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All Aboard the HM Train
A small Illinois hospital has joined the ranks of facilities—including its neighbors—in adding a hospital medicine (HM) program. The Genesis Medical Center, Illini Campus, in Silvas, Ill., began providing full-time hospitalist coverage on Dec. 1.
As the influx of hospitalists allowed local primary care physicians to stop making hospital visits, the Illini Campus rushed to fill the gap with its own HM program. "We were the last acute care hospital to implement a hospitalist program," says Chuck Bruhn, CEO of Illini Campus. "It had become a medical community issue."
Illini Campus, located near the Quad Cities on the western Illinois-eastern Iowa border, is a 149-bed facility with an average daily census of 50 to 55 patients. Its sister facility, the Genesis Medical Center in Davenport, Iowa, has had a successful hospital medicine program since 2005. Genesis' agreement with Cogent Healthcare, Inc., recently expanded to manage the program at Illini Campus, with round-the-clock coverage, including one full-time hospitalist.
Just two weeks after implementation, "the hospitalist program is growing much more rapidly than we had anticipated," Bruhn says. "They’re already covering a census of 14 patients a day. We're already talking about adding a physician extender."
Bruhn is pleased with the way the fledgling program has taken root. "We see it as a definite improvement, not only to quality and continuity of care, but to expediency of care. And the hospitalists provide additional support; they provide education to our clinical staff."
A small Illinois hospital has joined the ranks of facilities—including its neighbors—in adding a hospital medicine (HM) program. The Genesis Medical Center, Illini Campus, in Silvas, Ill., began providing full-time hospitalist coverage on Dec. 1.
As the influx of hospitalists allowed local primary care physicians to stop making hospital visits, the Illini Campus rushed to fill the gap with its own HM program. "We were the last acute care hospital to implement a hospitalist program," says Chuck Bruhn, CEO of Illini Campus. "It had become a medical community issue."
Illini Campus, located near the Quad Cities on the western Illinois-eastern Iowa border, is a 149-bed facility with an average daily census of 50 to 55 patients. Its sister facility, the Genesis Medical Center in Davenport, Iowa, has had a successful hospital medicine program since 2005. Genesis' agreement with Cogent Healthcare, Inc., recently expanded to manage the program at Illini Campus, with round-the-clock coverage, including one full-time hospitalist.
Just two weeks after implementation, "the hospitalist program is growing much more rapidly than we had anticipated," Bruhn says. "They’re already covering a census of 14 patients a day. We're already talking about adding a physician extender."
Bruhn is pleased with the way the fledgling program has taken root. "We see it as a definite improvement, not only to quality and continuity of care, but to expediency of care. And the hospitalists provide additional support; they provide education to our clinical staff."
A small Illinois hospital has joined the ranks of facilities—including its neighbors—in adding a hospital medicine (HM) program. The Genesis Medical Center, Illini Campus, in Silvas, Ill., began providing full-time hospitalist coverage on Dec. 1.
As the influx of hospitalists allowed local primary care physicians to stop making hospital visits, the Illini Campus rushed to fill the gap with its own HM program. "We were the last acute care hospital to implement a hospitalist program," says Chuck Bruhn, CEO of Illini Campus. "It had become a medical community issue."
Illini Campus, located near the Quad Cities on the western Illinois-eastern Iowa border, is a 149-bed facility with an average daily census of 50 to 55 patients. Its sister facility, the Genesis Medical Center in Davenport, Iowa, has had a successful hospital medicine program since 2005. Genesis' agreement with Cogent Healthcare, Inc., recently expanded to manage the program at Illini Campus, with round-the-clock coverage, including one full-time hospitalist.
Just two weeks after implementation, "the hospitalist program is growing much more rapidly than we had anticipated," Bruhn says. "They’re already covering a census of 14 patients a day. We're already talking about adding a physician extender."
Bruhn is pleased with the way the fledgling program has taken root. "We see it as a definite improvement, not only to quality and continuity of care, but to expediency of care. And the hospitalists provide additional support; they provide education to our clinical staff."
NFL Star’s Injury Spotlights Reporting Requirements
The recent suspension of a New York City doctor who failed to report a gunshot wound suffered by a football star is an opportunity for hospitalists to revisit their own reporting requirements, the president of SHM's NYC chapter says.
Josyann Abisaab, MD, of New York-Presbyterian Hospital/Weill Cornell Medical Center, was suspended after treating New York Giants wide receiver Plaxico Burress on Nov. 29. Less than a year after catching the winning touchdown pass in the Giants' Super Bowl victory, Burress, who told police he accidentally shot himself in the thigh at a NYC nightclub, has been suspended by the league and charged with criminal possession of a gun.
"I was not aware that something like this needed a report to the police," says Bradley Flansbaum, DO, MPH, chief of hospitalist services at Lenox Hill Hospital in Manhattan and president of SHM’s NYC chapter. "It opened up space in my brain. If I were confronted with this, when would I know when to and when not to call the police?"
Complicating matters is the fact hospitalists may have to report issues to more than just law enforcement; depending on diagnoses and patient histories, doctors may have to notify state and federal health agencies or social service departments. Rules vary by state, so Dr. Flansbaum says hospitalists would do well to brush up on their requirements and liabilities.
"I may not know the rules," Dr. Flansbaum said, "but I certainly would speak to the right people here and ask them: 'What are my obligations? How do I protect myself and the patient?' " He recommends hospitalists verify local requirements with their hospital administration.
The recent suspension of a New York City doctor who failed to report a gunshot wound suffered by a football star is an opportunity for hospitalists to revisit their own reporting requirements, the president of SHM's NYC chapter says.
Josyann Abisaab, MD, of New York-Presbyterian Hospital/Weill Cornell Medical Center, was suspended after treating New York Giants wide receiver Plaxico Burress on Nov. 29. Less than a year after catching the winning touchdown pass in the Giants' Super Bowl victory, Burress, who told police he accidentally shot himself in the thigh at a NYC nightclub, has been suspended by the league and charged with criminal possession of a gun.
"I was not aware that something like this needed a report to the police," says Bradley Flansbaum, DO, MPH, chief of hospitalist services at Lenox Hill Hospital in Manhattan and president of SHM’s NYC chapter. "It opened up space in my brain. If I were confronted with this, when would I know when to and when not to call the police?"
Complicating matters is the fact hospitalists may have to report issues to more than just law enforcement; depending on diagnoses and patient histories, doctors may have to notify state and federal health agencies or social service departments. Rules vary by state, so Dr. Flansbaum says hospitalists would do well to brush up on their requirements and liabilities.
"I may not know the rules," Dr. Flansbaum said, "but I certainly would speak to the right people here and ask them: 'What are my obligations? How do I protect myself and the patient?' " He recommends hospitalists verify local requirements with their hospital administration.
The recent suspension of a New York City doctor who failed to report a gunshot wound suffered by a football star is an opportunity for hospitalists to revisit their own reporting requirements, the president of SHM's NYC chapter says.
Josyann Abisaab, MD, of New York-Presbyterian Hospital/Weill Cornell Medical Center, was suspended after treating New York Giants wide receiver Plaxico Burress on Nov. 29. Less than a year after catching the winning touchdown pass in the Giants' Super Bowl victory, Burress, who told police he accidentally shot himself in the thigh at a NYC nightclub, has been suspended by the league and charged with criminal possession of a gun.
"I was not aware that something like this needed a report to the police," says Bradley Flansbaum, DO, MPH, chief of hospitalist services at Lenox Hill Hospital in Manhattan and president of SHM’s NYC chapter. "It opened up space in my brain. If I were confronted with this, when would I know when to and when not to call the police?"
Complicating matters is the fact hospitalists may have to report issues to more than just law enforcement; depending on diagnoses and patient histories, doctors may have to notify state and federal health agencies or social service departments. Rules vary by state, so Dr. Flansbaum says hospitalists would do well to brush up on their requirements and liabilities.
"I may not know the rules," Dr. Flansbaum said, "but I certainly would speak to the right people here and ask them: 'What are my obligations? How do I protect myself and the patient?' " He recommends hospitalists verify local requirements with their hospital administration.
Research Roundup
Question: Is sodium bicarbonate superior to sodium chloride in preventing contrast-induced nephropathy in patients with chronic kidney disease (CKD) undergoing coronary angiography?
Background: Sodium bicarbonate has been suggested as a possible strategy to prevent contrast-induced nephropathy—a condition that can lead to prolonged hospitalization, increased healthcare costs, and substantial morbidity and mortality.
Study design: Randomized, controlled, single-blind study.
Setting: Kaiser Permanente Medical Center, Los Angeles.
Synopsis: Data were collected over 12 months by selecting 353 patients with stable CKD undergoing coronary angiography who were 18 or older and had an estimated glomerular filtration rate (GFR) of 60mL/min/1.73m2 or less and one or more of diabetes mellitus, congestive heart failure, hypertension, or age older than 75 years. Patients were randomized to received sodium chloride (n=178) and sodium bicarbonate (n=175) at the same rate and duration.
There was no statistical difference in the primary endpoint (p=0.82), which was a 25% or greater decrease in the GFR on days 1 through 4 after contrast exposure.
Study results were limited by several factors; most importantly, it was not a double-blinded study and was performed at a single center. Also, the sodium content of the two fluids varied; normal saline carried 154mEq and sodium bicarbonate 130mEq of sodium, respectively.
Bottom line: Hydration with sodium bicarbonate is not superior to sodium chloride in preventing contrast-induced nephropathy in patients with moderate to severe CKD undergoing coronary angiography.
Citation: JAMA. 2008;300(9):1038-1046
—Reviewed for the e-wire by Elbert Chun, MD, John Vazquez, MD, Larry Beer, MD, Maged Doss, MD, Vana Bollineni, MD, Mohammed S. Singapuri, MD, Dan Dressler, MD, MsCR, Emory University Hospital, Atlanta
Question: Is sodium bicarbonate superior to sodium chloride in preventing contrast-induced nephropathy in patients with chronic kidney disease (CKD) undergoing coronary angiography?
Background: Sodium bicarbonate has been suggested as a possible strategy to prevent contrast-induced nephropathy—a condition that can lead to prolonged hospitalization, increased healthcare costs, and substantial morbidity and mortality.
Study design: Randomized, controlled, single-blind study.
Setting: Kaiser Permanente Medical Center, Los Angeles.
Synopsis: Data were collected over 12 months by selecting 353 patients with stable CKD undergoing coronary angiography who were 18 or older and had an estimated glomerular filtration rate (GFR) of 60mL/min/1.73m2 or less and one or more of diabetes mellitus, congestive heart failure, hypertension, or age older than 75 years. Patients were randomized to received sodium chloride (n=178) and sodium bicarbonate (n=175) at the same rate and duration.
There was no statistical difference in the primary endpoint (p=0.82), which was a 25% or greater decrease in the GFR on days 1 through 4 after contrast exposure.
Study results were limited by several factors; most importantly, it was not a double-blinded study and was performed at a single center. Also, the sodium content of the two fluids varied; normal saline carried 154mEq and sodium bicarbonate 130mEq of sodium, respectively.
Bottom line: Hydration with sodium bicarbonate is not superior to sodium chloride in preventing contrast-induced nephropathy in patients with moderate to severe CKD undergoing coronary angiography.
Citation: JAMA. 2008;300(9):1038-1046
—Reviewed for the e-wire by Elbert Chun, MD, John Vazquez, MD, Larry Beer, MD, Maged Doss, MD, Vana Bollineni, MD, Mohammed S. Singapuri, MD, Dan Dressler, MD, MsCR, Emory University Hospital, Atlanta
Question: Is sodium bicarbonate superior to sodium chloride in preventing contrast-induced nephropathy in patients with chronic kidney disease (CKD) undergoing coronary angiography?
Background: Sodium bicarbonate has been suggested as a possible strategy to prevent contrast-induced nephropathy—a condition that can lead to prolonged hospitalization, increased healthcare costs, and substantial morbidity and mortality.
Study design: Randomized, controlled, single-blind study.
Setting: Kaiser Permanente Medical Center, Los Angeles.
Synopsis: Data were collected over 12 months by selecting 353 patients with stable CKD undergoing coronary angiography who were 18 or older and had an estimated glomerular filtration rate (GFR) of 60mL/min/1.73m2 or less and one or more of diabetes mellitus, congestive heart failure, hypertension, or age older than 75 years. Patients were randomized to received sodium chloride (n=178) and sodium bicarbonate (n=175) at the same rate and duration.
There was no statistical difference in the primary endpoint (p=0.82), which was a 25% or greater decrease in the GFR on days 1 through 4 after contrast exposure.
Study results were limited by several factors; most importantly, it was not a double-blinded study and was performed at a single center. Also, the sodium content of the two fluids varied; normal saline carried 154mEq and sodium bicarbonate 130mEq of sodium, respectively.
Bottom line: Hydration with sodium bicarbonate is not superior to sodium chloride in preventing contrast-induced nephropathy in patients with moderate to severe CKD undergoing coronary angiography.
Citation: JAMA. 2008;300(9):1038-1046
—Reviewed for the e-wire by Elbert Chun, MD, John Vazquez, MD, Larry Beer, MD, Maged Doss, MD, Vana Bollineni, MD, Mohammed S. Singapuri, MD, Dan Dressler, MD, MsCR, Emory University Hospital, Atlanta
Study shows imatinib response is durable and improves with time
SAN FRANCISCO—The longest duration study of imatinib treatment for patients with Ph+ CML shows 86% of patients are still alive 7 years after beginning therapy.
The International Randomized Interferon versus STI571 (IRIS) study revealed only 1 early chronic-phase patient progressed to a more advanced phase between years 6 and 7, Stephen O’Brien, MD, PhD, of Newcastle University in the UK, said at the 50th Annual Meeting of the American Society of Hematology.
IRIS is an open-label, phase 3 clinical trial enrolling 1106 newly diagnosed patients with chronic phase Ph+ CML in 177 centers across 16 countries. One group of 553 patients received imatinib 400 mg per day. Another group of 553 patients received a target dose of interferon (IFN) of 5 MIU/m2/day in combination with cytarabine at 20 mg/m2/day for 10 days each month.
Because of tolerability issues, lack of response, or loss of response, 65% of patients in the IFN/cytarabine arm crossed over to the imatinib arm. Only 3% of patients in the imatinib arm crossed over to the IFN/cytarabine arm.
A low rate of progression has been reported every year since this trial began in 2001. Seven percent of patients treated with imatinib progressed to advanced phases of CML after 7 years. Of the 456 patients (82%) who achieved a complete cytogenetic response, 17% lost their response and 3% progressed to advanced phases.
“After 1 year of treatment, there is a small risk of progression,” Dr O’Brien said. “If patients achieve and maintain a complete cytogenetic response after 3 years, they are fairly safe.”
Treatment with imatinib in the IRIS study was well tolerated, he said. No new serious adverse events occurred between the sixth and seventh year of treatment.
The results from the IRIS study also reveal that, by year 6, 85% to 90% of patients still taking imatinib achieved a major molecular response. This key milestone indicates a reduction in the abnormal protein responsible for the uncontrolled production of abnormal white blood cells and may be a sensitive predictor of long-term progression-free survival.
“There was a steady improvement in major molecular responses between 4 and 7 years of treatment,” said Timothy Hughes, MD, of the Institute of Medical and Veterinary Science in Adelaide, Australia. “By 7 years, the vast majority of patients who achieved a complete cytogenetic response also achieved a major molecular response.”
A major molecular response at any time point represents a “safe haven” for patients, Dr Hughes said. Both molecular and cytogenetic evaluations should be used to guide treatment decisions until a complete cytogenetic response is achieved, followed by measurements of molecular assessments.
“In this, the seventh year of the IRIS study, CML patients treated with imatinib continue to demonstrate impressive long-term survival,” Dr O’Brien said. “Imatinib 400 mg daily is confirmed as the standard of care for the initial therapy of chronic-phase CML.”
Imatinib, the first therapy to inhibit the activity of Bcr-Abl, revolutionized the treatment of Ph+ CML, Dr O’Brien said. Prior to imatinib, about 50% of patients with Ph+ CML progressed from the initial phase to more advanced stages after 3 to 5 years. Once patients reached the final blast crisis phase, survival was generally 3 to 6 months. 
SAN FRANCISCO—The longest duration study of imatinib treatment for patients with Ph+ CML shows 86% of patients are still alive 7 years after beginning therapy.
The International Randomized Interferon versus STI571 (IRIS) study revealed only 1 early chronic-phase patient progressed to a more advanced phase between years 6 and 7, Stephen O’Brien, MD, PhD, of Newcastle University in the UK, said at the 50th Annual Meeting of the American Society of Hematology.
IRIS is an open-label, phase 3 clinical trial enrolling 1106 newly diagnosed patients with chronic phase Ph+ CML in 177 centers across 16 countries. One group of 553 patients received imatinib 400 mg per day. Another group of 553 patients received a target dose of interferon (IFN) of 5 MIU/m2/day in combination with cytarabine at 20 mg/m2/day for 10 days each month.
Because of tolerability issues, lack of response, or loss of response, 65% of patients in the IFN/cytarabine arm crossed over to the imatinib arm. Only 3% of patients in the imatinib arm crossed over to the IFN/cytarabine arm.
A low rate of progression has been reported every year since this trial began in 2001. Seven percent of patients treated with imatinib progressed to advanced phases of CML after 7 years. Of the 456 patients (82%) who achieved a complete cytogenetic response, 17% lost their response and 3% progressed to advanced phases.
“After 1 year of treatment, there is a small risk of progression,” Dr O’Brien said. “If patients achieve and maintain a complete cytogenetic response after 3 years, they are fairly safe.”
Treatment with imatinib in the IRIS study was well tolerated, he said. No new serious adverse events occurred between the sixth and seventh year of treatment.
The results from the IRIS study also reveal that, by year 6, 85% to 90% of patients still taking imatinib achieved a major molecular response. This key milestone indicates a reduction in the abnormal protein responsible for the uncontrolled production of abnormal white blood cells and may be a sensitive predictor of long-term progression-free survival.
“There was a steady improvement in major molecular responses between 4 and 7 years of treatment,” said Timothy Hughes, MD, of the Institute of Medical and Veterinary Science in Adelaide, Australia. “By 7 years, the vast majority of patients who achieved a complete cytogenetic response also achieved a major molecular response.”
A major molecular response at any time point represents a “safe haven” for patients, Dr Hughes said. Both molecular and cytogenetic evaluations should be used to guide treatment decisions until a complete cytogenetic response is achieved, followed by measurements of molecular assessments.
“In this, the seventh year of the IRIS study, CML patients treated with imatinib continue to demonstrate impressive long-term survival,” Dr O’Brien said. “Imatinib 400 mg daily is confirmed as the standard of care for the initial therapy of chronic-phase CML.”
Imatinib, the first therapy to inhibit the activity of Bcr-Abl, revolutionized the treatment of Ph+ CML, Dr O’Brien said. Prior to imatinib, about 50% of patients with Ph+ CML progressed from the initial phase to more advanced stages after 3 to 5 years. Once patients reached the final blast crisis phase, survival was generally 3 to 6 months.
SAN FRANCISCO—The longest duration study of imatinib treatment for patients with Ph+ CML shows 86% of patients are still alive 7 years after beginning therapy.
The International Randomized Interferon versus STI571 (IRIS) study revealed only 1 early chronic-phase patient progressed to a more advanced phase between years 6 and 7, Stephen O’Brien, MD, PhD, of Newcastle University in the UK, said at the 50th Annual Meeting of the American Society of Hematology.
IRIS is an open-label, phase 3 clinical trial enrolling 1106 newly diagnosed patients with chronic phase Ph+ CML in 177 centers across 16 countries. One group of 553 patients received imatinib 400 mg per day. Another group of 553 patients received a target dose of interferon (IFN) of 5 MIU/m2/day in combination with cytarabine at 20 mg/m2/day for 10 days each month.
Because of tolerability issues, lack of response, or loss of response, 65% of patients in the IFN/cytarabine arm crossed over to the imatinib arm. Only 3% of patients in the imatinib arm crossed over to the IFN/cytarabine arm.
A low rate of progression has been reported every year since this trial began in 2001. Seven percent of patients treated with imatinib progressed to advanced phases of CML after 7 years. Of the 456 patients (82%) who achieved a complete cytogenetic response, 17% lost their response and 3% progressed to advanced phases.
“After 1 year of treatment, there is a small risk of progression,” Dr O’Brien said. “If patients achieve and maintain a complete cytogenetic response after 3 years, they are fairly safe.”
Treatment with imatinib in the IRIS study was well tolerated, he said. No new serious adverse events occurred between the sixth and seventh year of treatment.
The results from the IRIS study also reveal that, by year 6, 85% to 90% of patients still taking imatinib achieved a major molecular response. This key milestone indicates a reduction in the abnormal protein responsible for the uncontrolled production of abnormal white blood cells and may be a sensitive predictor of long-term progression-free survival.
“There was a steady improvement in major molecular responses between 4 and 7 years of treatment,” said Timothy Hughes, MD, of the Institute of Medical and Veterinary Science in Adelaide, Australia. “By 7 years, the vast majority of patients who achieved a complete cytogenetic response also achieved a major molecular response.”
A major molecular response at any time point represents a “safe haven” for patients, Dr Hughes said. Both molecular and cytogenetic evaluations should be used to guide treatment decisions until a complete cytogenetic response is achieved, followed by measurements of molecular assessments.
“In this, the seventh year of the IRIS study, CML patients treated with imatinib continue to demonstrate impressive long-term survival,” Dr O’Brien said. “Imatinib 400 mg daily is confirmed as the standard of care for the initial therapy of chronic-phase CML.”
Imatinib, the first therapy to inhibit the activity of Bcr-Abl, revolutionized the treatment of Ph+ CML, Dr O’Brien said. Prior to imatinib, about 50% of patients with Ph+ CML progressed from the initial phase to more advanced stages after 3 to 5 years. Once patients reached the final blast crisis phase, survival was generally 3 to 6 months.
Dabigatran safe, effective in elderly surgery patients
San Francisco—Researchers confirmed the safety and efficacy of a lower dose of dabigatran etexilate in elderly hip and total knee replacement surgery patients.
Dabigatran is a new oral thrombin inhibitor recently approved in Europe for the prevention of VTE in patients undergoing this surgery. Ola E. Dahl, MD, of the Thrombosis Research Institute in London, reported the results of a post hoc pooled analysis of 2 pivotal trials comparing dabigatran with enoxaparin at the 50th Annual Meeting of the American Society of Hematology.
Dr Dahl and colleagues analyzed 883 patients older than 75 years who were enrolled in the RE-MODEL and RE-NOVATE trials. Researchers evaluated 220 mg and 150 mg once-daily doses of dabigatran compared to a 40 mg daily dose of enoxaparin.
The primary efficacy endpoint was total number of VTEs and all-cause mortality. Both doses of dabigatran reduced total VTEs compared to enoxaparin, though not significantly.
However, the higher dose of dabigatran produced a significant difference in the secondary endpoint, major VTEs and VTE-related mortality. Four of 216 patients (1.9%) receiving the 220 mg dose had a major VTE, compared with 13 of 218 patients receiving enoxaparin (P=0.045).
The safety endpoint was the difference in major bleeding events, including surgical site bleeding, which accounts for up to 90% of bleeding in these patients. Major bleeding events occurred in 3.7% of the patients receiving dabigatran at 220 mg and 1.4% receiving 150 mg, compared to 2.9% in the enoxaparin group. The study was not powered to show significance in the safety endpoint.
“If you look into the dabigatran regimens versus enoxaparin, you see that we have more efficacious 200 mg dosing with slightly increased bleeding,” Dr Dahl said. “The 150 mg dose has the same efficacy level, but with a little less bleeding. And that is exactly the profile we are looking for in the elderly.”
San Francisco—Researchers confirmed the safety and efficacy of a lower dose of dabigatran etexilate in elderly hip and total knee replacement surgery patients.
Dabigatran is a new oral thrombin inhibitor recently approved in Europe for the prevention of VTE in patients undergoing this surgery. Ola E. Dahl, MD, of the Thrombosis Research Institute in London, reported the results of a post hoc pooled analysis of 2 pivotal trials comparing dabigatran with enoxaparin at the 50th Annual Meeting of the American Society of Hematology.
Dr Dahl and colleagues analyzed 883 patients older than 75 years who were enrolled in the RE-MODEL and RE-NOVATE trials. Researchers evaluated 220 mg and 150 mg once-daily doses of dabigatran compared to a 40 mg daily dose of enoxaparin.
The primary efficacy endpoint was total number of VTEs and all-cause mortality. Both doses of dabigatran reduced total VTEs compared to enoxaparin, though not significantly.
However, the higher dose of dabigatran produced a significant difference in the secondary endpoint, major VTEs and VTE-related mortality. Four of 216 patients (1.9%) receiving the 220 mg dose had a major VTE, compared with 13 of 218 patients receiving enoxaparin (P=0.045).
The safety endpoint was the difference in major bleeding events, including surgical site bleeding, which accounts for up to 90% of bleeding in these patients. Major bleeding events occurred in 3.7% of the patients receiving dabigatran at 220 mg and 1.4% receiving 150 mg, compared to 2.9% in the enoxaparin group. The study was not powered to show significance in the safety endpoint.
“If you look into the dabigatran regimens versus enoxaparin, you see that we have more efficacious 200 mg dosing with slightly increased bleeding,” Dr Dahl said. “The 150 mg dose has the same efficacy level, but with a little less bleeding. And that is exactly the profile we are looking for in the elderly.”
San Francisco—Researchers confirmed the safety and efficacy of a lower dose of dabigatran etexilate in elderly hip and total knee replacement surgery patients.
Dabigatran is a new oral thrombin inhibitor recently approved in Europe for the prevention of VTE in patients undergoing this surgery. Ola E. Dahl, MD, of the Thrombosis Research Institute in London, reported the results of a post hoc pooled analysis of 2 pivotal trials comparing dabigatran with enoxaparin at the 50th Annual Meeting of the American Society of Hematology.
Dr Dahl and colleagues analyzed 883 patients older than 75 years who were enrolled in the RE-MODEL and RE-NOVATE trials. Researchers evaluated 220 mg and 150 mg once-daily doses of dabigatran compared to a 40 mg daily dose of enoxaparin.
The primary efficacy endpoint was total number of VTEs and all-cause mortality. Both doses of dabigatran reduced total VTEs compared to enoxaparin, though not significantly.
However, the higher dose of dabigatran produced a significant difference in the secondary endpoint, major VTEs and VTE-related mortality. Four of 216 patients (1.9%) receiving the 220 mg dose had a major VTE, compared with 13 of 218 patients receiving enoxaparin (P=0.045).
The safety endpoint was the difference in major bleeding events, including surgical site bleeding, which accounts for up to 90% of bleeding in these patients. Major bleeding events occurred in 3.7% of the patients receiving dabigatran at 220 mg and 1.4% receiving 150 mg, compared to 2.9% in the enoxaparin group. The study was not powered to show significance in the safety endpoint.
“If you look into the dabigatran regimens versus enoxaparin, you see that we have more efficacious 200 mg dosing with slightly increased bleeding,” Dr Dahl said. “The 150 mg dose has the same efficacy level, but with a little less bleeding. And that is exactly the profile we are looking for in the elderly.”
Fostamatinib for Lymphoma, Leukemia
Dr. Jonathan Friedberg discusses an experimental targeted oral agent, fostamatinib, that's being used to treat diffuse large B-cell lymphoma and chronic lymphocytic leukemia. Jane MacNeil of Elsevier Global Medical News (EGMN) reports from the annual meeting of the American Society of Hematology.
Dr. Jonathan Friedberg discusses an experimental targeted oral agent, fostamatinib, that's being used to treat diffuse large B-cell lymphoma and chronic lymphocytic leukemia. Jane MacNeil of Elsevier Global Medical News (EGMN) reports from the annual meeting of the American Society of Hematology.
Dr. Jonathan Friedberg discusses an experimental targeted oral agent, fostamatinib, that's being used to treat diffuse large B-cell lymphoma and chronic lymphocytic leukemia. Jane MacNeil of Elsevier Global Medical News (EGMN) reports from the annual meeting of the American Society of Hematology.
Eltrombopag in Chronic ITP
Dr. Gregory Cheng says patients with chronic idiopathic thrombocytopenia purpura are more likely to achieve target platelet counts when treated with oral eltrombopag. Jane MacNeil of Elsevier Global Medical News (EGMN) reports from the annual meeting of the American Society of Hematology.
Dr. Gregory Cheng says patients with chronic idiopathic thrombocytopenia purpura are more likely to achieve target platelet counts when treated with oral eltrombopag. Jane MacNeil of Elsevier Global Medical News (EGMN) reports from the annual meeting of the American Society of Hematology.
Dr. Gregory Cheng says patients with chronic idiopathic thrombocytopenia purpura are more likely to achieve target platelet counts when treated with oral eltrombopag. Jane MacNeil of Elsevier Global Medical News (EGMN) reports from the annual meeting of the American Society of Hematology.
IOM Recommends Resident Duty Hour Revisions
The Institute of Medicine (IOM) issued a report this month calling for limits to shifts worked by residents, a move that, if implemented, likely means more work for in-house hospitalists, according to one hospital medicine leader.
IOM recommends no change to the current maximum 80-hour workweek for residents, or to the maximum shift length of 30 hours. The report does, however, recommend residents only treat patients for up to 16 hours during their shift, down from the current recommendation of 24 hours. It also suggests residents take an uninterrupted five hours for a continuous sleep period between 10 p.m. and 8 a.m.
In 2003, the Accreditation Council for Graduate Medical Education restricted resident workweeks in order to protect patients and residents from unsafe conditions resulting from excessive fatigue. As mentioned in "While Residents Rest…" in The Hospitalist (August 2006), the resulting shift in workload stressed many hospitals relying on residents for coverage, and some believe it helped boost the need for hospitalists.
In teaching hospitals that follow the IOM recommendations, "I do think this work will go to hospitalists," says Sameer Badlani, MD, a hospitalist and instructor at the University of Chicago. "This is a good thing, in my opinion, as it will enhance the value a hospitalist program brings to an institution."
Dr. Badlani warns hospitals must be willing to help supplement additional costs to their hospitalist service.
The IOM report, "Resident Duty Hours: Enhancing Sleep, Supervision, and Safety," is available for purchase online, or you can download a report brief at www.iom.edu/CMS/3809/48553/60449.aspx.
The Institute of Medicine (IOM) issued a report this month calling for limits to shifts worked by residents, a move that, if implemented, likely means more work for in-house hospitalists, according to one hospital medicine leader.
IOM recommends no change to the current maximum 80-hour workweek for residents, or to the maximum shift length of 30 hours. The report does, however, recommend residents only treat patients for up to 16 hours during their shift, down from the current recommendation of 24 hours. It also suggests residents take an uninterrupted five hours for a continuous sleep period between 10 p.m. and 8 a.m.
In 2003, the Accreditation Council for Graduate Medical Education restricted resident workweeks in order to protect patients and residents from unsafe conditions resulting from excessive fatigue. As mentioned in "While Residents Rest…" in The Hospitalist (August 2006), the resulting shift in workload stressed many hospitals relying on residents for coverage, and some believe it helped boost the need for hospitalists.
In teaching hospitals that follow the IOM recommendations, "I do think this work will go to hospitalists," says Sameer Badlani, MD, a hospitalist and instructor at the University of Chicago. "This is a good thing, in my opinion, as it will enhance the value a hospitalist program brings to an institution."
Dr. Badlani warns hospitals must be willing to help supplement additional costs to their hospitalist service.
The IOM report, "Resident Duty Hours: Enhancing Sleep, Supervision, and Safety," is available for purchase online, or you can download a report brief at www.iom.edu/CMS/3809/48553/60449.aspx.
The Institute of Medicine (IOM) issued a report this month calling for limits to shifts worked by residents, a move that, if implemented, likely means more work for in-house hospitalists, according to one hospital medicine leader.
IOM recommends no change to the current maximum 80-hour workweek for residents, or to the maximum shift length of 30 hours. The report does, however, recommend residents only treat patients for up to 16 hours during their shift, down from the current recommendation of 24 hours. It also suggests residents take an uninterrupted five hours for a continuous sleep period between 10 p.m. and 8 a.m.
In 2003, the Accreditation Council for Graduate Medical Education restricted resident workweeks in order to protect patients and residents from unsafe conditions resulting from excessive fatigue. As mentioned in "While Residents Rest…" in The Hospitalist (August 2006), the resulting shift in workload stressed many hospitals relying on residents for coverage, and some believe it helped boost the need for hospitalists.
In teaching hospitals that follow the IOM recommendations, "I do think this work will go to hospitalists," says Sameer Badlani, MD, a hospitalist and instructor at the University of Chicago. "This is a good thing, in my opinion, as it will enhance the value a hospitalist program brings to an institution."
Dr. Badlani warns hospitals must be willing to help supplement additional costs to their hospitalist service.
The IOM report, "Resident Duty Hours: Enhancing Sleep, Supervision, and Safety," is available for purchase online, or you can download a report brief at www.iom.edu/CMS/3809/48553/60449.aspx.
Therapeutic Hypothermia in Cardiac Arrest
Mortality data estimates that there are about 400,000 to 460,000 sudden cardiac deaths (SCD) in the United States.1 In resuscitated cardiac arrest patients, morbidity and mortality remains high due to cerebral ischemic anoxia. Currently it is believed that following return of spontaneous circulation (ROSC) from successful resuscitation, secondary inflammatory responses characterized by the generation of chemical mediators and free radicals, as well as increased microvascular permeability, lead to further brain injury.2 Recently, 2 randomized controlled trials (RCT) showed that induced mild hypothermia (32C‐34C) in comatose patients after out‐of‐hospital cardiac arrest leads to improved neurologic outcomes and survival.3, 4 In 2002, the International Liaison Committee on Resuscitation (ILCOR) recommended induced mild hypothermia for the management of comatose patients with ROSC after cardiac arrest.5 Despite the recommendations by ILCOR and the supporting body of evidence proving the benefit of therapeutic hypothermia after cardiac arrest, this treatment remains underused.68
We present a case series of 8 cardiac arrest survivors treated using a hypothermia protocol at a community hospital.
TREATMENT PROTOCOL
Between June 2006 and December 2006, 8 patients presented to Unity Hospital, (a 200‐bed community teaching hospital with a 20‐bed intensive care unit [ICU]) in coma following cardiac arrest with ROSC after resuscitation. All the patients were managed using therapeutic hypothermia.
The hospital protocol, developed using the ILCOR guidelines, was used on all patients. The aim was to achieve a core temperature of 32C to 34C within 6 to 8 hours and maintain this for 24 hours from the start of cooling. The inclusion criteria were as follows: (1) coma within a 6‐hour postcardiac arrest window preceded by either ventricular fibrillation (VF), pulseless ventricular tachycardia, pulseless electrical activity, or asystole; (2) ability to maintain a blood pressure with or without pressors and/or fluid volume resuscitation after cardiopulmonary resuscitation; and (3) comatose at the time of cooling. The exclusion criteria were as follows: (1) coma from drug overdose, head trauma, stroke, or overt status epilepticus; (2) pregnancy; (3) temperature of 30C; (4) recent major surgery within 14 days; (5) systemic infections; (6) patients with known terminal illness; (7) Glasgow coma scale (GCS) of 10 and above; or (8) known bleeding diathesis or ongoing bleeding.
The Advanced Cardiac Life Support (ACLS) protocol was implemented in both in‐hospital and out‐of‐hospital cardiac arrests. The decision to initiate the protocol was made by the intensivist; however, in out‐of‐hospital cardiac arrest, the decision was taken in conjunction with the emergency room physician. A bladder temperature probe was used to monitor core body temperature. Cooling was achieved using iced saline gastric lavage and ice packs to the patient's neck, axillae, and groin while a cooling blanket (Mul‐T‐Blanket; Gaymar Industries, New York) was placed over and beneath the patient. In some cases, a Blanketrol cooling machine (Blanketrol II; CSZ Products, Inc., Cincinnati, OH) was used when available. All patients were maintained at a PaO2 above 90 mm Hg and PaCO2 around 35 mm Hg. Cisatacurium and midazolam were used to control shivering. Regular insulin intravenous drip was used to maintain tight blood glucose control (target blood glucose level of 140 mg/dL) when necessary. Target systolic and mean arterial blood pressures were 90 mm Hg and 80 mm Hg, respectively. Potassium was replaced to 3.4 mmol/L but not within 8 hours of commencing rewarming. Rewarming was started after 24 hours at a rate of not more than 1C in 4 hours. Clinical and laboratory parameters were continuously recorded and all patients were evaluated for complications, including electrolyte imbalance, cardiac arrhythmias, and seizures.
CASES
Table 1 summarizes all the cases. There were 4 men and 4 women. The mean age was 70 14 years (range, 44‐88 years). The main comorbidities were coronary artery disease (n = 6), hypertension (n = 5), diabetes mellitus (n = 5), and chronic or recurrent cardiac arrhythmia (n = 4). Cardiac arrest occurred out‐of‐hospital in 5 of 8 patients and was witnessed in 6 of the 8 cases. Ventricular fibrillation (VF) was the initial presenting rhythm in 5 of the 8 cases. The mean time from ROSC to initiation of cooling was 3 1.6 hours. The mean time from ROSC and attaining target temperature (34C) was 8.1 4.7 hours. The mean duration of cooling (initiation of cooling to onset of rewarming) was 23.8 0.6 hours. The mean duration at which target temperature was maintained (attainment of 32C‐34C to onset of rewarming) was 18.6 4.6 hours. The median time from onset of passive rewarming to attaining temperature of 36C was 7.25 hours. Two patients survived and were discharged to home (Patients B and C). Patient B had mild cognitive deficits on discharge.
| Patients | Age (Years) | Sex | Comorbidities | Location at the Time of Arrest | Witnessed Arrest? | Initial Rhythm | Time of Collapse to ROSC | Presenting GCS | Time from ROSC to Cooling Initiation (Hours) | Time from ROSC to Target Temperature of 34C (Hours) | Duration of Cooling (Cooling Initiation to Rewarming) (Hours) | Duration of Target Temperature Maintenance (Hours) | Onset of Passive Rewarming to Attainment of Temperature of >36C (Hours) | Complications by Day 5 | Outcome at Discharge |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| |||||||||||||||
| A | 64 | M | DM, CAD, SSS, PTCA, PM, CHF, COPD | OOH | Yes | VF | 8 min | 3 | 1.7 | 1.7 | 16.9 | 24 | 6 | Pneumonia, hypokalemia, seizures | Death |
| B | 43 | F | Mitral valve prolapse | OOH | Yes | VF | 12 min | 5 | 6.3 | 5.3 | 12.0 | 24 | 7 | Hypokalemia | Good recovery |
| C | 64 | M | CAD, CABG | IH | No | VF | 7 min | 5 | 1.4 | 1.5 | 10.0 | 24 | 7.5 | Good recovery | |
| D | 76 | F | DM, HTN, CAD, PM | OOH | Yes | PEA | 36 min | 6 | 1.7 | 1.6 | 4.2 | 24 | 5 | Hypokalemia | Death |
| E | 88 | F | DM, HTN, CAD, AFIB, CHF, COPD | IH | Yes | Asystole | 6 min | 3 | 1.9 | 4.9 | 5.2 | 22.2 | 9.3 | Hypokalemia, elevated creatinine | Death |
| F | 70 | F | DM, HTN, CABG, PTCA, COPD | OOH | Yes | VF | 15 min | 5 | 1.4 | 2.1 | 5.6 | 18.3 | 3 | Seizures | Death |
| G | 71 | M | CAD, CABG, AICD | OOH | No | VF | >20 min | 3 | 4.7 | 4.6 | 6.7 | 22.5 | 12.3 | Hypokalemia, elevated creatinine, VT and VF | Death |
| H | 82 | M | HTN, CAD, AFIB, CHF | IH | Yes | Asystole | 19 min | 3 | 2.8 | 2.5 | 4.3 | 22.5 | 51 | Elevated creatinine | Death |
DISCUSSION
There is substantial clinical and public health concern over increasing incidence of sudden cardiac deaths despite decreasing overall mortality from coronary heart disease.6
Supportive management has been the norm for comatose patients following cardiac arrest until recently, when induced hypothermia was shown to have favorable outcomes in 2 landmark prospective RCTs.3, 4 Supportive management often led to prolonged unconsciousness due to severe anoxic brain injury, which eventually led to high morbidity and mortality rates.9, 10 The Hypothermia after Cardiac Arrest Study Group (HACA) study4 revealed that 6 patients would need to be treated with therapeutic hypothermia to prevent an adverse neurologic outcome, while 7 patients would need to be treated to prevent 1 death. Other authors have reported improved outcomes with induced hypothermia used in patients resuscitated following cardiac arrest.1114
Despite strong and encouraging evidence, therapeutic hypothermia has not been readily accepted into daily clinical critical care practice.68 In an Internet‐based survey of physicians by Abella et al.,6 87% of respondents (comprised of emergency medicine and critical care physicians, and cardiologists) had not used this treatment modality following cardiac arrest. Reasons given by most physicians included insufficient data to support the use of therapeutic hypothermia, technical difficulties including the immense amount of resources required, as well as inadequate training. Merchant et al.,7 using an Internet‐based survey also sought to ascertain the degree of therapeutic hypothermia use from physicians in the United States, the United Kingdom, Australia, and Finland. They found that 74% of respondents in the United States and 64% of respondents outside of the United States were yet to use induced therapeutic hypothermia. Factors predicting the use of therapeutic hypothermia by physicians were found to include practice in an academic hospital with more than 250 beds, critical care specialty training, and location of the hospital outside of the United States. Similarly, the major reasons given for nonutilization of therapeutic hypothermia in this study include lack of supportive data and technical difficulties. In yet another study by Laver et al.,8 73% of respondents (ICUs in the United Kingdom) revealed that therapeutic hypothermia after cardiac arrest had not been used in their service. They also gave the same reasons for nonusage as in the aforementioned studies.
In this case series we have presented our experience with therapeutic hypothermia in comatose patients following cardiac arrest. Evaluation of our cooling process compares favorably with the findings of the HACA study4: In our study, the mean time from ROSC to cooling initiation was 180 66 minutes compared to a median of 105 minutes (interquartile range, 61192 minutes) in the HACA study; mean time between ROSC and attaining target temperature was 8.1 4.7 hours in our study compared to a median of 8 hours in the HACA study; mean duration of cooling in our study was 23.8 0.6 hours compared to a median of 24 hours in the HACA study; target temperature was maintained for a mean duration of 18.6 4.6 hours in our study compared to a median of 24 hours in the HACA study; and last, median time from passive rewarming to attainment of temperature greater than 36C in our study was 7.25 hours compared to 8 hours in the HACA study.
There were few complications observed in this case series. These include hypokalemia, mildly elevated creatinine levels, and seizures. One patient developed pneumonia. Other potential complications of therapeutic hypothermia include cardiac arrhythmias, sepsis, hyperglycemia, coagulopathy, acid‐base disturbances, and electrolyte imbalance.15 The studies by Bernard et al.3 and the HACA;4 however, revealed no clinically significant unfavorable outcomes in the patients randomized to receive hypothermia treatment.
Our experience based on this case series leads us to conclude that therapeutic hypothermia is feasible in the community hospital setting. In our 200‐bed community teaching hospital, a multidisciplinary approach involving intensivists, emergency room physicians, internists, residents, and nursing staff lessens the technical difficulties associated with implementing a seemingly cumbersome yet inexpensive and effective treatment modality. Therapeutic hypothermia should be considered in appropriate patients in coma after resuscitation from cardiac arrest.
- Centers for Disease Control and Prevention.State specific mortality data from sudden cardiac death—United States, 1999.MMWR Morb Mortal Wkly Rep.2002;51(6):123– 126.
- .Bench to bedside: brain edema and cerebral resuscitation: the present and future.Acad Emerg Med.2002;9(9):933–946.
- ,,, et al.Treatment of comatose survivors of out of hospital cardiac arrest with induced hypothermia.N Engl J Med.2002;346(8):557–563.
- Hypothermia after Cardiac Arrest Study Group.Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest.N Engl J Med.2002;346(8):549–556.
- Therapeutic hypothermia after cardiac arrest: an advisory statement by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation.Circulation.2003;108:118–121.
- ,,, et al.Induced hypothermia is underused after resuscitation from cardiac arrest: a current practice survey.Resuscitation.2005;64:181–186.
- ,,, et al.Therapeutic hypothermia utilization among physicians after resuscitation from cardiac arrest.Crit Care Med.2006;34(7):1935–1940.
- ,,, et al.Therapeutic hypothermia after cardiac arrest: a survey of practice in intensive care units in the United Kingdom.Anaesthesia2006;61:873–877.
- .Hypothermia improves outcome from cardiac arrest.Crit Care Resusc.2005;7(4):325–327.
- ,,.Sudden cardiac death: epidemiology, transient risk, and intervention assessment.Ann Intern Med.1993;119(12):1187–1197.
- ,,, et al.Mild hypothermia induced by a helmet device: a clinical feasibility study.Resuscitation.2001;51:275–281.
- ,,, et al.Implementation of a standardized treatment protocol for post resuscitation care after out‐of‐hospital cardiac arrest.Resuscitation.2007;73(1):29–39.
- ,,,.Induced hypothermia following out‐of‐hospital cardiac arrest; initial experience in a community hospital.Clin Cardiol.2006;29(12):525–529.
- ,,,,.From evidence to clinical practice: effective implementation of therapeutic hypothermia to improve patient outcome after cardiac arrest.Crit Care Med.2006;34(7):1865–1873.
- ,.Induced hypothermia in critical care medicine: a review.Crit Care Med.2003;31(7):2041–2051.
Mortality data estimates that there are about 400,000 to 460,000 sudden cardiac deaths (SCD) in the United States.1 In resuscitated cardiac arrest patients, morbidity and mortality remains high due to cerebral ischemic anoxia. Currently it is believed that following return of spontaneous circulation (ROSC) from successful resuscitation, secondary inflammatory responses characterized by the generation of chemical mediators and free radicals, as well as increased microvascular permeability, lead to further brain injury.2 Recently, 2 randomized controlled trials (RCT) showed that induced mild hypothermia (32C‐34C) in comatose patients after out‐of‐hospital cardiac arrest leads to improved neurologic outcomes and survival.3, 4 In 2002, the International Liaison Committee on Resuscitation (ILCOR) recommended induced mild hypothermia for the management of comatose patients with ROSC after cardiac arrest.5 Despite the recommendations by ILCOR and the supporting body of evidence proving the benefit of therapeutic hypothermia after cardiac arrest, this treatment remains underused.68
We present a case series of 8 cardiac arrest survivors treated using a hypothermia protocol at a community hospital.
TREATMENT PROTOCOL
Between June 2006 and December 2006, 8 patients presented to Unity Hospital, (a 200‐bed community teaching hospital with a 20‐bed intensive care unit [ICU]) in coma following cardiac arrest with ROSC after resuscitation. All the patients were managed using therapeutic hypothermia.
The hospital protocol, developed using the ILCOR guidelines, was used on all patients. The aim was to achieve a core temperature of 32C to 34C within 6 to 8 hours and maintain this for 24 hours from the start of cooling. The inclusion criteria were as follows: (1) coma within a 6‐hour postcardiac arrest window preceded by either ventricular fibrillation (VF), pulseless ventricular tachycardia, pulseless electrical activity, or asystole; (2) ability to maintain a blood pressure with or without pressors and/or fluid volume resuscitation after cardiopulmonary resuscitation; and (3) comatose at the time of cooling. The exclusion criteria were as follows: (1) coma from drug overdose, head trauma, stroke, or overt status epilepticus; (2) pregnancy; (3) temperature of 30C; (4) recent major surgery within 14 days; (5) systemic infections; (6) patients with known terminal illness; (7) Glasgow coma scale (GCS) of 10 and above; or (8) known bleeding diathesis or ongoing bleeding.
The Advanced Cardiac Life Support (ACLS) protocol was implemented in both in‐hospital and out‐of‐hospital cardiac arrests. The decision to initiate the protocol was made by the intensivist; however, in out‐of‐hospital cardiac arrest, the decision was taken in conjunction with the emergency room physician. A bladder temperature probe was used to monitor core body temperature. Cooling was achieved using iced saline gastric lavage and ice packs to the patient's neck, axillae, and groin while a cooling blanket (Mul‐T‐Blanket; Gaymar Industries, New York) was placed over and beneath the patient. In some cases, a Blanketrol cooling machine (Blanketrol II; CSZ Products, Inc., Cincinnati, OH) was used when available. All patients were maintained at a PaO2 above 90 mm Hg and PaCO2 around 35 mm Hg. Cisatacurium and midazolam were used to control shivering. Regular insulin intravenous drip was used to maintain tight blood glucose control (target blood glucose level of 140 mg/dL) when necessary. Target systolic and mean arterial blood pressures were 90 mm Hg and 80 mm Hg, respectively. Potassium was replaced to 3.4 mmol/L but not within 8 hours of commencing rewarming. Rewarming was started after 24 hours at a rate of not more than 1C in 4 hours. Clinical and laboratory parameters were continuously recorded and all patients were evaluated for complications, including electrolyte imbalance, cardiac arrhythmias, and seizures.
CASES
Table 1 summarizes all the cases. There were 4 men and 4 women. The mean age was 70 14 years (range, 44‐88 years). The main comorbidities were coronary artery disease (n = 6), hypertension (n = 5), diabetes mellitus (n = 5), and chronic or recurrent cardiac arrhythmia (n = 4). Cardiac arrest occurred out‐of‐hospital in 5 of 8 patients and was witnessed in 6 of the 8 cases. Ventricular fibrillation (VF) was the initial presenting rhythm in 5 of the 8 cases. The mean time from ROSC to initiation of cooling was 3 1.6 hours. The mean time from ROSC and attaining target temperature (34C) was 8.1 4.7 hours. The mean duration of cooling (initiation of cooling to onset of rewarming) was 23.8 0.6 hours. The mean duration at which target temperature was maintained (attainment of 32C‐34C to onset of rewarming) was 18.6 4.6 hours. The median time from onset of passive rewarming to attaining temperature of 36C was 7.25 hours. Two patients survived and were discharged to home (Patients B and C). Patient B had mild cognitive deficits on discharge.
| Patients | Age (Years) | Sex | Comorbidities | Location at the Time of Arrest | Witnessed Arrest? | Initial Rhythm | Time of Collapse to ROSC | Presenting GCS | Time from ROSC to Cooling Initiation (Hours) | Time from ROSC to Target Temperature of 34C (Hours) | Duration of Cooling (Cooling Initiation to Rewarming) (Hours) | Duration of Target Temperature Maintenance (Hours) | Onset of Passive Rewarming to Attainment of Temperature of >36C (Hours) | Complications by Day 5 | Outcome at Discharge |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| |||||||||||||||
| A | 64 | M | DM, CAD, SSS, PTCA, PM, CHF, COPD | OOH | Yes | VF | 8 min | 3 | 1.7 | 1.7 | 16.9 | 24 | 6 | Pneumonia, hypokalemia, seizures | Death |
| B | 43 | F | Mitral valve prolapse | OOH | Yes | VF | 12 min | 5 | 6.3 | 5.3 | 12.0 | 24 | 7 | Hypokalemia | Good recovery |
| C | 64 | M | CAD, CABG | IH | No | VF | 7 min | 5 | 1.4 | 1.5 | 10.0 | 24 | 7.5 | Good recovery | |
| D | 76 | F | DM, HTN, CAD, PM | OOH | Yes | PEA | 36 min | 6 | 1.7 | 1.6 | 4.2 | 24 | 5 | Hypokalemia | Death |
| E | 88 | F | DM, HTN, CAD, AFIB, CHF, COPD | IH | Yes | Asystole | 6 min | 3 | 1.9 | 4.9 | 5.2 | 22.2 | 9.3 | Hypokalemia, elevated creatinine | Death |
| F | 70 | F | DM, HTN, CABG, PTCA, COPD | OOH | Yes | VF | 15 min | 5 | 1.4 | 2.1 | 5.6 | 18.3 | 3 | Seizures | Death |
| G | 71 | M | CAD, CABG, AICD | OOH | No | VF | >20 min | 3 | 4.7 | 4.6 | 6.7 | 22.5 | 12.3 | Hypokalemia, elevated creatinine, VT and VF | Death |
| H | 82 | M | HTN, CAD, AFIB, CHF | IH | Yes | Asystole | 19 min | 3 | 2.8 | 2.5 | 4.3 | 22.5 | 51 | Elevated creatinine | Death |
DISCUSSION
There is substantial clinical and public health concern over increasing incidence of sudden cardiac deaths despite decreasing overall mortality from coronary heart disease.6
Supportive management has been the norm for comatose patients following cardiac arrest until recently, when induced hypothermia was shown to have favorable outcomes in 2 landmark prospective RCTs.3, 4 Supportive management often led to prolonged unconsciousness due to severe anoxic brain injury, which eventually led to high morbidity and mortality rates.9, 10 The Hypothermia after Cardiac Arrest Study Group (HACA) study4 revealed that 6 patients would need to be treated with therapeutic hypothermia to prevent an adverse neurologic outcome, while 7 patients would need to be treated to prevent 1 death. Other authors have reported improved outcomes with induced hypothermia used in patients resuscitated following cardiac arrest.1114
Despite strong and encouraging evidence, therapeutic hypothermia has not been readily accepted into daily clinical critical care practice.68 In an Internet‐based survey of physicians by Abella et al.,6 87% of respondents (comprised of emergency medicine and critical care physicians, and cardiologists) had not used this treatment modality following cardiac arrest. Reasons given by most physicians included insufficient data to support the use of therapeutic hypothermia, technical difficulties including the immense amount of resources required, as well as inadequate training. Merchant et al.,7 using an Internet‐based survey also sought to ascertain the degree of therapeutic hypothermia use from physicians in the United States, the United Kingdom, Australia, and Finland. They found that 74% of respondents in the United States and 64% of respondents outside of the United States were yet to use induced therapeutic hypothermia. Factors predicting the use of therapeutic hypothermia by physicians were found to include practice in an academic hospital with more than 250 beds, critical care specialty training, and location of the hospital outside of the United States. Similarly, the major reasons given for nonutilization of therapeutic hypothermia in this study include lack of supportive data and technical difficulties. In yet another study by Laver et al.,8 73% of respondents (ICUs in the United Kingdom) revealed that therapeutic hypothermia after cardiac arrest had not been used in their service. They also gave the same reasons for nonusage as in the aforementioned studies.
In this case series we have presented our experience with therapeutic hypothermia in comatose patients following cardiac arrest. Evaluation of our cooling process compares favorably with the findings of the HACA study4: In our study, the mean time from ROSC to cooling initiation was 180 66 minutes compared to a median of 105 minutes (interquartile range, 61192 minutes) in the HACA study; mean time between ROSC and attaining target temperature was 8.1 4.7 hours in our study compared to a median of 8 hours in the HACA study; mean duration of cooling in our study was 23.8 0.6 hours compared to a median of 24 hours in the HACA study; target temperature was maintained for a mean duration of 18.6 4.6 hours in our study compared to a median of 24 hours in the HACA study; and last, median time from passive rewarming to attainment of temperature greater than 36C in our study was 7.25 hours compared to 8 hours in the HACA study.
There were few complications observed in this case series. These include hypokalemia, mildly elevated creatinine levels, and seizures. One patient developed pneumonia. Other potential complications of therapeutic hypothermia include cardiac arrhythmias, sepsis, hyperglycemia, coagulopathy, acid‐base disturbances, and electrolyte imbalance.15 The studies by Bernard et al.3 and the HACA;4 however, revealed no clinically significant unfavorable outcomes in the patients randomized to receive hypothermia treatment.
Our experience based on this case series leads us to conclude that therapeutic hypothermia is feasible in the community hospital setting. In our 200‐bed community teaching hospital, a multidisciplinary approach involving intensivists, emergency room physicians, internists, residents, and nursing staff lessens the technical difficulties associated with implementing a seemingly cumbersome yet inexpensive and effective treatment modality. Therapeutic hypothermia should be considered in appropriate patients in coma after resuscitation from cardiac arrest.
Mortality data estimates that there are about 400,000 to 460,000 sudden cardiac deaths (SCD) in the United States.1 In resuscitated cardiac arrest patients, morbidity and mortality remains high due to cerebral ischemic anoxia. Currently it is believed that following return of spontaneous circulation (ROSC) from successful resuscitation, secondary inflammatory responses characterized by the generation of chemical mediators and free radicals, as well as increased microvascular permeability, lead to further brain injury.2 Recently, 2 randomized controlled trials (RCT) showed that induced mild hypothermia (32C‐34C) in comatose patients after out‐of‐hospital cardiac arrest leads to improved neurologic outcomes and survival.3, 4 In 2002, the International Liaison Committee on Resuscitation (ILCOR) recommended induced mild hypothermia for the management of comatose patients with ROSC after cardiac arrest.5 Despite the recommendations by ILCOR and the supporting body of evidence proving the benefit of therapeutic hypothermia after cardiac arrest, this treatment remains underused.68
We present a case series of 8 cardiac arrest survivors treated using a hypothermia protocol at a community hospital.
TREATMENT PROTOCOL
Between June 2006 and December 2006, 8 patients presented to Unity Hospital, (a 200‐bed community teaching hospital with a 20‐bed intensive care unit [ICU]) in coma following cardiac arrest with ROSC after resuscitation. All the patients were managed using therapeutic hypothermia.
The hospital protocol, developed using the ILCOR guidelines, was used on all patients. The aim was to achieve a core temperature of 32C to 34C within 6 to 8 hours and maintain this for 24 hours from the start of cooling. The inclusion criteria were as follows: (1) coma within a 6‐hour postcardiac arrest window preceded by either ventricular fibrillation (VF), pulseless ventricular tachycardia, pulseless electrical activity, or asystole; (2) ability to maintain a blood pressure with or without pressors and/or fluid volume resuscitation after cardiopulmonary resuscitation; and (3) comatose at the time of cooling. The exclusion criteria were as follows: (1) coma from drug overdose, head trauma, stroke, or overt status epilepticus; (2) pregnancy; (3) temperature of 30C; (4) recent major surgery within 14 days; (5) systemic infections; (6) patients with known terminal illness; (7) Glasgow coma scale (GCS) of 10 and above; or (8) known bleeding diathesis or ongoing bleeding.
The Advanced Cardiac Life Support (ACLS) protocol was implemented in both in‐hospital and out‐of‐hospital cardiac arrests. The decision to initiate the protocol was made by the intensivist; however, in out‐of‐hospital cardiac arrest, the decision was taken in conjunction with the emergency room physician. A bladder temperature probe was used to monitor core body temperature. Cooling was achieved using iced saline gastric lavage and ice packs to the patient's neck, axillae, and groin while a cooling blanket (Mul‐T‐Blanket; Gaymar Industries, New York) was placed over and beneath the patient. In some cases, a Blanketrol cooling machine (Blanketrol II; CSZ Products, Inc., Cincinnati, OH) was used when available. All patients were maintained at a PaO2 above 90 mm Hg and PaCO2 around 35 mm Hg. Cisatacurium and midazolam were used to control shivering. Regular insulin intravenous drip was used to maintain tight blood glucose control (target blood glucose level of 140 mg/dL) when necessary. Target systolic and mean arterial blood pressures were 90 mm Hg and 80 mm Hg, respectively. Potassium was replaced to 3.4 mmol/L but not within 8 hours of commencing rewarming. Rewarming was started after 24 hours at a rate of not more than 1C in 4 hours. Clinical and laboratory parameters were continuously recorded and all patients were evaluated for complications, including electrolyte imbalance, cardiac arrhythmias, and seizures.
CASES
Table 1 summarizes all the cases. There were 4 men and 4 women. The mean age was 70 14 years (range, 44‐88 years). The main comorbidities were coronary artery disease (n = 6), hypertension (n = 5), diabetes mellitus (n = 5), and chronic or recurrent cardiac arrhythmia (n = 4). Cardiac arrest occurred out‐of‐hospital in 5 of 8 patients and was witnessed in 6 of the 8 cases. Ventricular fibrillation (VF) was the initial presenting rhythm in 5 of the 8 cases. The mean time from ROSC to initiation of cooling was 3 1.6 hours. The mean time from ROSC and attaining target temperature (34C) was 8.1 4.7 hours. The mean duration of cooling (initiation of cooling to onset of rewarming) was 23.8 0.6 hours. The mean duration at which target temperature was maintained (attainment of 32C‐34C to onset of rewarming) was 18.6 4.6 hours. The median time from onset of passive rewarming to attaining temperature of 36C was 7.25 hours. Two patients survived and were discharged to home (Patients B and C). Patient B had mild cognitive deficits on discharge.
| Patients | Age (Years) | Sex | Comorbidities | Location at the Time of Arrest | Witnessed Arrest? | Initial Rhythm | Time of Collapse to ROSC | Presenting GCS | Time from ROSC to Cooling Initiation (Hours) | Time from ROSC to Target Temperature of 34C (Hours) | Duration of Cooling (Cooling Initiation to Rewarming) (Hours) | Duration of Target Temperature Maintenance (Hours) | Onset of Passive Rewarming to Attainment of Temperature of >36C (Hours) | Complications by Day 5 | Outcome at Discharge |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| |||||||||||||||
| A | 64 | M | DM, CAD, SSS, PTCA, PM, CHF, COPD | OOH | Yes | VF | 8 min | 3 | 1.7 | 1.7 | 16.9 | 24 | 6 | Pneumonia, hypokalemia, seizures | Death |
| B | 43 | F | Mitral valve prolapse | OOH | Yes | VF | 12 min | 5 | 6.3 | 5.3 | 12.0 | 24 | 7 | Hypokalemia | Good recovery |
| C | 64 | M | CAD, CABG | IH | No | VF | 7 min | 5 | 1.4 | 1.5 | 10.0 | 24 | 7.5 | Good recovery | |
| D | 76 | F | DM, HTN, CAD, PM | OOH | Yes | PEA | 36 min | 6 | 1.7 | 1.6 | 4.2 | 24 | 5 | Hypokalemia | Death |
| E | 88 | F | DM, HTN, CAD, AFIB, CHF, COPD | IH | Yes | Asystole | 6 min | 3 | 1.9 | 4.9 | 5.2 | 22.2 | 9.3 | Hypokalemia, elevated creatinine | Death |
| F | 70 | F | DM, HTN, CABG, PTCA, COPD | OOH | Yes | VF | 15 min | 5 | 1.4 | 2.1 | 5.6 | 18.3 | 3 | Seizures | Death |
| G | 71 | M | CAD, CABG, AICD | OOH | No | VF | >20 min | 3 | 4.7 | 4.6 | 6.7 | 22.5 | 12.3 | Hypokalemia, elevated creatinine, VT and VF | Death |
| H | 82 | M | HTN, CAD, AFIB, CHF | IH | Yes | Asystole | 19 min | 3 | 2.8 | 2.5 | 4.3 | 22.5 | 51 | Elevated creatinine | Death |
DISCUSSION
There is substantial clinical and public health concern over increasing incidence of sudden cardiac deaths despite decreasing overall mortality from coronary heart disease.6
Supportive management has been the norm for comatose patients following cardiac arrest until recently, when induced hypothermia was shown to have favorable outcomes in 2 landmark prospective RCTs.3, 4 Supportive management often led to prolonged unconsciousness due to severe anoxic brain injury, which eventually led to high morbidity and mortality rates.9, 10 The Hypothermia after Cardiac Arrest Study Group (HACA) study4 revealed that 6 patients would need to be treated with therapeutic hypothermia to prevent an adverse neurologic outcome, while 7 patients would need to be treated to prevent 1 death. Other authors have reported improved outcomes with induced hypothermia used in patients resuscitated following cardiac arrest.1114
Despite strong and encouraging evidence, therapeutic hypothermia has not been readily accepted into daily clinical critical care practice.68 In an Internet‐based survey of physicians by Abella et al.,6 87% of respondents (comprised of emergency medicine and critical care physicians, and cardiologists) had not used this treatment modality following cardiac arrest. Reasons given by most physicians included insufficient data to support the use of therapeutic hypothermia, technical difficulties including the immense amount of resources required, as well as inadequate training. Merchant et al.,7 using an Internet‐based survey also sought to ascertain the degree of therapeutic hypothermia use from physicians in the United States, the United Kingdom, Australia, and Finland. They found that 74% of respondents in the United States and 64% of respondents outside of the United States were yet to use induced therapeutic hypothermia. Factors predicting the use of therapeutic hypothermia by physicians were found to include practice in an academic hospital with more than 250 beds, critical care specialty training, and location of the hospital outside of the United States. Similarly, the major reasons given for nonutilization of therapeutic hypothermia in this study include lack of supportive data and technical difficulties. In yet another study by Laver et al.,8 73% of respondents (ICUs in the United Kingdom) revealed that therapeutic hypothermia after cardiac arrest had not been used in their service. They also gave the same reasons for nonusage as in the aforementioned studies.
In this case series we have presented our experience with therapeutic hypothermia in comatose patients following cardiac arrest. Evaluation of our cooling process compares favorably with the findings of the HACA study4: In our study, the mean time from ROSC to cooling initiation was 180 66 minutes compared to a median of 105 minutes (interquartile range, 61192 minutes) in the HACA study; mean time between ROSC and attaining target temperature was 8.1 4.7 hours in our study compared to a median of 8 hours in the HACA study; mean duration of cooling in our study was 23.8 0.6 hours compared to a median of 24 hours in the HACA study; target temperature was maintained for a mean duration of 18.6 4.6 hours in our study compared to a median of 24 hours in the HACA study; and last, median time from passive rewarming to attainment of temperature greater than 36C in our study was 7.25 hours compared to 8 hours in the HACA study.
There were few complications observed in this case series. These include hypokalemia, mildly elevated creatinine levels, and seizures. One patient developed pneumonia. Other potential complications of therapeutic hypothermia include cardiac arrhythmias, sepsis, hyperglycemia, coagulopathy, acid‐base disturbances, and electrolyte imbalance.15 The studies by Bernard et al.3 and the HACA;4 however, revealed no clinically significant unfavorable outcomes in the patients randomized to receive hypothermia treatment.
Our experience based on this case series leads us to conclude that therapeutic hypothermia is feasible in the community hospital setting. In our 200‐bed community teaching hospital, a multidisciplinary approach involving intensivists, emergency room physicians, internists, residents, and nursing staff lessens the technical difficulties associated with implementing a seemingly cumbersome yet inexpensive and effective treatment modality. Therapeutic hypothermia should be considered in appropriate patients in coma after resuscitation from cardiac arrest.
- Centers for Disease Control and Prevention.State specific mortality data from sudden cardiac death—United States, 1999.MMWR Morb Mortal Wkly Rep.2002;51(6):123– 126.
- .Bench to bedside: brain edema and cerebral resuscitation: the present and future.Acad Emerg Med.2002;9(9):933–946.
- ,,, et al.Treatment of comatose survivors of out of hospital cardiac arrest with induced hypothermia.N Engl J Med.2002;346(8):557–563.
- Hypothermia after Cardiac Arrest Study Group.Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest.N Engl J Med.2002;346(8):549–556.
- Therapeutic hypothermia after cardiac arrest: an advisory statement by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation.Circulation.2003;108:118–121.
- ,,, et al.Induced hypothermia is underused after resuscitation from cardiac arrest: a current practice survey.Resuscitation.2005;64:181–186.
- ,,, et al.Therapeutic hypothermia utilization among physicians after resuscitation from cardiac arrest.Crit Care Med.2006;34(7):1935–1940.
- ,,, et al.Therapeutic hypothermia after cardiac arrest: a survey of practice in intensive care units in the United Kingdom.Anaesthesia2006;61:873–877.
- .Hypothermia improves outcome from cardiac arrest.Crit Care Resusc.2005;7(4):325–327.
- ,,.Sudden cardiac death: epidemiology, transient risk, and intervention assessment.Ann Intern Med.1993;119(12):1187–1197.
- ,,, et al.Mild hypothermia induced by a helmet device: a clinical feasibility study.Resuscitation.2001;51:275–281.
- ,,, et al.Implementation of a standardized treatment protocol for post resuscitation care after out‐of‐hospital cardiac arrest.Resuscitation.2007;73(1):29–39.
- ,,,.Induced hypothermia following out‐of‐hospital cardiac arrest; initial experience in a community hospital.Clin Cardiol.2006;29(12):525–529.
- ,,,,.From evidence to clinical practice: effective implementation of therapeutic hypothermia to improve patient outcome after cardiac arrest.Crit Care Med.2006;34(7):1865–1873.
- ,.Induced hypothermia in critical care medicine: a review.Crit Care Med.2003;31(7):2041–2051.
- Centers for Disease Control and Prevention.State specific mortality data from sudden cardiac death—United States, 1999.MMWR Morb Mortal Wkly Rep.2002;51(6):123– 126.
- .Bench to bedside: brain edema and cerebral resuscitation: the present and future.Acad Emerg Med.2002;9(9):933–946.
- ,,, et al.Treatment of comatose survivors of out of hospital cardiac arrest with induced hypothermia.N Engl J Med.2002;346(8):557–563.
- Hypothermia after Cardiac Arrest Study Group.Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest.N Engl J Med.2002;346(8):549–556.
- Therapeutic hypothermia after cardiac arrest: an advisory statement by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation.Circulation.2003;108:118–121.
- ,,, et al.Induced hypothermia is underused after resuscitation from cardiac arrest: a current practice survey.Resuscitation.2005;64:181–186.
- ,,, et al.Therapeutic hypothermia utilization among physicians after resuscitation from cardiac arrest.Crit Care Med.2006;34(7):1935–1940.
- ,,, et al.Therapeutic hypothermia after cardiac arrest: a survey of practice in intensive care units in the United Kingdom.Anaesthesia2006;61:873–877.
- .Hypothermia improves outcome from cardiac arrest.Crit Care Resusc.2005;7(4):325–327.
- ,,.Sudden cardiac death: epidemiology, transient risk, and intervention assessment.Ann Intern Med.1993;119(12):1187–1197.
- ,,, et al.Mild hypothermia induced by a helmet device: a clinical feasibility study.Resuscitation.2001;51:275–281.
- ,,, et al.Implementation of a standardized treatment protocol for post resuscitation care after out‐of‐hospital cardiac arrest.Resuscitation.2007;73(1):29–39.
- ,,,.Induced hypothermia following out‐of‐hospital cardiac arrest; initial experience in a community hospital.Clin Cardiol.2006;29(12):525–529.
- ,,,,.From evidence to clinical practice: effective implementation of therapeutic hypothermia to improve patient outcome after cardiac arrest.Crit Care Med.2006;34(7):1865–1873.
- ,.Induced hypothermia in critical care medicine: a review.Crit Care Med.2003;31(7):2041–2051.
Engaging Patients at Hospital Discharge
I first met G.M. (a pseudonym) a year ago during a hospitalization for a flare of his Crohn's disease. At the age of 26, he had accrued nearly 400 hospital days in more than 10 institutionsranging from academic to community medical centers from the East Coast to the West Coast. He had been admitted and discharged more than 25 times and endured several surgeries, intermittent struggles with chronic pain and depression, and mishaps due to poor discharge planning. He referred to discharge as the most chaotic time of hospitalization, a comment that prompted a memorable discussion.
He began by describing the emotions he felt when first told about being discharged, using words such as fear and helplessness. He repeatedly talked about the lack of planning and anticipation of discharge as well as the frustration of watching a system that required fixing. Speaking with tremendous emotion and insight, he also pointed out the discharge experiences that maintained his trust and faith in the system. The conversation then shifted to his mother, who pointed out that her experiences as the caretaker were quite different than her son's. She was equally passionate and genuine in trying to characterize the hospital discharge process.
The conversation was so moving that I asked G.M. and his mother to jot down their thoughts on discharge as well as participate in a multidisciplinary patient safety conference. The following are excerpts from our conversation, their letters, and the conference.
THE PATIENT'S VIEW
You never go into the hospital wanting to stay there, but you also worry tremendously about adjusting back to home life. In my case, I was often on heavy pain medications with a PCA (patient‐controlled analgesia), so the transition to orals always created a source of stress, particularly when the transition happened right at discharge. I've had a number of experiences when they told me I was going home, stopped the PCA, and then simply sent me on my way. Nothing is worse than being discharged from the hospital, spending the car ride home doubled over in pain, and then not being able to get pain meds from the pharmacy until the next day. On the other hand, I've had discharges that were better anticipated, so I could participate in the process. This made all the difference in the world. I don't think people realize that when you're on a PCA right up to discharge, you're not really in a state to receive counseling, education, or instructions about follow‐up plansI was just trying to get better.
Many times, I knew I was getting close to discharge, but I often didn't see anyone owning the process. Information would be fragmented or inconsistent, and while I may have been ready for discharge, I wasn't prepared for discharge. This was a combination of paperwork being incomplete or being left to arrange my own follow‐up appointments after getting home. When you're sick and depressed, you fall through the cracks of the system. You just don't have the resolve to make things happen.
Ultimately, a well orchestrated discharge prepared me to be independent on some level. I felt comfortable and ready for life outside the hospital. I didn't feel helpless because I was only responsible for getting wellnot for arranging my follow‐up appointments, ensuring the home care nurse was coming by, and confirming that my primary doctor knew what was going on. In these situations, there was always a discharge planner serving as a patient advocate of sorts. I also can't imagine what I would have done if I didn't have my mom with me all the time. She's my mom, my advocate, and my caretaker and I don't know how patients survive without someone like that.
HIS MOTHER'S VIEW
I wasn't the sick and helpless one but rather the one who was expected to make it all happen: keep tabs on the medications, understand the details of the discharge plan, and ultimately manage the execution of care postdischarge. In the majority of cases when we had a bad discharge experience, it was because the goals were confused. It became about the bed that was needed for the person still sitting in the emergency department. They may not have realized it, but we fully understood the tension, and we very much felt it during the spotty discharge communications. Safety for the patient being discharged seemed to fall off the radar.
The goals of the process must be clear. In good discharges, caregivers clearly outline the transition plan, transfer records to the outpatient physicians, and arrange referrals to specialists as needed. Perhaps equally important is addressing the patient's emotional state for discharge. This isn't about convincing us that he's safe to go home, but a simple acknowledgement of the difficult transitionparticularly after a long hospitalizationgoes a far way in providing reassurance and decreasing fear and anxiety. If the issue is always one about beds and cost, I would think someone would figure out that a good discharge prevents readmissions, which would have to be a cost‐effective investment.
DISCUSSION
The voice of the patient (or family member) is incredibly powerful. Rather than having a trainee present a case history to illustrate teaching points, it is sometimes more meaningful and instructive to let patients tell their own stories. We invited G.M. and his mother to discuss their discharge experiences at a multidisciplinary patient safety conference. There, representative members of the discharge team (eg, house staff, attending, bedside nurse, pharmacist, and discharge planner) responded to their comments and discussed their roles in the discharge process. Ultimately, the patient and his mother taught us the most about what we can do to improve a process fraught with complexity and the potential for errors: communicate and work better as a team.
G.M. and his mother listened to each of the experts discuss the tasks they must complete to ensure a smooth discharge. Each provider expressed how committed they were to safe discharges, yet all of them shared how easy it is for one to go awry. They knew their individual roles, but all relied on each other to make the process completehighlighting that communication failures frequently lead to poor discharge experiences for patients. Engaging patients in the process should not transfer ownership of discharge to them (ie, making them responsible to ensure we do our jobs), though our patient and his mother presented several examples of how they owned the process because it was clear no one else did.
Evaluating our hospital discharge systems must include identifying methods to improve communication with outpatient providers, ensuring medications are available to patients on discharge, and providing written instructions (including follow‐up appointments) to patients before they leave the hospital. G.M. and his mother remind us that the best systems still need to engage patients, make them an active part of the discharge process (rather than an outcome of it), and never underestimate what patients suffer through emotionally prior to discharge.
Providers often feel uneasy when having to explain to patients that they no longer require hospitalization and perhaps avoid emotional engagement in those discussions because of the fear that some patients may become upset about a planned discharge. Communicating with patients about discharge plans should be handled with the same compassion, patience, and skill as delivering bad news. Patients entrust their lives to our clinical decision making, and abandoning this trust just as they leave the hospital is an unintended message that our patient and his mother perceived during their poor discharge experiences.
In my practice, I frequently include trainees in bedside discussions with patients and families, both to illustrate how important these conversations are and to model skills I was taught during my training. I now use discussions about discharge as a specific bedside teaching moment as well, hoping to impress on trainees the overriding message shared by G.M. and his mother: do not forget to engage patients in a process that is designed for them rather than to them.
Many physicians remain dedicated to improving hospital systems, but perhaps we should all be including our patients more in quality improvement activities and hospital committee work, as they provide perspectives not easily captured by administrative data and run charts.
Acknowledgements
The author thanks G.M. and his mother for candidly sharing their thoughts and feelings about the discharge process. He also thanks Erin Hartman, MS, for her invaluable editorial assistance in preparing this manuscript. The patient safety conference described was part of the Triad for Optimal Patient Safety (TOPS), a project funded by the Gorden & Betty Moore Foundation.
I first met G.M. (a pseudonym) a year ago during a hospitalization for a flare of his Crohn's disease. At the age of 26, he had accrued nearly 400 hospital days in more than 10 institutionsranging from academic to community medical centers from the East Coast to the West Coast. He had been admitted and discharged more than 25 times and endured several surgeries, intermittent struggles with chronic pain and depression, and mishaps due to poor discharge planning. He referred to discharge as the most chaotic time of hospitalization, a comment that prompted a memorable discussion.
He began by describing the emotions he felt when first told about being discharged, using words such as fear and helplessness. He repeatedly talked about the lack of planning and anticipation of discharge as well as the frustration of watching a system that required fixing. Speaking with tremendous emotion and insight, he also pointed out the discharge experiences that maintained his trust and faith in the system. The conversation then shifted to his mother, who pointed out that her experiences as the caretaker were quite different than her son's. She was equally passionate and genuine in trying to characterize the hospital discharge process.
The conversation was so moving that I asked G.M. and his mother to jot down their thoughts on discharge as well as participate in a multidisciplinary patient safety conference. The following are excerpts from our conversation, their letters, and the conference.
THE PATIENT'S VIEW
You never go into the hospital wanting to stay there, but you also worry tremendously about adjusting back to home life. In my case, I was often on heavy pain medications with a PCA (patient‐controlled analgesia), so the transition to orals always created a source of stress, particularly when the transition happened right at discharge. I've had a number of experiences when they told me I was going home, stopped the PCA, and then simply sent me on my way. Nothing is worse than being discharged from the hospital, spending the car ride home doubled over in pain, and then not being able to get pain meds from the pharmacy until the next day. On the other hand, I've had discharges that were better anticipated, so I could participate in the process. This made all the difference in the world. I don't think people realize that when you're on a PCA right up to discharge, you're not really in a state to receive counseling, education, or instructions about follow‐up plansI was just trying to get better.
Many times, I knew I was getting close to discharge, but I often didn't see anyone owning the process. Information would be fragmented or inconsistent, and while I may have been ready for discharge, I wasn't prepared for discharge. This was a combination of paperwork being incomplete or being left to arrange my own follow‐up appointments after getting home. When you're sick and depressed, you fall through the cracks of the system. You just don't have the resolve to make things happen.
Ultimately, a well orchestrated discharge prepared me to be independent on some level. I felt comfortable and ready for life outside the hospital. I didn't feel helpless because I was only responsible for getting wellnot for arranging my follow‐up appointments, ensuring the home care nurse was coming by, and confirming that my primary doctor knew what was going on. In these situations, there was always a discharge planner serving as a patient advocate of sorts. I also can't imagine what I would have done if I didn't have my mom with me all the time. She's my mom, my advocate, and my caretaker and I don't know how patients survive without someone like that.
HIS MOTHER'S VIEW
I wasn't the sick and helpless one but rather the one who was expected to make it all happen: keep tabs on the medications, understand the details of the discharge plan, and ultimately manage the execution of care postdischarge. In the majority of cases when we had a bad discharge experience, it was because the goals were confused. It became about the bed that was needed for the person still sitting in the emergency department. They may not have realized it, but we fully understood the tension, and we very much felt it during the spotty discharge communications. Safety for the patient being discharged seemed to fall off the radar.
The goals of the process must be clear. In good discharges, caregivers clearly outline the transition plan, transfer records to the outpatient physicians, and arrange referrals to specialists as needed. Perhaps equally important is addressing the patient's emotional state for discharge. This isn't about convincing us that he's safe to go home, but a simple acknowledgement of the difficult transitionparticularly after a long hospitalizationgoes a far way in providing reassurance and decreasing fear and anxiety. If the issue is always one about beds and cost, I would think someone would figure out that a good discharge prevents readmissions, which would have to be a cost‐effective investment.
DISCUSSION
The voice of the patient (or family member) is incredibly powerful. Rather than having a trainee present a case history to illustrate teaching points, it is sometimes more meaningful and instructive to let patients tell their own stories. We invited G.M. and his mother to discuss their discharge experiences at a multidisciplinary patient safety conference. There, representative members of the discharge team (eg, house staff, attending, bedside nurse, pharmacist, and discharge planner) responded to their comments and discussed their roles in the discharge process. Ultimately, the patient and his mother taught us the most about what we can do to improve a process fraught with complexity and the potential for errors: communicate and work better as a team.
G.M. and his mother listened to each of the experts discuss the tasks they must complete to ensure a smooth discharge. Each provider expressed how committed they were to safe discharges, yet all of them shared how easy it is for one to go awry. They knew their individual roles, but all relied on each other to make the process completehighlighting that communication failures frequently lead to poor discharge experiences for patients. Engaging patients in the process should not transfer ownership of discharge to them (ie, making them responsible to ensure we do our jobs), though our patient and his mother presented several examples of how they owned the process because it was clear no one else did.
Evaluating our hospital discharge systems must include identifying methods to improve communication with outpatient providers, ensuring medications are available to patients on discharge, and providing written instructions (including follow‐up appointments) to patients before they leave the hospital. G.M. and his mother remind us that the best systems still need to engage patients, make them an active part of the discharge process (rather than an outcome of it), and never underestimate what patients suffer through emotionally prior to discharge.
Providers often feel uneasy when having to explain to patients that they no longer require hospitalization and perhaps avoid emotional engagement in those discussions because of the fear that some patients may become upset about a planned discharge. Communicating with patients about discharge plans should be handled with the same compassion, patience, and skill as delivering bad news. Patients entrust their lives to our clinical decision making, and abandoning this trust just as they leave the hospital is an unintended message that our patient and his mother perceived during their poor discharge experiences.
In my practice, I frequently include trainees in bedside discussions with patients and families, both to illustrate how important these conversations are and to model skills I was taught during my training. I now use discussions about discharge as a specific bedside teaching moment as well, hoping to impress on trainees the overriding message shared by G.M. and his mother: do not forget to engage patients in a process that is designed for them rather than to them.
Many physicians remain dedicated to improving hospital systems, but perhaps we should all be including our patients more in quality improvement activities and hospital committee work, as they provide perspectives not easily captured by administrative data and run charts.
Acknowledgements
The author thanks G.M. and his mother for candidly sharing their thoughts and feelings about the discharge process. He also thanks Erin Hartman, MS, for her invaluable editorial assistance in preparing this manuscript. The patient safety conference described was part of the Triad for Optimal Patient Safety (TOPS), a project funded by the Gorden & Betty Moore Foundation.
I first met G.M. (a pseudonym) a year ago during a hospitalization for a flare of his Crohn's disease. At the age of 26, he had accrued nearly 400 hospital days in more than 10 institutionsranging from academic to community medical centers from the East Coast to the West Coast. He had been admitted and discharged more than 25 times and endured several surgeries, intermittent struggles with chronic pain and depression, and mishaps due to poor discharge planning. He referred to discharge as the most chaotic time of hospitalization, a comment that prompted a memorable discussion.
He began by describing the emotions he felt when first told about being discharged, using words such as fear and helplessness. He repeatedly talked about the lack of planning and anticipation of discharge as well as the frustration of watching a system that required fixing. Speaking with tremendous emotion and insight, he also pointed out the discharge experiences that maintained his trust and faith in the system. The conversation then shifted to his mother, who pointed out that her experiences as the caretaker were quite different than her son's. She was equally passionate and genuine in trying to characterize the hospital discharge process.
The conversation was so moving that I asked G.M. and his mother to jot down their thoughts on discharge as well as participate in a multidisciplinary patient safety conference. The following are excerpts from our conversation, their letters, and the conference.
THE PATIENT'S VIEW
You never go into the hospital wanting to stay there, but you also worry tremendously about adjusting back to home life. In my case, I was often on heavy pain medications with a PCA (patient‐controlled analgesia), so the transition to orals always created a source of stress, particularly when the transition happened right at discharge. I've had a number of experiences when they told me I was going home, stopped the PCA, and then simply sent me on my way. Nothing is worse than being discharged from the hospital, spending the car ride home doubled over in pain, and then not being able to get pain meds from the pharmacy until the next day. On the other hand, I've had discharges that were better anticipated, so I could participate in the process. This made all the difference in the world. I don't think people realize that when you're on a PCA right up to discharge, you're not really in a state to receive counseling, education, or instructions about follow‐up plansI was just trying to get better.
Many times, I knew I was getting close to discharge, but I often didn't see anyone owning the process. Information would be fragmented or inconsistent, and while I may have been ready for discharge, I wasn't prepared for discharge. This was a combination of paperwork being incomplete or being left to arrange my own follow‐up appointments after getting home. When you're sick and depressed, you fall through the cracks of the system. You just don't have the resolve to make things happen.
Ultimately, a well orchestrated discharge prepared me to be independent on some level. I felt comfortable and ready for life outside the hospital. I didn't feel helpless because I was only responsible for getting wellnot for arranging my follow‐up appointments, ensuring the home care nurse was coming by, and confirming that my primary doctor knew what was going on. In these situations, there was always a discharge planner serving as a patient advocate of sorts. I also can't imagine what I would have done if I didn't have my mom with me all the time. She's my mom, my advocate, and my caretaker and I don't know how patients survive without someone like that.
HIS MOTHER'S VIEW
I wasn't the sick and helpless one but rather the one who was expected to make it all happen: keep tabs on the medications, understand the details of the discharge plan, and ultimately manage the execution of care postdischarge. In the majority of cases when we had a bad discharge experience, it was because the goals were confused. It became about the bed that was needed for the person still sitting in the emergency department. They may not have realized it, but we fully understood the tension, and we very much felt it during the spotty discharge communications. Safety for the patient being discharged seemed to fall off the radar.
The goals of the process must be clear. In good discharges, caregivers clearly outline the transition plan, transfer records to the outpatient physicians, and arrange referrals to specialists as needed. Perhaps equally important is addressing the patient's emotional state for discharge. This isn't about convincing us that he's safe to go home, but a simple acknowledgement of the difficult transitionparticularly after a long hospitalizationgoes a far way in providing reassurance and decreasing fear and anxiety. If the issue is always one about beds and cost, I would think someone would figure out that a good discharge prevents readmissions, which would have to be a cost‐effective investment.
DISCUSSION
The voice of the patient (or family member) is incredibly powerful. Rather than having a trainee present a case history to illustrate teaching points, it is sometimes more meaningful and instructive to let patients tell their own stories. We invited G.M. and his mother to discuss their discharge experiences at a multidisciplinary patient safety conference. There, representative members of the discharge team (eg, house staff, attending, bedside nurse, pharmacist, and discharge planner) responded to their comments and discussed their roles in the discharge process. Ultimately, the patient and his mother taught us the most about what we can do to improve a process fraught with complexity and the potential for errors: communicate and work better as a team.
G.M. and his mother listened to each of the experts discuss the tasks they must complete to ensure a smooth discharge. Each provider expressed how committed they were to safe discharges, yet all of them shared how easy it is for one to go awry. They knew their individual roles, but all relied on each other to make the process completehighlighting that communication failures frequently lead to poor discharge experiences for patients. Engaging patients in the process should not transfer ownership of discharge to them (ie, making them responsible to ensure we do our jobs), though our patient and his mother presented several examples of how they owned the process because it was clear no one else did.
Evaluating our hospital discharge systems must include identifying methods to improve communication with outpatient providers, ensuring medications are available to patients on discharge, and providing written instructions (including follow‐up appointments) to patients before they leave the hospital. G.M. and his mother remind us that the best systems still need to engage patients, make them an active part of the discharge process (rather than an outcome of it), and never underestimate what patients suffer through emotionally prior to discharge.
Providers often feel uneasy when having to explain to patients that they no longer require hospitalization and perhaps avoid emotional engagement in those discussions because of the fear that some patients may become upset about a planned discharge. Communicating with patients about discharge plans should be handled with the same compassion, patience, and skill as delivering bad news. Patients entrust their lives to our clinical decision making, and abandoning this trust just as they leave the hospital is an unintended message that our patient and his mother perceived during their poor discharge experiences.
In my practice, I frequently include trainees in bedside discussions with patients and families, both to illustrate how important these conversations are and to model skills I was taught during my training. I now use discussions about discharge as a specific bedside teaching moment as well, hoping to impress on trainees the overriding message shared by G.M. and his mother: do not forget to engage patients in a process that is designed for them rather than to them.
Many physicians remain dedicated to improving hospital systems, but perhaps we should all be including our patients more in quality improvement activities and hospital committee work, as they provide perspectives not easily captured by administrative data and run charts.
Acknowledgements
The author thanks G.M. and his mother for candidly sharing their thoughts and feelings about the discharge process. He also thanks Erin Hartman, MS, for her invaluable editorial assistance in preparing this manuscript. The patient safety conference described was part of the Triad for Optimal Patient Safety (TOPS), a project funded by the Gorden & Betty Moore Foundation.