disrespectful behavior is rooted, in part, in characteristics such as insecurity, immaturity, and aggressiveness; however, it can also be learned, tolerated, and reinforced in the hierarchical hospital culture.11

Other intrinsic factors that may contribute to DPB include lack of emotional intelligence, poor social skills, cultural and ethnic issues, and generation and gender bias.12 Identifying the root causes of DPB can be challenging due to the complexity of the interaction between the healthcare environment and the key players within it; nevertheless, awareness of the contributing factors and early recognition are important. Those who take on the mantle of leadership within hospitals should be educated in this regard.

 

 

Repercussions of Disruptive Physician Behavior

An institution’s organizational culture often has an impact on how DPB is addressed. Tolerance of such behavior can have far-reaching consequences. The central tenets of a “culture of safety and respect”–teamwork across disciplines and a blame-free environment in which every member of the healthcare team feels equally empowered to report errors and openly discuss safety issues–would be negatively impacted.

DPB can diminish the quality of care provided, increase the risk of medical errors, and adversely affect patient safety and satisfaction.11-13 Such behavior can cause erosion of relationships and communication between individuals and contribute to a hostile work environment. For instance, nurses or trainees may be afraid to question a physician because of the fear of getting yelled at or being humiliated. Consequently, improperly written orders may be overlooked or a potentially “wrong-site” surgical procedure may not be questioned for fear of provoking a hostile response.

DPB can increase litigation risk and financial costs to institutions. Provider retention may be adversely affected; valued staff may leave hospitals and need to be replaced, and productivity may suffer. When physicians in training observe how their superiors model disruptive behaviors with impunity, a concerning problem that arises is that DPB becomes normalized in the workplace culture, especially if such behaviors are tolerated and result in a perceived gain.

Proposed Interventions

Perhaps the initial step in addressing DPB is prevention. Considering the role of external factors, it is necessary to encourage initiatives to foster “whole health” and a peaceful environment in the workplace. Physician health and wellness are key to maintaining professionalism and should be prioritized in the healthcare environment. Individuals should be encouraged to seek professional care when their physical or mental health is compromised.12 (Table 2)

Confrontation of DPB can be challenging without appropriate infrastructure. Healthcare facilities should have a fair system in place for reliable reporting and monitoring of DPB, including a complaints’ verification process, appeals process, and an option for fair hearing.

It is best to initially address the issue in a direct, timely, yet informal manner through counseling or a verbal warning. In several situations, such informal counseling opportunities create a mindful awareness of the problem and the problematic behavior ceases without the need for further action.

When informal intervention is either not appropriate (eg, if the alleged event involved an assault or other illegal behavior) or has already been offered in the past, more formal intervention is required. Institutional progressive disciplinary polices should be in place and adhered to. For example, repeat offenders may be issued written warnings or even temporary suspension of privileges.

Institutional resources such as human resources departments, office of general counsel, office of medical affairs, and the hospital’s medical board may be consulted. Some medical centers have “employee assistance programs” staffed with clinicians skilled in dealing with DPB. Individuals diagnosed with substance abuse or a mental health disorder may require consultation with mental health professionals.14

Special “Professionalism Committees” can be instituted and tasked with investigating complaints and making recommendations for the involvement of resources outside the institution, such as a state medical society.15

Conclusion

Although the vast majority of physicians are well-behaved, it is important to acknowledge that disruptive behaviors can occur in the healthcare environment. Such behaviors have a major impact on workplace culture and patient safety and must be recognized early. Hospital executives and leaders must ensure that appropriate interventions are undertaken—before the quality of patient care is affected and before lives are endangered.

Acknowledgment

The authors would like to thank Ansu John for providing editorial assistance with the manuscript.

Disclosures 

The authors have nothing to disclose (Conflict of Interest Form submitted as separate PDF document). Dr. Heitt consults with local hospitals, medical practices, and licensing boards regarding physicians and other healthcare practitioners who have been accused of engaging in disruptive behavior. In these situations he may be paid by the board, medical society, hospital, practice or the professional (patient).

References

1. Accreditation Council for Graduate Medical Education. Common program requirements: general competencies. https://www.acgme.org/Portals/0/PDFs/Common_Program_Requirements_07012011[2].pdf. Accessed July 25, 2017.
2. Porto G, Lauve R. Disruptive clinician behavior: a persistent threat to patient safety. Patient safety and quality healthcare. Lionheart Publishing, Inc. 2006;3:16-24 https://www.psqh.com/julaug06/disruptive.html. Accessed October 1, 2017.
3. American Medical Association. Opinion E- 9.045–Physicians with disruptive behavior. Chicago, IL American Medical Association 2008.
4. Joint Commission: Behaviors that undermine a culture of safety. Sentinel event alert, July 9, 2008:40. http://www.jointcommission.org/sentinel_event_alert_issue_40_behaviors_that_undermine_a_culture_of_safety/. Accessed October 1, 2017.
5. Leape LL, Fromson JA. Problem doctors: is there a system-level solution? Ann Int Med. 2006;144:107-115. PubMed
6. Rosenstein AH, O’Daniel M. A survey of the impact of disruptive behaviors and communication defects on patient safety. Jt Comm J Qual Patient Saf. 2008;34(8):464-471. PubMed
7. Weber DO. Poll Results: Doctors’ disruptive behavior disturbs physician leaders. The Physician Executive. 2004;30(5):6. PubMed
8. Center C, Davis M, Detre T, et al. Confronting depression and suicide in physicians: a consensus statement. JAMA. 2003;289(23):3161-3166. PubMed
9. Brown S, Goske M, Johnson C. Beyond substance abuse: stress, burnout and depression as causes of physician impairment and disruptive behavior. J Am Coll Radiol. 2009 6;(7):479-485. PubMed
10. Reynolds NT. Disruptive physician behavior: use and misuse of the label. J Med Regulation. 2012;98(1):8-19. 
11. Leape LL, Shore MF, Dienstag JL, et al. Perspective: a culture of respect, part 1: the nature and causes of disrespectful behavior by physicians. Acad Med. 2012;87(7):845-852. PubMed
12. Rosenstein AH, O’Daniel M. Impact and implications of disruptive behavior in the perioperative arena. J Am Coll Surg. 2006;203(1):96-105. PubMed
13. Patient Safety Primer: Disruptive and unprofessional behavior. Available at AHRQ Patient Safety Network: https://psnet.ahrq.gov/primers/primer/15/disruptive-and-unprofessional-behavior(Accessed October 1, 2017.
14. Williams BW, Williams MV. The disruptive physician: conceptual organization. JMed Licensure Discipline. 2008;94(3):12-19. 
15. Speck R, Foster J, Mulhem V, et al. Development of a professionalism committee approach to address unprofessional medical staff behavior at an academic medical center. Jt Comm J Qual Patient Saf. 2004;40(4):161-167. PubMed

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Dramatic stories of disruptive physician behavior (DPB) appear occasionally in the news, such as the physician who shot and killed a colleague within hospital confines or the gynecologist who secretly took photographs using a camera disguised as a pen during pelvic examinations. More common in hospitals, however, are incidents of inappropriate behavior that may generate complaints from patients or other providers and at times snowball into administrative or legal challenges.

“Professionalism” is one of the six competencies listed by the Accreditation Council for Graduate Medical Education (ACGME)1 and the American Board of Medical Specialties. Unfortunately, incidents of disruptive behavior can result in violation of the tenets of professionalism in the healthcare environment. These behaviors fall along a continuum ranging from outwardly aggressive and uncivil to overly passive and insidious. Although these behaviors can occur across all healthcare disciplines and settings and are not just limited to physicians, the behaviors of physicians often have a much greater impact on the healthcare system as a whole because of their positions of relative “power” within the system.2 Hence, this problem requires greater awareness and education. In this context, the aim of this article is to discuss disruptive behaviors in physicians.

The AMA defines DPB as “personal conduct, verbal or physical that has the potential to negatively affect patient care or the ability to work with other members of the healthcare team.”3 The definition of DPB by the Joint Commission includes “all behaviors that undermine a culture of safety.”4 Both the Joint Commission and the AMA recognize the significance and patient safety implications of such behavior. Policy statements by both these organizations underscore the importance of confronting and remedying these potentially dangerous interpersonal behaviors.

Data regarding the prevalence of DPB have been inconsistent. One study estimated that 3%–5% of physicians demonstrate this behavior,5 whereas another study reported a DPB prevalence of 97% among physicians and nurses in the workplace.6 According to a 2004 survey of physician executives, more than 95% of them reported regular encounters of DPB.7

The etiology of such disruptive behaviors is multifactorial and complex. Explanations associated with ‘nature versus nurture’ have ranged from physician psychopathology to unhealthy modeling during training. Both extrinsic and intrinsic factors may also contribute to DPB. External stressors and negative experiences–professional and/or personal–can provoke disruptive behaviors. Overwork, fatigue, strife, and a dysfunctional environment that can arise in both work and home environments can contribute to the development of mental health problems. Stress, burnout, and depression have increasingly become prevalent among physicians and can play a significant role in causing impaired patterns of professional conduct.8, 9 These mental health problems can cause physicians to acquire maladaptive coping strategies such as substance abuse and drug or alcohol dependence. However, it is important to note that physician impairment and substance abuse are not the most frequent causes of DPB. In fact, fewer than 10% of physician behavior issues have been related to substance abuse.2, 5

Intrinsic factors that contribute to DPB include personality traits and disorders, psychiatric diagnoses, and even medical conditions (eg, age and disease-related cognitive impairment).5 Personality disorders have been implicated in causing DPB and constitute varying levels of pathology that may exist in several shades along a continuum. A single individual may fit into multiple different personality disorders (eg, narcissistic, borderline, and antisocial).10 As a result, making a clear diagnosis is often difficult for mental health professionals. Occasionally, it is simpler to conceptualize DPB in the context of subclinical personality traits, rather than diagnosable personality disorders. Not all these personality traits are pathologic—in fact, some are desirable (Table 1).10

Psychiatric disorders such as major depression and bipolar and anxiety disorders may also contribute to DPB.10 Most of these disorders (except for schizophrenia) are likely as common among physicians as among the general public.9 An essential clarification is that although DPB can be a manifestation of personality disorders or psychiatric disorders, it does not always stem from underlying psychopathology. Clarifying these distinctions is important for managing the problem and calls for expert professional evaluation in some cases.10

A person’s behavior is shaped by character, values, perceptions, and attitudes. Individuals who engage in DPB typically lack insight and justify their behaviors as a means to achieve a goal. Disrespectful behavior is rooted, in part, in characteristics such as insecurity, immaturity, and aggressiveness; however, it can also be learned, tolerated, and reinforced in the hierarchical hospital culture.11

Other intrinsic factors that may contribute to DPB include lack of emotional intelligence, poor social skills, cultural and ethnic issues, and generation and gender bias.12 Identifying the root causes of DPB can be challenging due to the complexity of the interaction between the healthcare environment and the key players within it; nevertheless, awareness of the contributing factors and early recognition are important. Those who take on the mantle of leadership within hospitals should be educated in this regard.

 

 

Repercussions of Disruptive Physician Behavior

An institution’s organizational culture often has an impact on how DPB is addressed. Tolerance of such behavior can have far-reaching consequences. The central tenets of a “culture of safety and respect”–teamwork across disciplines and a blame-free environment in which every member of the healthcare team feels equally empowered to report errors and openly discuss safety issues–would be negatively impacted.

DPB can diminish the quality of care provided, increase the risk of medical errors, and adversely affect patient safety and satisfaction.11-13 Such behavior can cause erosion of relationships and communication between individuals and contribute to a hostile work environment. For instance, nurses or trainees may be afraid to question a physician because of the fear of getting yelled at or being humiliated. Consequently, improperly written orders may be overlooked or a potentially “wrong-site” surgical procedure may not be questioned for fear of provoking a hostile response.

DPB can increase litigation risk and financial costs to institutions. Provider retention may be adversely affected; valued staff may leave hospitals and need to be replaced, and productivity may suffer. When physicians in training observe how their superiors model disruptive behaviors with impunity, a concerning problem that arises is that DPB becomes normalized in the workplace culture, especially if such behaviors are tolerated and result in a perceived gain.

Proposed Interventions

Perhaps the initial step in addressing DPB is prevention. Considering the role of external factors, it is necessary to encourage initiatives to foster “whole health” and a peaceful environment in the workplace. Physician health and wellness are key to maintaining professionalism and should be prioritized in the healthcare environment. Individuals should be encouraged to seek professional care when their physical or mental health is compromised.12 (Table 2)

Confrontation of DPB can be challenging without appropriate infrastructure. Healthcare facilities should have a fair system in place for reliable reporting and monitoring of DPB, including a complaints’ verification process, appeals process, and an option for fair hearing.

It is best to initially address the issue in a direct, timely, yet informal manner through counseling or a verbal warning. In several situations, such informal counseling opportunities create a mindful awareness of the problem and the problematic behavior ceases without the need for further action.

When informal intervention is either not appropriate (eg, if the alleged event involved an assault or other illegal behavior) or has already been offered in the past, more formal intervention is required. Institutional progressive disciplinary polices should be in place and adhered to. For example, repeat offenders may be issued written warnings or even temporary suspension of privileges.

Institutional resources such as human resources departments, office of general counsel, office of medical affairs, and the hospital’s medical board may be consulted. Some medical centers have “employee assistance programs” staffed with clinicians skilled in dealing with DPB. Individuals diagnosed with substance abuse or a mental health disorder may require consultation with mental health professionals.14

Special “Professionalism Committees” can be instituted and tasked with investigating complaints and making recommendations for the involvement of resources outside the institution, such as a state medical society.15

Conclusion

Although the vast majority of physicians are well-behaved, it is important to acknowledge that disruptive behaviors can occur in the healthcare environment. Such behaviors have a major impact on workplace culture and patient safety and must be recognized early. Hospital executives and leaders must ensure that appropriate interventions are undertaken—before the quality of patient care is affected and before lives are endangered.

Acknowledgment

The authors would like to thank Ansu John for providing editorial assistance with the manuscript.

Disclosures 

The authors have nothing to disclose (Conflict of Interest Form submitted as separate PDF document). Dr. Heitt consults with local hospitals, medical practices, and licensing boards regarding physicians and other healthcare practitioners who have been accused of engaging in disruptive behavior. In these situations he may be paid by the board, medical society, hospital, practice or the professional (patient).

Dramatic stories of disruptive physician behavior (DPB) appear occasionally in the news, such as the physician who shot and killed a colleague within hospital confines or the gynecologist who secretly took photographs using a camera disguised as a pen during pelvic examinations. More common in hospitals, however, are incidents of inappropriate behavior that may generate complaints from patients or other providers and at times snowball into administrative or legal challenges.

“Professionalism” is one of the six competencies listed by the Accreditation Council for Graduate Medical Education (ACGME)1 and the American Board of Medical Specialties. Unfortunately, incidents of disruptive behavior can result in violation of the tenets of professionalism in the healthcare environment. These behaviors fall along a continuum ranging from outwardly aggressive and uncivil to overly passive and insidious. Although these behaviors can occur across all healthcare disciplines and settings and are not just limited to physicians, the behaviors of physicians often have a much greater impact on the healthcare system as a whole because of their positions of relative “power” within the system.2 Hence, this problem requires greater awareness and education. In this context, the aim of this article is to discuss disruptive behaviors in physicians.

The AMA defines DPB as “personal conduct, verbal or physical that has the potential to negatively affect patient care or the ability to work with other members of the healthcare team.”3 The definition of DPB by the Joint Commission includes “all behaviors that undermine a culture of safety.”4 Both the Joint Commission and the AMA recognize the significance and patient safety implications of such behavior. Policy statements by both these organizations underscore the importance of confronting and remedying these potentially dangerous interpersonal behaviors.

Data regarding the prevalence of DPB have been inconsistent. One study estimated that 3%–5% of physicians demonstrate this behavior,5 whereas another study reported a DPB prevalence of 97% among physicians and nurses in the workplace.6 According to a 2004 survey of physician executives, more than 95% of them reported regular encounters of DPB.7

The etiology of such disruptive behaviors is multifactorial and complex. Explanations associated with ‘nature versus nurture’ have ranged from physician psychopathology to unhealthy modeling during training. Both extrinsic and intrinsic factors may also contribute to DPB. External stressors and negative experiences–professional and/or personal–can provoke disruptive behaviors. Overwork, fatigue, strife, and a dysfunctional environment that can arise in both work and home environments can contribute to the development of mental health problems. Stress, burnout, and depression have increasingly become prevalent among physicians and can play a significant role in causing impaired patterns of professional conduct.8, 9 These mental health problems can cause physicians to acquire maladaptive coping strategies such as substance abuse and drug or alcohol dependence. However, it is important to note that physician impairment and substance abuse are not the most frequent causes of DPB. In fact, fewer than 10% of physician behavior issues have been related to substance abuse.2, 5

Intrinsic factors that contribute to DPB include personality traits and disorders, psychiatric diagnoses, and even medical conditions (eg, age and disease-related cognitive impairment).5 Personality disorders have been implicated in causing DPB and constitute varying levels of pathology that may exist in several shades along a continuum. A single individual may fit into multiple different personality disorders (eg, narcissistic, borderline, and antisocial).10 As a result, making a clear diagnosis is often difficult for mental health professionals. Occasionally, it is simpler to conceptualize DPB in the context of subclinical personality traits, rather than diagnosable personality disorders. Not all these personality traits are pathologic—in fact, some are desirable (Table 1).10

Psychiatric disorders such as major depression and bipolar and anxiety disorders may also contribute to DPB.10 Most of these disorders (except for schizophrenia) are likely as common among physicians as among the general public.9 An essential clarification is that although DPB can be a manifestation of personality disorders or psychiatric disorders, it does not always stem from underlying psychopathology. Clarifying these distinctions is important for managing the problem and calls for expert professional evaluation in some cases.10

A person’s behavior is shaped by character, values, perceptions, and attitudes. Individuals who engage in DPB typically lack insight and justify their behaviors as a means to achieve a goal. Disrespectful behavior is rooted, in part, in characteristics such as insecurity, immaturity, and aggressiveness; however, it can also be learned, tolerated, and reinforced in the hierarchical hospital culture.11

Other intrinsic factors that may contribute to DPB include lack of emotional intelligence, poor social skills, cultural and ethnic issues, and generation and gender bias.12 Identifying the root causes of DPB can be challenging due to the complexity of the interaction between the healthcare environment and the key players within it; nevertheless, awareness of the contributing factors and early recognition are important. Those who take on the mantle of leadership within hospitals should be educated in this regard.

 

 

Repercussions of Disruptive Physician Behavior

An institution’s organizational culture often has an impact on how DPB is addressed. Tolerance of such behavior can have far-reaching consequences. The central tenets of a “culture of safety and respect”–teamwork across disciplines and a blame-free environment in which every member of the healthcare team feels equally empowered to report errors and openly discuss safety issues–would be negatively impacted.

DPB can diminish the quality of care provided, increase the risk of medical errors, and adversely affect patient safety and satisfaction.11-13 Such behavior can cause erosion of relationships and communication between individuals and contribute to a hostile work environment. For instance, nurses or trainees may be afraid to question a physician because of the fear of getting yelled at or being humiliated. Consequently, improperly written orders may be overlooked or a potentially “wrong-site” surgical procedure may not be questioned for fear of provoking a hostile response.

DPB can increase litigation risk and financial costs to institutions. Provider retention may be adversely affected; valued staff may leave hospitals and need to be replaced, and productivity may suffer. When physicians in training observe how their superiors model disruptive behaviors with impunity, a concerning problem that arises is that DPB becomes normalized in the workplace culture, especially if such behaviors are tolerated and result in a perceived gain.

Proposed Interventions

Perhaps the initial step in addressing DPB is prevention. Considering the role of external factors, it is necessary to encourage initiatives to foster “whole health” and a peaceful environment in the workplace. Physician health and wellness are key to maintaining professionalism and should be prioritized in the healthcare environment. Individuals should be encouraged to seek professional care when their physical or mental health is compromised.12 (Table 2)

Confrontation of DPB can be challenging without appropriate infrastructure. Healthcare facilities should have a fair system in place for reliable reporting and monitoring of DPB, including a complaints’ verification process, appeals process, and an option for fair hearing.

It is best to initially address the issue in a direct, timely, yet informal manner through counseling or a verbal warning. In several situations, such informal counseling opportunities create a mindful awareness of the problem and the problematic behavior ceases without the need for further action.

When informal intervention is either not appropriate (eg, if the alleged event involved an assault or other illegal behavior) or has already been offered in the past, more formal intervention is required. Institutional progressive disciplinary polices should be in place and adhered to. For example, repeat offenders may be issued written warnings or even temporary suspension of privileges.

Institutional resources such as human resources departments, office of general counsel, office of medical affairs, and the hospital’s medical board may be consulted. Some medical centers have “employee assistance programs” staffed with clinicians skilled in dealing with DPB. Individuals diagnosed with substance abuse or a mental health disorder may require consultation with mental health professionals.14

Special “Professionalism Committees” can be instituted and tasked with investigating complaints and making recommendations for the involvement of resources outside the institution, such as a state medical society.15

Conclusion

Although the vast majority of physicians are well-behaved, it is important to acknowledge that disruptive behaviors can occur in the healthcare environment. Such behaviors have a major impact on workplace culture and patient safety and must be recognized early. Hospital executives and leaders must ensure that appropriate interventions are undertaken—before the quality of patient care is affected and before lives are endangered.

Acknowledgment

The authors would like to thank Ansu John for providing editorial assistance with the manuscript.

Disclosures 

The authors have nothing to disclose (Conflict of Interest Form submitted as separate PDF document). Dr. Heitt consults with local hospitals, medical practices, and licensing boards regarding physicians and other healthcare practitioners who have been accused of engaging in disruptive behavior. In these situations he may be paid by the board, medical society, hospital, practice or the professional (patient).

References

1. Accreditation Council for Graduate Medical Education. Common program requirements: general competencies. https://www.acgme.org/Portals/0/PDFs/Common_Program_Requirements_07012011[2].pdf. Accessed July 25, 2017.
2. Porto G, Lauve R. Disruptive clinician behavior: a persistent threat to patient safety. Patient safety and quality healthcare. Lionheart Publishing, Inc. 2006;3:16-24 https://www.psqh.com/julaug06/disruptive.html. Accessed October 1, 2017.
3. American Medical Association. Opinion E- 9.045–Physicians with disruptive behavior. Chicago, IL American Medical Association 2008.
4. Joint Commission: Behaviors that undermine a culture of safety. Sentinel event alert, July 9, 2008:40. http://www.jointcommission.org/sentinel_event_alert_issue_40_behaviors_that_undermine_a_culture_of_safety/. Accessed October 1, 2017.
5. Leape LL, Fromson JA. Problem doctors: is there a system-level solution? Ann Int Med. 2006;144:107-115. PubMed
6. Rosenstein AH, O’Daniel M. A survey of the impact of disruptive behaviors and communication defects on patient safety. Jt Comm J Qual Patient Saf. 2008;34(8):464-471. PubMed
7. Weber DO. Poll Results: Doctors’ disruptive behavior disturbs physician leaders. The Physician Executive. 2004;30(5):6. PubMed
8. Center C, Davis M, Detre T, et al. Confronting depression and suicide in physicians: a consensus statement. JAMA. 2003;289(23):3161-3166. PubMed
9. Brown S, Goske M, Johnson C. Beyond substance abuse: stress, burnout and depression as causes of physician impairment and disruptive behavior. J Am Coll Radiol. 2009 6;(7):479-485. PubMed
10. Reynolds NT. Disruptive physician behavior: use and misuse of the label. J Med Regulation. 2012;98(1):8-19. 
11. Leape LL, Shore MF, Dienstag JL, et al. Perspective: a culture of respect, part 1: the nature and causes of disrespectful behavior by physicians. Acad Med. 2012;87(7):845-852. PubMed
12. Rosenstein AH, O’Daniel M. Impact and implications of disruptive behavior in the perioperative arena. J Am Coll Surg. 2006;203(1):96-105. PubMed
13. Patient Safety Primer: Disruptive and unprofessional behavior. Available at AHRQ Patient Safety Network: https://psnet.ahrq.gov/primers/primer/15/disruptive-and-unprofessional-behavior(Accessed October 1, 2017.
14. Williams BW, Williams MV. The disruptive physician: conceptual organization. JMed Licensure Discipline. 2008;94(3):12-19. 
15. Speck R, Foster J, Mulhem V, et al. Development of a professionalism committee approach to address unprofessional medical staff behavior at an academic medical center. Jt Comm J Qual Patient Saf. 2004;40(4):161-167. PubMed

References

1. Accreditation Council for Graduate Medical Education. Common program requirements: general competencies. https://www.acgme.org/Portals/0/PDFs/Common_Program_Requirements_07012011[2].pdf. Accessed July 25, 2017.
2. Porto G, Lauve R. Disruptive clinician behavior: a persistent threat to patient safety. Patient safety and quality healthcare. Lionheart Publishing, Inc. 2006;3:16-24 https://www.psqh.com/julaug06/disruptive.html. Accessed October 1, 2017.
3. American Medical Association. Opinion E- 9.045–Physicians with disruptive behavior. Chicago, IL American Medical Association 2008.
4. Joint Commission: Behaviors that undermine a culture of safety. Sentinel event alert, July 9, 2008:40. http://www.jointcommission.org/sentinel_event_alert_issue_40_behaviors_that_undermine_a_culture_of_safety/. Accessed October 1, 2017.
5. Leape LL, Fromson JA. Problem doctors: is there a system-level solution? Ann Int Med. 2006;144:107-115. PubMed
6. Rosenstein AH, O’Daniel M. A survey of the impact of disruptive behaviors and communication defects on patient safety. Jt Comm J Qual Patient Saf. 2008;34(8):464-471. PubMed
7. Weber DO. Poll Results: Doctors’ disruptive behavior disturbs physician leaders. The Physician Executive. 2004;30(5):6. PubMed
8. Center C, Davis M, Detre T, et al. Confronting depression and suicide in physicians: a consensus statement. JAMA. 2003;289(23):3161-3166. PubMed
9. Brown S, Goske M, Johnson C. Beyond substance abuse: stress, burnout and depression as causes of physician impairment and disruptive behavior. J Am Coll Radiol. 2009 6;(7):479-485. PubMed
10. Reynolds NT. Disruptive physician behavior: use and misuse of the label. J Med Regulation. 2012;98(1):8-19. 
11. Leape LL, Shore MF, Dienstag JL, et al. Perspective: a culture of respect, part 1: the nature and causes of disrespectful behavior by physicians. Acad Med. 2012;87(7):845-852. PubMed
12. Rosenstein AH, O’Daniel M. Impact and implications of disruptive behavior in the perioperative arena. J Am Coll Surg. 2006;203(1):96-105. PubMed
13. Patient Safety Primer: Disruptive and unprofessional behavior. Available at AHRQ Patient Safety Network: https://psnet.ahrq.gov/primers/primer/15/disruptive-and-unprofessional-behavior(Accessed October 1, 2017.
14. Williams BW, Williams MV. The disruptive physician: conceptual organization. JMed Licensure Discipline. 2008;94(3):12-19. 
15. Speck R, Foster J, Mulhem V, et al. Development of a professionalism committee approach to address unprofessional medical staff behavior at an academic medical center. Jt Comm J Qual Patient Saf. 2004;40(4):161-167. PubMed

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Denah Joseph: “In the Hospital”

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We recently spoke with Denah Joseph, a clinical chaplain who works with the Palliative Care team to provide spiritual services to patients with serious illness. In addition, Denah leads efforts to address burnout among healthcare providers.

Denah, tell us about yourself.

My first career was actually in clinical psychology, but I’ve been a Palliative Care chaplain for 15 years. I also teach skill-building for providers around burnout and resilience.

What brought you to Palliative Care?

I’ve lost three sisters and a partner to breast cancer, and my dad died when I was quite young, so I’ve had a lot of exposure to loss. The other big thread in my life has been my spiritual practice. My father was an Orthodox Jew, but exceptionally ecumenical for his time. His first wife was Irish Catholic, and my father used to go to church, sit, kneel, and say the rosary, and light candles for his Catholic friends. Three hundred nuns from the local diocese all came to my dad’s funeral. It was really remarkable.

I’ve been a practicing Buddhist since I was 19. When I went back to school to become a chaplain I wanted to bring more of my spiritual interest into counseling work, so chaplaincy seemed like a really interesting way to do that.

Tell us more about what a chaplain actually does.

As a field, healthcare chaplaincy is relatively new. The old model was if a person was religious, somebody would arrange for a rabbi or an imam or a priest to come into the hospital and take care of the pastoral needs of that patient. In the last 10 to 15 years, the consensus guidelines for quality patient care now include addressing the spiritual dimension of patients’ lives. Instead of relying on volunteers from the community with no quality assurance, it’s required that any hospital over 200 beds have spiritual care available. In order to be a board-certified chaplain, you need to be endorsed by a faith community, and have an advanced degree in either Pastoral Counseling or Theology.

Everybody has spiritual needs even if they don’t use that word “spiritual.” We define it in terms of meaning, relationships, impact on one’s life, hope, fears, reconciliation issues, legacy issues, etc. Approximately 80% of patients want their physicians to understand a little bit about their spiritual/existential/emotional world, and only 20% of doctors ask—so there’s a really big gap. This can be a 5-minute conversation about who are you, what’s important to you, what’s the biggest struggle with your illness that is not medically oriented.

Can you share a patient encounter where you learned something?

Recently I cared for a patient whose wish was to survive to see his only son graduate from college. His wife and son both were like, “You’ve got to hang in there, Dad. You’ve got to hang in there.” He had very advanced pancreatic cancer, and the chances of him making it to graduation were exceedingly small, but nobody was dealing with this.

During the hospitalization, I went to the patient and his wife and I said, “We’re all hoping that you’re going to make it until the graduation but in the event you don’t, would you like to write a letter to your son?” In the Jewish tradition, it is called an ethical will. It’s the idea of legacy work. Just like you would make a will for your material possessions, an ethical will expresses what you value, what you hope for and dream for your beloved. He wanted to do it. His wife said, “Absolutely not, that’s like believing you’re not going to make it.” He was a very gentle guy. He would generally completely defer to his wife, but this time he said, “No, I want to do this.”

So I met with the patient and asked questions like, “What are the things you would hope to be remembered for? What are you most proud of that you want your son to know? What would you want your son to know if he became a father?”

I had him just talk, while I took notes. Later on, I wrote it up on official stationery and gave it to the patient.

 

 

What was his reaction when you gave the letter to him?

He started to cry. He said it was perfect. I usually read it to them so they can make edits if they want to. It sort of brings the grief forward when you imagine talking to a beloved that you’re leaving behind.

A few days later the patient died in the hospital surrounded by family members.

His wife, who had advocated so strongly against the letter, hugged me. She said, “That letter is the most important thing that happened here in the hospital.” I was shocked she said that, I had no idea he even shared it with her.

If people have the opportunity to share what’s important to them, particularly generationally, it could address a very deep need to be remembered.

Reflecting on it, I actually see myself as a healer and all my work is in healing, whether it’s working with physicians or working with patients or working with students or working with people in my private practice. It’s a theme that runs through everything. It’s not a word we hear often enough in medicine.

Why not?

The culture of medicine has lost its roots, in that sense. I hear a lot of people say, “There’s nothing we can do medically, so we’re just supporting them through this.” Supporting people through the experience is often seen as less valuable, but I think, particularly for serious, terminal illness, supporting people is not optional.

Switching gears a bit, tell us about the skill-building and resilience work you’ve done.

I think if you don’t proactively care for the rest of your life then your work life takes over. Although it’s pronounced in medicine, it’s in all fields. The pace and stress of our contemporary culture can be contrary to well-being in general.

When I first came to UCSF, I saw a culture of silence around stress, anxiety, and burnout. I started reading about burnout and the numbers of people who qualified to be burnt out at any given time, which may be at least 50% and trending upward. It just seemed to me that in any other profession if half the workforce was impaired, somebody would be doing something. I’ve really become passionate about this in the last couple of years.

So I developed a burnout prevention and resilience skills training class for providers. We work on mindfulness, social connection and support, positive psychology emotions like gratitude, appreciation, self-compassion, and humor, and delve into the sources of meaning in our work.

Based on your work, what would you say are the key stressors in medicine, generally?

Well there’s research on the electronic medical record and the increasing focus on metrics and “value-driven medicine,” which can lead to reduced connection with patients. I hope that what I’m doing makes some difference, but fundamentally, I believe there needs to be a real commitment on the part of the health system, to understand and make the changes that need to happen.

What is the fundamental problem? How do you define that?

Well I don’t think anybody knows. I think that’s what we’re saying. How can it be that so many people aren’t happy in such privileged work? It’s not clinical. It’s the system. It’s yet another flow sheet that you have to fill out; the actual amount of time spent with patients is low. No wonder we get burned out. We’re just doing orders all the time and answering phone calls.

It’s the loss of interconnectedness.

Yes, it’s the loss of connection. That goes back to even why chaplains may not be recognized as adding value. You can’t put a metric on connection. You can’t say, “I made 5 connections.”

Anything else you would like to share?

I don’t know how you feel about it, but I feel so grateful to have the opportunity to be in people’s lives in the intimate way we get to be and I, especially, get to be in a way sometimes even more than doctors. You get to be there, and you may even want to talk about the things that we were mentioning, but they’re asking you about their creatinine and their platelets and their urinary incontinence, so that’s what you’re having to talk about. I don’t have to do that, so I feel like I get the best seat in the house that way.

I think the seriously ill have so much to share and often are wise, particularly the young ones, from having dealt with illness. I’m really interested in that idea of wisdom and how you develop wisdom. Traditionally wisdom is associated with being an elder and having lived a long time and having a lot of experience. I think our work gives us that opportunity. We don’t have to necessarily live through everything to develop that kind of wisdom, but just to be with people who are living through these things.

So here I am, almost 70. I’m working harder than I’ve ever worked in my life. My partner is retired. She’s like, “Come on, let’s play.” She rides bikes, takes the dog out, cooks, reads. But I just can’t stop. I think it’s because I feel like, what else would I want to be doing with my time? I think that’s an amazing thing to be given that gift that I learn from my patients all the time and learn about what’s important. Obviously people are different, but it all boils down to relationships in the end.

That’s the promise of medicine, and I think that’s the great sadness of what’s going on with the epidemic of burnout. People lose connection to that.

 

 

There is some element to being present in these hard and difficult times that can bring perspective to life; and to know the sadness, in some ways

…is to know the joy.

Thank you, Denah, for sharing your thoughts with us.

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We recently spoke with Denah Joseph, a clinical chaplain who works with the Palliative Care team to provide spiritual services to patients with serious illness. In addition, Denah leads efforts to address burnout among healthcare providers.

Denah, tell us about yourself.

My first career was actually in clinical psychology, but I’ve been a Palliative Care chaplain for 15 years. I also teach skill-building for providers around burnout and resilience.

What brought you to Palliative Care?

I’ve lost three sisters and a partner to breast cancer, and my dad died when I was quite young, so I’ve had a lot of exposure to loss. The other big thread in my life has been my spiritual practice. My father was an Orthodox Jew, but exceptionally ecumenical for his time. His first wife was Irish Catholic, and my father used to go to church, sit, kneel, and say the rosary, and light candles for his Catholic friends. Three hundred nuns from the local diocese all came to my dad’s funeral. It was really remarkable.

I’ve been a practicing Buddhist since I was 19. When I went back to school to become a chaplain I wanted to bring more of my spiritual interest into counseling work, so chaplaincy seemed like a really interesting way to do that.

Tell us more about what a chaplain actually does.

As a field, healthcare chaplaincy is relatively new. The old model was if a person was religious, somebody would arrange for a rabbi or an imam or a priest to come into the hospital and take care of the pastoral needs of that patient. In the last 10 to 15 years, the consensus guidelines for quality patient care now include addressing the spiritual dimension of patients’ lives. Instead of relying on volunteers from the community with no quality assurance, it’s required that any hospital over 200 beds have spiritual care available. In order to be a board-certified chaplain, you need to be endorsed by a faith community, and have an advanced degree in either Pastoral Counseling or Theology.

Everybody has spiritual needs even if they don’t use that word “spiritual.” We define it in terms of meaning, relationships, impact on one’s life, hope, fears, reconciliation issues, legacy issues, etc. Approximately 80% of patients want their physicians to understand a little bit about their spiritual/existential/emotional world, and only 20% of doctors ask—so there’s a really big gap. This can be a 5-minute conversation about who are you, what’s important to you, what’s the biggest struggle with your illness that is not medically oriented.

Can you share a patient encounter where you learned something?

Recently I cared for a patient whose wish was to survive to see his only son graduate from college. His wife and son both were like, “You’ve got to hang in there, Dad. You’ve got to hang in there.” He had very advanced pancreatic cancer, and the chances of him making it to graduation were exceedingly small, but nobody was dealing with this.

During the hospitalization, I went to the patient and his wife and I said, “We’re all hoping that you’re going to make it until the graduation but in the event you don’t, would you like to write a letter to your son?” In the Jewish tradition, it is called an ethical will. It’s the idea of legacy work. Just like you would make a will for your material possessions, an ethical will expresses what you value, what you hope for and dream for your beloved. He wanted to do it. His wife said, “Absolutely not, that’s like believing you’re not going to make it.” He was a very gentle guy. He would generally completely defer to his wife, but this time he said, “No, I want to do this.”

So I met with the patient and asked questions like, “What are the things you would hope to be remembered for? What are you most proud of that you want your son to know? What would you want your son to know if he became a father?”

I had him just talk, while I took notes. Later on, I wrote it up on official stationery and gave it to the patient.

 

 

What was his reaction when you gave the letter to him?

He started to cry. He said it was perfect. I usually read it to them so they can make edits if they want to. It sort of brings the grief forward when you imagine talking to a beloved that you’re leaving behind.

A few days later the patient died in the hospital surrounded by family members.

His wife, who had advocated so strongly against the letter, hugged me. She said, “That letter is the most important thing that happened here in the hospital.” I was shocked she said that, I had no idea he even shared it with her.

If people have the opportunity to share what’s important to them, particularly generationally, it could address a very deep need to be remembered.

Reflecting on it, I actually see myself as a healer and all my work is in healing, whether it’s working with physicians or working with patients or working with students or working with people in my private practice. It’s a theme that runs through everything. It’s not a word we hear often enough in medicine.

Why not?

The culture of medicine has lost its roots, in that sense. I hear a lot of people say, “There’s nothing we can do medically, so we’re just supporting them through this.” Supporting people through the experience is often seen as less valuable, but I think, particularly for serious, terminal illness, supporting people is not optional.

Switching gears a bit, tell us about the skill-building and resilience work you’ve done.

I think if you don’t proactively care for the rest of your life then your work life takes over. Although it’s pronounced in medicine, it’s in all fields. The pace and stress of our contemporary culture can be contrary to well-being in general.

When I first came to UCSF, I saw a culture of silence around stress, anxiety, and burnout. I started reading about burnout and the numbers of people who qualified to be burnt out at any given time, which may be at least 50% and trending upward. It just seemed to me that in any other profession if half the workforce was impaired, somebody would be doing something. I’ve really become passionate about this in the last couple of years.

So I developed a burnout prevention and resilience skills training class for providers. We work on mindfulness, social connection and support, positive psychology emotions like gratitude, appreciation, self-compassion, and humor, and delve into the sources of meaning in our work.

Based on your work, what would you say are the key stressors in medicine, generally?

Well there’s research on the electronic medical record and the increasing focus on metrics and “value-driven medicine,” which can lead to reduced connection with patients. I hope that what I’m doing makes some difference, but fundamentally, I believe there needs to be a real commitment on the part of the health system, to understand and make the changes that need to happen.

What is the fundamental problem? How do you define that?

Well I don’t think anybody knows. I think that’s what we’re saying. How can it be that so many people aren’t happy in such privileged work? It’s not clinical. It’s the system. It’s yet another flow sheet that you have to fill out; the actual amount of time spent with patients is low. No wonder we get burned out. We’re just doing orders all the time and answering phone calls.

It’s the loss of interconnectedness.

Yes, it’s the loss of connection. That goes back to even why chaplains may not be recognized as adding value. You can’t put a metric on connection. You can’t say, “I made 5 connections.”

Anything else you would like to share?

I don’t know how you feel about it, but I feel so grateful to have the opportunity to be in people’s lives in the intimate way we get to be and I, especially, get to be in a way sometimes even more than doctors. You get to be there, and you may even want to talk about the things that we were mentioning, but they’re asking you about their creatinine and their platelets and their urinary incontinence, so that’s what you’re having to talk about. I don’t have to do that, so I feel like I get the best seat in the house that way.

I think the seriously ill have so much to share and often are wise, particularly the young ones, from having dealt with illness. I’m really interested in that idea of wisdom and how you develop wisdom. Traditionally wisdom is associated with being an elder and having lived a long time and having a lot of experience. I think our work gives us that opportunity. We don’t have to necessarily live through everything to develop that kind of wisdom, but just to be with people who are living through these things.

So here I am, almost 70. I’m working harder than I’ve ever worked in my life. My partner is retired. She’s like, “Come on, let’s play.” She rides bikes, takes the dog out, cooks, reads. But I just can’t stop. I think it’s because I feel like, what else would I want to be doing with my time? I think that’s an amazing thing to be given that gift that I learn from my patients all the time and learn about what’s important. Obviously people are different, but it all boils down to relationships in the end.

That’s the promise of medicine, and I think that’s the great sadness of what’s going on with the epidemic of burnout. People lose connection to that.

 

 

There is some element to being present in these hard and difficult times that can bring perspective to life; and to know the sadness, in some ways

…is to know the joy.

Thank you, Denah, for sharing your thoughts with us.

We recently spoke with Denah Joseph, a clinical chaplain who works with the Palliative Care team to provide spiritual services to patients with serious illness. In addition, Denah leads efforts to address burnout among healthcare providers.

Denah, tell us about yourself.

My first career was actually in clinical psychology, but I’ve been a Palliative Care chaplain for 15 years. I also teach skill-building for providers around burnout and resilience.

What brought you to Palliative Care?

I’ve lost three sisters and a partner to breast cancer, and my dad died when I was quite young, so I’ve had a lot of exposure to loss. The other big thread in my life has been my spiritual practice. My father was an Orthodox Jew, but exceptionally ecumenical for his time. His first wife was Irish Catholic, and my father used to go to church, sit, kneel, and say the rosary, and light candles for his Catholic friends. Three hundred nuns from the local diocese all came to my dad’s funeral. It was really remarkable.

I’ve been a practicing Buddhist since I was 19. When I went back to school to become a chaplain I wanted to bring more of my spiritual interest into counseling work, so chaplaincy seemed like a really interesting way to do that.

Tell us more about what a chaplain actually does.

As a field, healthcare chaplaincy is relatively new. The old model was if a person was religious, somebody would arrange for a rabbi or an imam or a priest to come into the hospital and take care of the pastoral needs of that patient. In the last 10 to 15 years, the consensus guidelines for quality patient care now include addressing the spiritual dimension of patients’ lives. Instead of relying on volunteers from the community with no quality assurance, it’s required that any hospital over 200 beds have spiritual care available. In order to be a board-certified chaplain, you need to be endorsed by a faith community, and have an advanced degree in either Pastoral Counseling or Theology.

Everybody has spiritual needs even if they don’t use that word “spiritual.” We define it in terms of meaning, relationships, impact on one’s life, hope, fears, reconciliation issues, legacy issues, etc. Approximately 80% of patients want their physicians to understand a little bit about their spiritual/existential/emotional world, and only 20% of doctors ask—so there’s a really big gap. This can be a 5-minute conversation about who are you, what’s important to you, what’s the biggest struggle with your illness that is not medically oriented.

Can you share a patient encounter where you learned something?

Recently I cared for a patient whose wish was to survive to see his only son graduate from college. His wife and son both were like, “You’ve got to hang in there, Dad. You’ve got to hang in there.” He had very advanced pancreatic cancer, and the chances of him making it to graduation were exceedingly small, but nobody was dealing with this.

During the hospitalization, I went to the patient and his wife and I said, “We’re all hoping that you’re going to make it until the graduation but in the event you don’t, would you like to write a letter to your son?” In the Jewish tradition, it is called an ethical will. It’s the idea of legacy work. Just like you would make a will for your material possessions, an ethical will expresses what you value, what you hope for and dream for your beloved. He wanted to do it. His wife said, “Absolutely not, that’s like believing you’re not going to make it.” He was a very gentle guy. He would generally completely defer to his wife, but this time he said, “No, I want to do this.”

So I met with the patient and asked questions like, “What are the things you would hope to be remembered for? What are you most proud of that you want your son to know? What would you want your son to know if he became a father?”

I had him just talk, while I took notes. Later on, I wrote it up on official stationery and gave it to the patient.

 

 

What was his reaction when you gave the letter to him?

He started to cry. He said it was perfect. I usually read it to them so they can make edits if they want to. It sort of brings the grief forward when you imagine talking to a beloved that you’re leaving behind.

A few days later the patient died in the hospital surrounded by family members.

His wife, who had advocated so strongly against the letter, hugged me. She said, “That letter is the most important thing that happened here in the hospital.” I was shocked she said that, I had no idea he even shared it with her.

If people have the opportunity to share what’s important to them, particularly generationally, it could address a very deep need to be remembered.

Reflecting on it, I actually see myself as a healer and all my work is in healing, whether it’s working with physicians or working with patients or working with students or working with people in my private practice. It’s a theme that runs through everything. It’s not a word we hear often enough in medicine.

Why not?

The culture of medicine has lost its roots, in that sense. I hear a lot of people say, “There’s nothing we can do medically, so we’re just supporting them through this.” Supporting people through the experience is often seen as less valuable, but I think, particularly for serious, terminal illness, supporting people is not optional.

Switching gears a bit, tell us about the skill-building and resilience work you’ve done.

I think if you don’t proactively care for the rest of your life then your work life takes over. Although it’s pronounced in medicine, it’s in all fields. The pace and stress of our contemporary culture can be contrary to well-being in general.

When I first came to UCSF, I saw a culture of silence around stress, anxiety, and burnout. I started reading about burnout and the numbers of people who qualified to be burnt out at any given time, which may be at least 50% and trending upward. It just seemed to me that in any other profession if half the workforce was impaired, somebody would be doing something. I’ve really become passionate about this in the last couple of years.

So I developed a burnout prevention and resilience skills training class for providers. We work on mindfulness, social connection and support, positive psychology emotions like gratitude, appreciation, self-compassion, and humor, and delve into the sources of meaning in our work.

Based on your work, what would you say are the key stressors in medicine, generally?

Well there’s research on the electronic medical record and the increasing focus on metrics and “value-driven medicine,” which can lead to reduced connection with patients. I hope that what I’m doing makes some difference, but fundamentally, I believe there needs to be a real commitment on the part of the health system, to understand and make the changes that need to happen.

What is the fundamental problem? How do you define that?

Well I don’t think anybody knows. I think that’s what we’re saying. How can it be that so many people aren’t happy in such privileged work? It’s not clinical. It’s the system. It’s yet another flow sheet that you have to fill out; the actual amount of time spent with patients is low. No wonder we get burned out. We’re just doing orders all the time and answering phone calls.

It’s the loss of interconnectedness.

Yes, it’s the loss of connection. That goes back to even why chaplains may not be recognized as adding value. You can’t put a metric on connection. You can’t say, “I made 5 connections.”

Anything else you would like to share?

I don’t know how you feel about it, but I feel so grateful to have the opportunity to be in people’s lives in the intimate way we get to be and I, especially, get to be in a way sometimes even more than doctors. You get to be there, and you may even want to talk about the things that we were mentioning, but they’re asking you about their creatinine and their platelets and their urinary incontinence, so that’s what you’re having to talk about. I don’t have to do that, so I feel like I get the best seat in the house that way.

I think the seriously ill have so much to share and often are wise, particularly the young ones, from having dealt with illness. I’m really interested in that idea of wisdom and how you develop wisdom. Traditionally wisdom is associated with being an elder and having lived a long time and having a lot of experience. I think our work gives us that opportunity. We don’t have to necessarily live through everything to develop that kind of wisdom, but just to be with people who are living through these things.

So here I am, almost 70. I’m working harder than I’ve ever worked in my life. My partner is retired. She’s like, “Come on, let’s play.” She rides bikes, takes the dog out, cooks, reads. But I just can’t stop. I think it’s because I feel like, what else would I want to be doing with my time? I think that’s an amazing thing to be given that gift that I learn from my patients all the time and learn about what’s important. Obviously people are different, but it all boils down to relationships in the end.

That’s the promise of medicine, and I think that’s the great sadness of what’s going on with the epidemic of burnout. People lose connection to that.

 

 

There is some element to being present in these hard and difficult times that can bring perspective to life; and to know the sadness, in some ways

…is to know the joy.

Thank you, Denah, for sharing your thoughts with us.

Issue
Journal of Hospital Medicine 13(3)
Issue
Journal of Hospital Medicine 13(3)
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203-204
Page Number
203-204
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