Dr. Wachter

Anyone who has attended the closing session of an SHM Annual Meeting or read one of his editorial pieces in The Hospitalist or other publications knows that Bob Wachter, MD, sees the world in a unique and uniquely informed way.

This fall, Dr. Wachter—professor and associate chairman of the Department of Medicine at the University of California, San Francisco (UCSF), co-founder of SHM, and the man who coined the term “hospitalist” (along with Lee Goldman, MD)—will regularly share his one-of-a-kind perspective via a Weblog, or blog. Tentatively titled “Wachter’s World,” the hospital medicine blog will debut at www.the-hospitalist.org in time for the “Management of the Hospitalized Patient” session Oct. 4-6 at UCSF. The in-depth course serves as the West Coast regional meeting of SHM.

“Even an old guy like me realizes that blogs are incredibly hot,” says Dr. Wachter. “And as I read more of them and began relying on them more for information and insights, I started looking for one in our field that was lively, engaging and informative, one I’d like to read. I couldn’t find anything, so I thought I should start one.”

When Dr. Wachter approached SHM about hosting his blog, the organization’s leadership was quite interested—especially because SHM was already considering starting its own blog.

“SHM’s audience is perfect for the growing blog medium,” says Larry Wellikson, MD, the CEO of SHM. “We saw this with the enormous response to the SHM blogs at the May 2007 Annual Meeting.”

So “Wachter’s World” will be found on The Hospitalist’s Web site, where Dr. Wachter will post regular updates—he estimates typically three or four times a week.

“SHM’s partnership with Bob Wachter to launch an innovative blog, housed on the Web site for the most widely read publication in hospital medicine, SHM’s The Hospitalist, just makes sense as hospitalists need to hear new ideas and meet the challenge to be the change agents for the hospital of the future,” Dr. Wellikson says. “Wachter has proven himself a nationally sought-after thought leader who has something to say about hospital medicine, patient safety, improving quality, and the future of medicine.”

Dr. Wachter has a unique perspective on, well, everything. His years of experience working in hospital medicine as well as his high-level involvement in shaping the field—such as his position as chair of the American Board of Internal Medicine (ABIM) Committee on Hospital Medicine Focused Recognition—allows him ground-level and big-picture views of issues and trends that affect hospitalists’ work.

He often makes unique connections and forms original opinions on those issues—whether addressing road bumps a hospitalist runs into on the job or policy points that may change that job—and he plans to share those connections and opinions in his blog.

“I want to comment on the confluence of real stuff we all see day to day and the things that influence our field,” Dr. Wachter says. And he certainly has plenty of subjects to cover.

“There are so many issues that cross my retina every day that I think are of interest to hospitalists,” he says. “I see things in context—how they develop and how they all fit together, including trends as they develop. This blog will show my point of view—not on the differences in healthcare policy between Clinton’s camp and Obama’s camp—but closer to the ground. I’ll cover what relates to all of us.” TH

Dr. Wachter

Anyone who has attended the closing session of an SHM Annual Meeting or read one of his editorial pieces in The Hospitalist or other publications knows that Bob Wachter, MD, sees the world in a unique and uniquely informed way.

This fall, Dr. Wachter—professor and associate chairman of the Department of Medicine at the University of California, San Francisco (UCSF), co-founder of SHM, and the man who coined the term “hospitalist” (along with Lee Goldman, MD)—will regularly share his one-of-a-kind perspective via a Weblog, or blog. Tentatively titled “Wachter’s World,” the hospital medicine blog will debut at www.the-hospitalist.org in time for the “Management of the Hospitalized Patient” session Oct. 4-6 at UCSF. The in-depth course serves as the West Coast regional meeting of SHM.

“Even an old guy like me realizes that blogs are incredibly hot,” says Dr. Wachter. “And as I read more of them and began relying on them more for information and insights, I started looking for one in our field that was lively, engaging and informative, one I’d like to read. I couldn’t find anything, so I thought I should start one.”

When Dr. Wachter approached SHM about hosting his blog, the organization’s leadership was quite interested—especially because SHM was already considering starting its own blog.

“SHM’s audience is perfect for the growing blog medium,” says Larry Wellikson, MD, the CEO of SHM. “We saw this with the enormous response to the SHM blogs at the May 2007 Annual Meeting.”

So “Wachter’s World” will be found on The Hospitalist’s Web site, where Dr. Wachter will post regular updates—he estimates typically three or four times a week.

“SHM’s partnership with Bob Wachter to launch an innovative blog, housed on the Web site for the most widely read publication in hospital medicine, SHM’s The Hospitalist, just makes sense as hospitalists need to hear new ideas and meet the challenge to be the change agents for the hospital of the future,” Dr. Wellikson says. “Wachter has proven himself a nationally sought-after thought leader who has something to say about hospital medicine, patient safety, improving quality, and the future of medicine.”

Dr. Wachter has a unique perspective on, well, everything. His years of experience working in hospital medicine as well as his high-level involvement in shaping the field—such as his position as chair of the American Board of Internal Medicine (ABIM) Committee on Hospital Medicine Focused Recognition—allows him ground-level and big-picture views of issues and trends that affect hospitalists’ work.

He often makes unique connections and forms original opinions on those issues—whether addressing road bumps a hospitalist runs into on the job or policy points that may change that job—and he plans to share those connections and opinions in his blog.

“I want to comment on the confluence of real stuff we all see day to day and the things that influence our field,” Dr. Wachter says. And he certainly has plenty of subjects to cover.

“There are so many issues that cross my retina every day that I think are of interest to hospitalists,” he says. “I see things in context—how they develop and how they all fit together, including trends as they develop. This blog will show my point of view—not on the differences in healthcare policy between Clinton’s camp and Obama’s camp—but closer to the ground. I’ll cover what relates to all of us.” TH

Dr. Wachter

Anyone who has attended the closing session of an SHM Annual Meeting or read one of his editorial pieces in The Hospitalist or other publications knows that Bob Wachter, MD, sees the world in a unique and uniquely informed way.

This fall, Dr. Wachter—professor and associate chairman of the Department of Medicine at the University of California, San Francisco (UCSF), co-founder of SHM, and the man who coined the term “hospitalist” (along with Lee Goldman, MD)—will regularly share his one-of-a-kind perspective via a Weblog, or blog. Tentatively titled “Wachter’s World,” the hospital medicine blog will debut at www.the-hospitalist.org in time for the “Management of the Hospitalized Patient” session Oct. 4-6 at UCSF. The in-depth course serves as the West Coast regional meeting of SHM.

“Even an old guy like me realizes that blogs are incredibly hot,” says Dr. Wachter. “And as I read more of them and began relying on them more for information and insights, I started looking for one in our field that was lively, engaging and informative, one I’d like to read. I couldn’t find anything, so I thought I should start one.”

When Dr. Wachter approached SHM about hosting his blog, the organization’s leadership was quite interested—especially because SHM was already considering starting its own blog.

“SHM’s audience is perfect for the growing blog medium,” says Larry Wellikson, MD, the CEO of SHM. “We saw this with the enormous response to the SHM blogs at the May 2007 Annual Meeting.”

So “Wachter’s World” will be found on The Hospitalist’s Web site, where Dr. Wachter will post regular updates—he estimates typically three or four times a week.

“SHM’s partnership with Bob Wachter to launch an innovative blog, housed on the Web site for the most widely read publication in hospital medicine, SHM’s The Hospitalist, just makes sense as hospitalists need to hear new ideas and meet the challenge to be the change agents for the hospital of the future,” Dr. Wellikson says. “Wachter has proven himself a nationally sought-after thought leader who has something to say about hospital medicine, patient safety, improving quality, and the future of medicine.”

Dr. Wachter has a unique perspective on, well, everything. His years of experience working in hospital medicine as well as his high-level involvement in shaping the field—such as his position as chair of the American Board of Internal Medicine (ABIM) Committee on Hospital Medicine Focused Recognition—allows him ground-level and big-picture views of issues and trends that affect hospitalists’ work.

He often makes unique connections and forms original opinions on those issues—whether addressing road bumps a hospitalist runs into on the job or policy points that may change that job—and he plans to share those connections and opinions in his blog.

“I want to comment on the confluence of real stuff we all see day to day and the things that influence our field,” Dr. Wachter says. And he certainly has plenty of subjects to cover.

“There are so many issues that cross my retina every day that I think are of interest to hospitalists,” he says. “I see things in context—how they develop and how they all fit together, including trends as they develop. This blog will show my point of view—not on the differences in healthcare policy between Clinton’s camp and Obama’s camp—but closer to the ground. I’ll cover what relates to all of us.” TH

Patient-controlled analgesia (PCA), well accepted and widely used to quickly ease post-operative and acute pain, is safe and effective—in skilled hands. But there are complications, caveats, and safety concerns hospitalists should consider to incorporate this tool into their pain management routines and hospital protocols.

Studies show patients prefer the PCA compared with other analgesic routes.1-2 Less clear is whether it is more effective or leads to lower opioid use.

Some hospitalists use the PCA for their patients with pain—others defer to anesthesiologists, pain services, or palliative care consultants to manage the PCA and its multifaceted dosing requirements.

“There are a lot of misconceptions about the PCA,” says Deb Gordon, RN, MS, FAAN, senior clinical nurse specialist and pain consultant at the University of Wisconsin (UW) Medical Center in Madison. “There is a misunderstanding that the PCA is a magic black box for pain relief,” which can lead to its overuse. As a general rule of pain management, patients prefer the oral route of analgesic administration, Gordon says, unless that is a problem or rapid titration is needed.

“I don’t think [the PCA is] rocket science—it’s just a tool to deliver analgesics conveniently,” Gordon says. “I think every hospitalist should learn how to use the PCA, but there are always nuances of how to titrate opioids by any route.” UW has implemented PCA protocols, which staff can use for ballpark dosing recommendations.

How Hospitalists Use the PCA

The PCA delivers pain medication intravenously via a computerized pump with a button the patient can press when needed—without waiting for busy nurses to answer a call button and then confirm, prepare, and administer an analgesic treatment.

Hospitalists at UW, including Rob Hoffman, MD, often order the PCA. “It’s very well-liked by patients, who are not dependent on a busy nurse to get their analgesics administered,” Dr. Hoffman says. “The biggest concern, involving overdosing patients who are opioid-naïve, may be somewhat overblown. I haven’t experienced problems with my patients being over narcotized, but I start with a low dose and monitor them frequently.”

PCA technology can tabulate how much analgesic the patient has received during the previous 24 hours, Dr. Hoffman notes. “You know that’s a safe dose for the patient, and you can use it to make the transition to oral medications,” he says.

“Most of the patients I have on PCAs are palliative care patients,” says Rachelle Bernacki, MD, MS, a hospitalist, palliative care physician, and geriatrician at the University of California-San Francisco Medical Center. “I use it somewhat differently for the patients in my hospitalist practice—for example, for those who are experiencing intermittent, unpredictable episodes of abdominal pain. It’s also useful for patients with a need to feel in control of their situation. For constant, predictable pain, it’s better to use an around-the-clock schedule. I also send certain patients home on PCAs, especially if they are going to hospice care.”

Dr. Bernacki notes that some of her patients kiss the PCA button as if it were a long-lost friend, including one she recalls who had a bowel obstruction and had not found relief prior to starting on the PCA. But she also recalls a patient for whom the PCA was not a solution. “He was Cantonese-speaking,” she says. “Despite the presence of an interpreter and several attempts at education, he was never able to understand the connection between the PCA button and relief for his pain. We just couldn’t cross the cultural and language barriers.”

Hospitalists probably underuse the PCA, says Mahmood Shahlapour, MD, hospitalist and palliative care consultant at Chandler Regional Hospital in Chandler, Ariz. “Some hospitalists may feel uncomfortable with it,” he says. “I think it’s important for hospitalists to try to get more experience and comfort to be able to use it for the right patient and the right setting.”

What Is the PCA?

PCA technology as we know it today was pioneered in the early 1970s. Now it’s routine for post-surgical pain management. It is used for patients who have trouble taking oral medications or who need rapid response to acute pain crises. Increasingly, it is also used for patients with moderate to severe chronic pain related to cancer or who are being followed by hospice or palliative care services.

PCA refers both to the process of patient self-administration of parenteral analgesics and to the computerized infusion pump that makes this control possible. Recent advances in pain management also include patient-controlled epidural and transdermal analgesia systems—and other new pain modalities continue to be developed.3 Patients unable to operate the equipment themselves—for example, neonates or infants—may receive nurse-controlled analgesia, but experts say this should only be done within carefully defined parameters.

With the more typical intravenous PCA, the computerized pump allows for a number of variables, including:

• An initial bolus or loading dose to bring the pain under immediate control—an important but sometimes overlooked consideration in the successful use of PCAs;
• The patient-initiated or demand dose, available to the patient at the press of a button;
• The delay interval or lockout, typically between six and 15 minutes, allowing the analgesic to achieve its peak effect before another dose can be administered. The number of unsuccessful demands by patients during lockout periods is important for the physician to know;
• A continuous infusion or basal rate to provide continuous pain relief, although this may be contraindicated for opioid-naïve patients starting on PCAs.4 For those receiving opioids for chronic pain, the basal rate could be their current analgesic dose converted to the intravenous equivalent. Alternatively, the patient could receive this dose in a long-acting oral analgesic, with the PCA used for incidental or breakthrough pain. A basal rate also helps patients sleep, their pain controlled without having to wake up to press for a dose;
• A maximum volume of drug to be administered within a defined period of one, four, eight, or 24 hours, calculated to prevent an opioid overdose—regardless of how many times the PCA button gets pushed; and
• Monitoring devices such as pulse oximeter or end-tidal carbon dioxide monitor may be part of the PCA system to help warn of emerging respiratory depression.

The fundamental challenge for physicians lies in balancing the loading, basal, and patient-initiated doses with an appropriate maximum to make sure the patient gets adequate pain relief but doesn’t overdose. This is a more complex, multifaceted mathematical formula than ordering opioids to be administered two, three, or four times a day.

A basic safeguard of the PCA for preventing overdose is that when the opioid analgesic starts to make the patient drowsy, he or she is likely to stop pressing the button for another dose. However, for this to work, the PCA must be patient-controlled. If a nurse or family member pushes the button on the patient’s behalf out of a well-meaning desire to keep pain in check, this raises the risk of overdose.

In the past few years, several national quality and safety organizations have issued alerts about the danger of such patient-controlled analgesia by proxy. The Institute for Safe Medication Practices (ISMP) in Huntington Valley, Pa., issued two safety alerts in July 2003 discussing how potentially life-threatening errors can occur with PCAs and offering ways to prevent such errors.

U.S. Pharmacopeia’s summer 2004 USP Quality Review also offered safety recommendations based on analysis of medical errors directly resulting from PCA by proxy. The Joint Commission issued a Sentinel Alert on Dec. 20, 2004, noting that “serious adverse effects can occur when family members, caregivers or clinicians who are not authorized become involved in administering the analgesic for the patient by proxy.”5 Earlier this year the American Society for Pain Management Nursing issued clinical practice recommendations for how nurses can deal with the problem of PCA by proxy.6

Well-designed hospital PCA protocols will address this problem by including clear instructions to family members not to push the button for the patient, with an explanation of why this can be dangerous. Printed brochures and signs in the patient’s room are also helpful.

The Need for Training

“Physicians, as a rule, don’t receive adequate training in the PCA,” says Jean Youngwerth, MD, hospitalist, palliative care consultant and fellowship associate director at the University of Colorado Health Sciences Center in Denver. “Then you’re expected to know how to use it. There clearly is a need for this kind of training in the basics of the PCA, but a brief in-service should be sufficient.”

Dan Johnson, MD, regional department chief for palliative care for Kaiser-Permanente in Colorado, says the level of experience with the PCA is highly variable among physicians he works with. “Some know how to use the PCA and actually do it quite well. Many others are not adequately trained,” he says. “When I test residents with a few questions, they customarily do very poorly. Some of the answers I see make me nervous.”

Dr. Johnson offers a refresher on the PCA for hospitalists in the Denver area who attend an annual palliative care retreat. Those who come regularly seem to retain the information he offers. “If I were in a hospital that had not rolled out PCA standing orders, I’d make sure that there were educational units provided for hospitalists,” he says. “I’d also investigate how to develop standing orders for the hospital.” TH

Larry Beresford is a frequent contributor to The Hospitalist.

References

1. Hudcova J, McNicol E, Quah C, et al. Patient controlled opioid analgesia versus conventional opioid analgesia for postoperative pain. Cochrane Database Syst Rev. 2006;4.
2. Ballantyne JC, Carr DB, Chalmers TC. Postoperative patient-controlled analgesia: Meta-analyses of initial randomized controlled trials. J Clin Anesth. 1993 May/June;5(3):182-193.
3. D’Arcy Y. New pain management options: Delivery systems and techniques. Nursing. 2007 February; 37(2):26-27.
4. Pasero C, McCaffery M. Safe use of a continuous infusion with IV PCA. J PeriAnesthesia Nursing. 2004 Feb;19(1):42-45.
5. Joint Commission. Patient-controlled analgesia by proxy. Available at www.jointcommission.org/SentinelEvents/SentinelEventAlert/sea_33.htm. Last accessed July 12, 2007.
6. Wuhrman E, Cooney MF, Dunwoody CJ, et al. Authorized and unauthorized (“PCA by Proxy”) dosing of analgesic infusion pumps: Position statement with clinical practice recommendations. Pain Manag Nurs. 2007 Mar;8(1):4-11.
7. Prommer E. Fast Fact and Concept #92, Patient controlled analgesia in palliative care. End-of-Life/ Palliative Education Resource Center, Medical College of Wisconsin, Milwaukee:www.eperc.mcw.edu/ff_index.htm.
8. Owen H, Plummer JL, Armstrong I, et al. Variables of patient-controlled analgesia. 1. Bolus size. Anaesthesia.1989 Jan.;44(1):7-10.
9. Vicente KJ, Kada-Bekhaled K, Hillel G, et al. Programming errors contribute to death from patient-controlled analgesia. Can J Anesth. 2003;50:328-332.

Patient-controlled analgesia (PCA), well accepted and widely used to quickly ease post-operative and acute pain, is safe and effective—in skilled hands. But there are complications, caveats, and safety concerns hospitalists should consider to incorporate this tool into their pain management routines and hospital protocols.

Studies show patients prefer the PCA compared with other analgesic routes.1-2 Less clear is whether it is more effective or leads to lower opioid use.

Some hospitalists use the PCA for their patients with pain—others defer to anesthesiologists, pain services, or palliative care consultants to manage the PCA and its multifaceted dosing requirements.

“There are a lot of misconceptions about the PCA,” says Deb Gordon, RN, MS, FAAN, senior clinical nurse specialist and pain consultant at the University of Wisconsin (UW) Medical Center in Madison. “There is a misunderstanding that the PCA is a magic black box for pain relief,” which can lead to its overuse. As a general rule of pain management, patients prefer the oral route of analgesic administration, Gordon says, unless that is a problem or rapid titration is needed.

“I don’t think [the PCA is] rocket science—it’s just a tool to deliver analgesics conveniently,” Gordon says. “I think every hospitalist should learn how to use the PCA, but there are always nuances of how to titrate opioids by any route.” UW has implemented PCA protocols, which staff can use for ballpark dosing recommendations.

How Hospitalists Use the PCA

The PCA delivers pain medication intravenously via a computerized pump with a button the patient can press when needed—without waiting for busy nurses to answer a call button and then confirm, prepare, and administer an analgesic treatment.

Hospitalists at UW, including Rob Hoffman, MD, often order the PCA. “It’s very well-liked by patients, who are not dependent on a busy nurse to get their analgesics administered,” Dr. Hoffman says. “The biggest concern, involving overdosing patients who are opioid-naïve, may be somewhat overblown. I haven’t experienced problems with my patients being over narcotized, but I start with a low dose and monitor them frequently.”

PCA technology can tabulate how much analgesic the patient has received during the previous 24 hours, Dr. Hoffman notes. “You know that’s a safe dose for the patient, and you can use it to make the transition to oral medications,” he says.

“Most of the patients I have on PCAs are palliative care patients,” says Rachelle Bernacki, MD, MS, a hospitalist, palliative care physician, and geriatrician at the University of California-San Francisco Medical Center. “I use it somewhat differently for the patients in my hospitalist practice—for example, for those who are experiencing intermittent, unpredictable episodes of abdominal pain. It’s also useful for patients with a need to feel in control of their situation. For constant, predictable pain, it’s better to use an around-the-clock schedule. I also send certain patients home on PCAs, especially if they are going to hospice care.”

Dr. Bernacki notes that some of her patients kiss the PCA button as if it were a long-lost friend, including one she recalls who had a bowel obstruction and had not found relief prior to starting on the PCA. But she also recalls a patient for whom the PCA was not a solution. “He was Cantonese-speaking,” she says. “Despite the presence of an interpreter and several attempts at education, he was never able to understand the connection between the PCA button and relief for his pain. We just couldn’t cross the cultural and language barriers.”

Hospitalists probably underuse the PCA, says Mahmood Shahlapour, MD, hospitalist and palliative care consultant at Chandler Regional Hospital in Chandler, Ariz. “Some hospitalists may feel uncomfortable with it,” he says. “I think it’s important for hospitalists to try to get more experience and comfort to be able to use it for the right patient and the right setting.”

What Is the PCA?

PCA technology as we know it today was pioneered in the early 1970s. Now it’s routine for post-surgical pain management. It is used for patients who have trouble taking oral medications or who need rapid response to acute pain crises. Increasingly, it is also used for patients with moderate to severe chronic pain related to cancer or who are being followed by hospice or palliative care services.

PCA refers both to the process of patient self-administration of parenteral analgesics and to the computerized infusion pump that makes this control possible. Recent advances in pain management also include patient-controlled epidural and transdermal analgesia systems—and other new pain modalities continue to be developed.3 Patients unable to operate the equipment themselves—for example, neonates or infants—may receive nurse-controlled analgesia, but experts say this should only be done within carefully defined parameters.

With the more typical intravenous PCA, the computerized pump allows for a number of variables, including:

• An initial bolus or loading dose to bring the pain under immediate control—an important but sometimes overlooked consideration in the successful use of PCAs;
• The patient-initiated or demand dose, available to the patient at the press of a button;
• The delay interval or lockout, typically between six and 15 minutes, allowing the analgesic to achieve its peak effect before another dose can be administered. The number of unsuccessful demands by patients during lockout periods is important for the physician to know;
• A continuous infusion or basal rate to provide continuous pain relief, although this may be contraindicated for opioid-naïve patients starting on PCAs.4 For those receiving opioids for chronic pain, the basal rate could be their current analgesic dose converted to the intravenous equivalent. Alternatively, the patient could receive this dose in a long-acting oral analgesic, with the PCA used for incidental or breakthrough pain. A basal rate also helps patients sleep, their pain controlled without having to wake up to press for a dose;
• A maximum volume of drug to be administered within a defined period of one, four, eight, or 24 hours, calculated to prevent an opioid overdose—regardless of how many times the PCA button gets pushed; and
• Monitoring devices such as pulse oximeter or end-tidal carbon dioxide monitor may be part of the PCA system to help warn of emerging respiratory depression.

The fundamental challenge for physicians lies in balancing the loading, basal, and patient-initiated doses with an appropriate maximum to make sure the patient gets adequate pain relief but doesn’t overdose. This is a more complex, multifaceted mathematical formula than ordering opioids to be administered two, three, or four times a day.

A basic safeguard of the PCA for preventing overdose is that when the opioid analgesic starts to make the patient drowsy, he or she is likely to stop pressing the button for another dose. However, for this to work, the PCA must be patient-controlled. If a nurse or family member pushes the button on the patient’s behalf out of a well-meaning desire to keep pain in check, this raises the risk of overdose.

In the past few years, several national quality and safety organizations have issued alerts about the danger of such patient-controlled analgesia by proxy. The Institute for Safe Medication Practices (ISMP) in Huntington Valley, Pa., issued two safety alerts in July 2003 discussing how potentially life-threatening errors can occur with PCAs and offering ways to prevent such errors.

U.S. Pharmacopeia’s summer 2004 USP Quality Review also offered safety recommendations based on analysis of medical errors directly resulting from PCA by proxy. The Joint Commission issued a Sentinel Alert on Dec. 20, 2004, noting that “serious adverse effects can occur when family members, caregivers or clinicians who are not authorized become involved in administering the analgesic for the patient by proxy.”5 Earlier this year the American Society for Pain Management Nursing issued clinical practice recommendations for how nurses can deal with the problem of PCA by proxy.6

Well-designed hospital PCA protocols will address this problem by including clear instructions to family members not to push the button for the patient, with an explanation of why this can be dangerous. Printed brochures and signs in the patient’s room are also helpful.

The Need for Training

“Physicians, as a rule, don’t receive adequate training in the PCA,” says Jean Youngwerth, MD, hospitalist, palliative care consultant and fellowship associate director at the University of Colorado Health Sciences Center in Denver. “Then you’re expected to know how to use it. There clearly is a need for this kind of training in the basics of the PCA, but a brief in-service should be sufficient.”

Dan Johnson, MD, regional department chief for palliative care for Kaiser-Permanente in Colorado, says the level of experience with the PCA is highly variable among physicians he works with. “Some know how to use the PCA and actually do it quite well. Many others are not adequately trained,” he says. “When I test residents with a few questions, they customarily do very poorly. Some of the answers I see make me nervous.”

Dr. Johnson offers a refresher on the PCA for hospitalists in the Denver area who attend an annual palliative care retreat. Those who come regularly seem to retain the information he offers. “If I were in a hospital that had not rolled out PCA standing orders, I’d make sure that there were educational units provided for hospitalists,” he says. “I’d also investigate how to develop standing orders for the hospital.” TH

Larry Beresford is a frequent contributor to The Hospitalist.

References

1. Hudcova J, McNicol E, Quah C, et al. Patient controlled opioid analgesia versus conventional opioid analgesia for postoperative pain. Cochrane Database Syst Rev. 2006;4.
2. Ballantyne JC, Carr DB, Chalmers TC. Postoperative patient-controlled analgesia: Meta-analyses of initial randomized controlled trials. J Clin Anesth. 1993 May/June;5(3):182-193.
3. D’Arcy Y. New pain management options: Delivery systems and techniques. Nursing. 2007 February; 37(2):26-27.
4. Pasero C, McCaffery M. Safe use of a continuous infusion with IV PCA. J PeriAnesthesia Nursing. 2004 Feb;19(1):42-45.
5. Joint Commission. Patient-controlled analgesia by proxy. Available at www.jointcommission.org/SentinelEvents/SentinelEventAlert/sea_33.htm. Last accessed July 12, 2007.
6. Wuhrman E, Cooney MF, Dunwoody CJ, et al. Authorized and unauthorized (“PCA by Proxy”) dosing of analgesic infusion pumps: Position statement with clinical practice recommendations. Pain Manag Nurs. 2007 Mar;8(1):4-11.
7. Prommer E. Fast Fact and Concept #92, Patient controlled analgesia in palliative care. End-of-Life/ Palliative Education Resource Center, Medical College of Wisconsin, Milwaukee:www.eperc.mcw.edu/ff_index.htm.
8. Owen H, Plummer JL, Armstrong I, et al. Variables of patient-controlled analgesia. 1. Bolus size. Anaesthesia.1989 Jan.;44(1):7-10.
9. Vicente KJ, Kada-Bekhaled K, Hillel G, et al. Programming errors contribute to death from patient-controlled analgesia. Can J Anesth. 2003;50:328-332.

Patient-controlled analgesia (PCA), well accepted and widely used to quickly ease post-operative and acute pain, is safe and effective—in skilled hands. But there are complications, caveats, and safety concerns hospitalists should consider to incorporate this tool into their pain management routines and hospital protocols.

Studies show patients prefer the PCA compared with other analgesic routes.1-2 Less clear is whether it is more effective or leads to lower opioid use.

Some hospitalists use the PCA for their patients with pain—others defer to anesthesiologists, pain services, or palliative care consultants to manage the PCA and its multifaceted dosing requirements.

“There are a lot of misconceptions about the PCA,” says Deb Gordon, RN, MS, FAAN, senior clinical nurse specialist and pain consultant at the University of Wisconsin (UW) Medical Center in Madison. “There is a misunderstanding that the PCA is a magic black box for pain relief,” which can lead to its overuse. As a general rule of pain management, patients prefer the oral route of analgesic administration, Gordon says, unless that is a problem or rapid titration is needed.

“I don’t think [the PCA is] rocket science—it’s just a tool to deliver analgesics conveniently,” Gordon says. “I think every hospitalist should learn how to use the PCA, but there are always nuances of how to titrate opioids by any route.” UW has implemented PCA protocols, which staff can use for ballpark dosing recommendations.

How Hospitalists Use the PCA

The PCA delivers pain medication intravenously via a computerized pump with a button the patient can press when needed—without waiting for busy nurses to answer a call button and then confirm, prepare, and administer an analgesic treatment.

Hospitalists at UW, including Rob Hoffman, MD, often order the PCA. “It’s very well-liked by patients, who are not dependent on a busy nurse to get their analgesics administered,” Dr. Hoffman says. “The biggest concern, involving overdosing patients who are opioid-naïve, may be somewhat overblown. I haven’t experienced problems with my patients being over narcotized, but I start with a low dose and monitor them frequently.”

PCA technology can tabulate how much analgesic the patient has received during the previous 24 hours, Dr. Hoffman notes. “You know that’s a safe dose for the patient, and you can use it to make the transition to oral medications,” he says.

“Most of the patients I have on PCAs are palliative care patients,” says Rachelle Bernacki, MD, MS, a hospitalist, palliative care physician, and geriatrician at the University of California-San Francisco Medical Center. “I use it somewhat differently for the patients in my hospitalist practice—for example, for those who are experiencing intermittent, unpredictable episodes of abdominal pain. It’s also useful for patients with a need to feel in control of their situation. For constant, predictable pain, it’s better to use an around-the-clock schedule. I also send certain patients home on PCAs, especially if they are going to hospice care.”

Dr. Bernacki notes that some of her patients kiss the PCA button as if it were a long-lost friend, including one she recalls who had a bowel obstruction and had not found relief prior to starting on the PCA. But she also recalls a patient for whom the PCA was not a solution. “He was Cantonese-speaking,” she says. “Despite the presence of an interpreter and several attempts at education, he was never able to understand the connection between the PCA button and relief for his pain. We just couldn’t cross the cultural and language barriers.”

Hospitalists probably underuse the PCA, says Mahmood Shahlapour, MD, hospitalist and palliative care consultant at Chandler Regional Hospital in Chandler, Ariz. “Some hospitalists may feel uncomfortable with it,” he says. “I think it’s important for hospitalists to try to get more experience and comfort to be able to use it for the right patient and the right setting.”

What Is the PCA?

PCA technology as we know it today was pioneered in the early 1970s. Now it’s routine for post-surgical pain management. It is used for patients who have trouble taking oral medications or who need rapid response to acute pain crises. Increasingly, it is also used for patients with moderate to severe chronic pain related to cancer or who are being followed by hospice or palliative care services.

PCA refers both to the process of patient self-administration of parenteral analgesics and to the computerized infusion pump that makes this control possible. Recent advances in pain management also include patient-controlled epidural and transdermal analgesia systems—and other new pain modalities continue to be developed.3 Patients unable to operate the equipment themselves—for example, neonates or infants—may receive nurse-controlled analgesia, but experts say this should only be done within carefully defined parameters.

With the more typical intravenous PCA, the computerized pump allows for a number of variables, including:

• An initial bolus or loading dose to bring the pain under immediate control—an important but sometimes overlooked consideration in the successful use of PCAs;
• The patient-initiated or demand dose, available to the patient at the press of a button;
• The delay interval or lockout, typically between six and 15 minutes, allowing the analgesic to achieve its peak effect before another dose can be administered. The number of unsuccessful demands by patients during lockout periods is important for the physician to know;
• A continuous infusion or basal rate to provide continuous pain relief, although this may be contraindicated for opioid-naïve patients starting on PCAs.4 For those receiving opioids for chronic pain, the basal rate could be their current analgesic dose converted to the intravenous equivalent. Alternatively, the patient could receive this dose in a long-acting oral analgesic, with the PCA used for incidental or breakthrough pain. A basal rate also helps patients sleep, their pain controlled without having to wake up to press for a dose;
• A maximum volume of drug to be administered within a defined period of one, four, eight, or 24 hours, calculated to prevent an opioid overdose—regardless of how many times the PCA button gets pushed; and
• Monitoring devices such as pulse oximeter or end-tidal carbon dioxide monitor may be part of the PCA system to help warn of emerging respiratory depression.

The fundamental challenge for physicians lies in balancing the loading, basal, and patient-initiated doses with an appropriate maximum to make sure the patient gets adequate pain relief but doesn’t overdose. This is a more complex, multifaceted mathematical formula than ordering opioids to be administered two, three, or four times a day.

A basic safeguard of the PCA for preventing overdose is that when the opioid analgesic starts to make the patient drowsy, he or she is likely to stop pressing the button for another dose. However, for this to work, the PCA must be patient-controlled. If a nurse or family member pushes the button on the patient’s behalf out of a well-meaning desire to keep pain in check, this raises the risk of overdose.

In the past few years, several national quality and safety organizations have issued alerts about the danger of such patient-controlled analgesia by proxy. The Institute for Safe Medication Practices (ISMP) in Huntington Valley, Pa., issued two safety alerts in July 2003 discussing how potentially life-threatening errors can occur with PCAs and offering ways to prevent such errors.

U.S. Pharmacopeia’s summer 2004 USP Quality Review also offered safety recommendations based on analysis of medical errors directly resulting from PCA by proxy. The Joint Commission issued a Sentinel Alert on Dec. 20, 2004, noting that “serious adverse effects can occur when family members, caregivers or clinicians who are not authorized become involved in administering the analgesic for the patient by proxy.”5 Earlier this year the American Society for Pain Management Nursing issued clinical practice recommendations for how nurses can deal with the problem of PCA by proxy.6

Well-designed hospital PCA protocols will address this problem by including clear instructions to family members not to push the button for the patient, with an explanation of why this can be dangerous. Printed brochures and signs in the patient’s room are also helpful.

The Need for Training

“Physicians, as a rule, don’t receive adequate training in the PCA,” says Jean Youngwerth, MD, hospitalist, palliative care consultant and fellowship associate director at the University of Colorado Health Sciences Center in Denver. “Then you’re expected to know how to use it. There clearly is a need for this kind of training in the basics of the PCA, but a brief in-service should be sufficient.”

Dan Johnson, MD, regional department chief for palliative care for Kaiser-Permanente in Colorado, says the level of experience with the PCA is highly variable among physicians he works with. “Some know how to use the PCA and actually do it quite well. Many others are not adequately trained,” he says. “When I test residents with a few questions, they customarily do very poorly. Some of the answers I see make me nervous.”

Dr. Johnson offers a refresher on the PCA for hospitalists in the Denver area who attend an annual palliative care retreat. Those who come regularly seem to retain the information he offers. “If I were in a hospital that had not rolled out PCA standing orders, I’d make sure that there were educational units provided for hospitalists,” he says. “I’d also investigate how to develop standing orders for the hospital.” TH

Larry Beresford is a frequent contributor to The Hospitalist.

References

1. Hudcova J, McNicol E, Quah C, et al. Patient controlled opioid analgesia versus conventional opioid analgesia for postoperative pain. Cochrane Database Syst Rev. 2006;4.
2. Ballantyne JC, Carr DB, Chalmers TC. Postoperative patient-controlled analgesia: Meta-analyses of initial randomized controlled trials. J Clin Anesth. 1993 May/June;5(3):182-193.
3. D’Arcy Y. New pain management options: Delivery systems and techniques. Nursing. 2007 February; 37(2):26-27.
4. Pasero C, McCaffery M. Safe use of a continuous infusion with IV PCA. J PeriAnesthesia Nursing. 2004 Feb;19(1):42-45.
5. Joint Commission. Patient-controlled analgesia by proxy. Available at www.jointcommission.org/SentinelEvents/SentinelEventAlert/sea_33.htm. Last accessed July 12, 2007.
6. Wuhrman E, Cooney MF, Dunwoody CJ, et al. Authorized and unauthorized (“PCA by Proxy”) dosing of analgesic infusion pumps: Position statement with clinical practice recommendations. Pain Manag Nurs. 2007 Mar;8(1):4-11.
7. Prommer E. Fast Fact and Concept #92, Patient controlled analgesia in palliative care. End-of-Life/ Palliative Education Resource Center, Medical College of Wisconsin, Milwaukee:www.eperc.mcw.edu/ff_index.htm.
8. Owen H, Plummer JL, Armstrong I, et al. Variables of patient-controlled analgesia. 1. Bolus size. Anaesthesia.1989 Jan.;44(1):7-10.
9. Vicente KJ, Kada-Bekhaled K, Hillel G, et al. Programming errors contribute to death from patient-controlled analgesia. Can J Anesth. 2003;50:328-332.

Supplement Co-Editors and Supplement Co-Directors:
Amir K. Jaffer, MD, and Franklin A. Michota, Jr., MD

Summit Co-Directors:
Angela M. Bader, MD, MPH, and Raymond Borkowski, MD

Contents

Forword: New topics, returning features, tools for enduring challenges
Amir K. Jaffer, MD, and Franklin A. Michota, Jr., MD

Summit Faculty

Summit Program

IMPACT Consults

Are routine preoperative chest radiographs necessary in asymptomatic patients undergoing noncardiothoracic surgery?
Anitha Rajamanickam, MD, Preethi Patel, MD, and Ali Usmani, MD

Do preoperative nutritional interventions improve outcomes in malnourished patients undergoing elective surgery?
Ramnath Hebbar, MD, and Brian Harte, MD

Do all patients undergoing bariatric surgery need polysomnography to evaluate for obstructive sleep apnea?
Roop Kaw, MD, Vesselin Dimov, MD, and Charles Bae, MD

Can brain natriuretic peptide identify noncardiac surgery patients at high risk for cardiac events?
Ali Usmani, MD, Priyanka Sharma, MD, and Ashish Aneja, MD

What is the significance of an isolated elevated activated partial thromboplastin time in the preoperative setting?
William H. Morris, MD, and Ajay Kumar, MD

Does unrecognized diabetes in the preoperative period worsen postoperative outcomes?
Krista Andersen-Harris, DO, and Christopher Whinney, MD

Should an asymptomatic patient with an abnormal urinalysis (bacteriuria or pyuria) be treated with antibiotics prior to major joint replacement surgery?
Anitha Rajamanickam, MD, Saira Noor, MD, and Ali Usmani, MD

Does a carotid bruit predict cerebrovascular complications following noncardiac surgery in asymptomatic patients?
Robert Mayock, MD

What risks does a history of pulmonary hypertension present for patients undergoing noncardiac surgery?
Roop Kaw, MD, Priyanka Sharma, MD, and Omar A. Minai, MD

Does a systolic murmur heard in the aortic area need to be further evaluated prior to elective surgery?
Thadeo Catacutan, MD, Ali Usmani, MD, and Ashish Aneja, MD

Abstracts

Oral Abstracts
Preoperative electrocardiograms: Patient factors predictive of abnormalities
Darin Correll, David Hepner, Lawrence Tsen, Candace Chang, Angela Bader

Impact of combination medical therapy on mortality in vascular surgery patients
Thomas Barrett, Motomi Mori, Caroline Koudelka

Do large electronic medical record databases permit collection of reliable and valid data for quality improvement purposes?
Ashish Aneja, Eric Hixson, Brian Harte, Vesselin Dimov, Amir Jaffer

Poster Abstracts
Innovations in Perioperative Medicine
Abstract 1: PONV: 'An ounce of prevention is worth a pound of cure'
Catherine Capitula, Shari Duguay

Abstract 2: Optimization of perioperative processes through innovation and technology for the orthopaedic operating room of the future
J.H. James Choi, Jennifer Blueter, Barbara Fahey, James Leonard, Ted Omilanowski, Vincent Riley, Mark Schauer, Timothy Sullivan, Viktor Krebs, Jonathan Schaffer

Abstract 3: A systematic approach to interpreting electrocardiograms by using two mnemonics
Vesselin Dimov, Kalina Uzunova-Dimova, Ajay Kumar, Ashish Aneja

Abstract 4: Improving and standardizing medicine consultation
Benny Gavi, Lisa Shieh, Keith Posley, Shahram Sepehri, Phil Pang

Abstract 5: Medical students' assessment of a required rotation in perioperative medicine and pain
Amir Jaffer, Samuel Irefin, John Tetzlaff, J. Harry Isaacson

Abstract 6: Improving safety for adult surgical patients with obstructive sleep apnea
Karen Watkins

Abstract 7: A multidisciplinary approach to improving the safety of high-risk spine surgery: The complex spine protocol
Peter Kallas, Anjali Desai, Andrew Naidech, Tyler Koski, Steve Ondra, Mary Lou Green

Abstract 8: The nurse practitioner role in evidence-based medication strategies
Patricia Kidik, Kathleen Holbrook

Abstract 9: Use of the motivator/hygiene theory of motivation to guide quality efforts
Ronald Kratz

Abstract 10: A novel care model coordinating inpatient and outpatient perioperative care, utilizing a computerized patient tracking system
Diane Levitan, Dominic Reilly, Christopher Wong, Kara Mitchell, Philip Vedovatti, Nason Hamlin

Abstract 11: The development of an admitting team
Kathleen McGrath, Janet Piatek, Jeanne Lanchester

Abstract 12: Improve communication among caregivers: Eliminating unauthorized abbreviations on hospital medical records
Magdalena G. Smith, Maura Walsh, Laurie Walsh, Marjorie Guglin, Dio Sumaygaysay, Evangelina Sapalasan, Frances Haug, Olivia Voellmicke, Mahin Sanjari, Nancy Cimitile, Mariya Chernyatskaya

Abstract 13: Improve preadmission testing process
Magdalena G. Smith, Tak Tam, Rita Medrozo, Maura Walsh, Laurie Walsh, Marjorie Guglin

Perioperative Clinical Vignettes
Abstract 14: Chronic renal insufficiency: An oft-forgotten component of the revised cardiac risk index
Vesselin Dimov, Ashish Aneja, Kalina Uzunova-Dimova

Abstract 15: When is a stress test indicated in patients with chronic kidney disease evaluated for noncardiac surgery?
Vesselin Dimov, Kalina Uzunova-Dimova, Mitko Badov, Saira Noor

Abstract 16: When to correct hyperkalemia in patients with chronic kidney disease prior to noncardiac surgery?
Vesselin Dimov, Kalina Uzunova-Dimova, Ajay Kumar, Anitha Rajamanickam, Mitko Badov

Abstract 17: What is the optimal time frame for performing hemodialysis in patients with end-stage renal disease prior to surgery?
Vesselin Dimov, Kalina Uzunova-Dimova, Mitko Badov, Ajay Kumar

Abstract 18: A recent vascular graft in a patient with end-stage renal disease on hemodialysis and the need for preoperative antibiotic prophylaxis
Vesselin Dimov, Kalina Uzunova-Dimova, Mitko Badov, Ajay Kumar

Abstract 19: Postoperative risk of acute kidney injury in patients with chronic kidney disease
Vesselin Dimov, Kalina Uzunova-Dimova, Ali Usmani, Ajay Kumar

Abstract 20: Preoperative hypoglycemia in a patient on detemir insulin
Ronad P. Olson, M. Angelyn Bethel, Lillian F. Lien

Abstract 21: Evaluation of Mobitz I atrioventricular block in a preoperative patient
Margaret Pothier

Abstract 22: Perioperative cardiac arrest in a patient with aortic stenosis: Is it preventable?
Zdravka Zafirova, Bobbie Sweitzer

Abstract 23: Antiplatelet therapy interruption and perioperative stent thrombosis: Too much, too early
Zdravka Zafirova, Bobbie Sweitzer

Research in Perioperative Medicine
Abstract 24: Use of an at-home internet-based patient evaluation tool for preoperative assessment
Margaret Pothier, David Hepner, Darrin Correll, Thomas Ho, Alina Lazar, Angela Bader

Abstract 25: The utility of a preoperative clinic questionnaire to predict postoperative delirium risk
David Hepner, Darin Correll, Thomas Ho, Juergen Bludau, Jhoanna Santos, Angela Bader

Abstract 26: A drug by any other name: Preoperative insulin regimens
Carlee Clark, Vivek Moitra, Bobbie Jean Sweitzer

Abstract 27: Preoperative cardiovascular risk factor assessment in morbidly obese patients with an abnormal electrocardiogram
Girish Mood, Roomana Akhtar, Rajagopal Reddy Edula, Gunjana Bhandari, Vishal Gupta, Michael Koch

Abstract 28: Cardiac testing prior to nonvascular surgery: The results from a newly formed preoperative clinic
Sheela Pai, Giang Tran, Alvin Blaustein, Prasad Atluri, Salwa Shenaq

Abstract 29: Which is better—half-dose or no insulin on day of surgery?
Kirk Smith, Vivek Moitra, Melinda Drum, Bobbie Jean Sweitzer

Index of Authors

Supplement Co-Editors and Supplement Co-Directors:
Amir K. Jaffer, MD, and Franklin A. Michota, Jr., MD

Summit Co-Directors:
Angela M. Bader, MD, MPH, and Raymond Borkowski, MD

Contents

Forword: New topics, returning features, tools for enduring challenges
Amir K. Jaffer, MD, and Franklin A. Michota, Jr., MD

Summit Faculty

Summit Program

IMPACT Consults

Are routine preoperative chest radiographs necessary in asymptomatic patients undergoing noncardiothoracic surgery?
Anitha Rajamanickam, MD, Preethi Patel, MD, and Ali Usmani, MD

Do preoperative nutritional interventions improve outcomes in malnourished patients undergoing elective surgery?
Ramnath Hebbar, MD, and Brian Harte, MD

Do all patients undergoing bariatric surgery need polysomnography to evaluate for obstructive sleep apnea?
Roop Kaw, MD, Vesselin Dimov, MD, and Charles Bae, MD

Can brain natriuretic peptide identify noncardiac surgery patients at high risk for cardiac events?
Ali Usmani, MD, Priyanka Sharma, MD, and Ashish Aneja, MD

What is the significance of an isolated elevated activated partial thromboplastin time in the preoperative setting?
William H. Morris, MD, and Ajay Kumar, MD

Does unrecognized diabetes in the preoperative period worsen postoperative outcomes?
Krista Andersen-Harris, DO, and Christopher Whinney, MD

Should an asymptomatic patient with an abnormal urinalysis (bacteriuria or pyuria) be treated with antibiotics prior to major joint replacement surgery?
Anitha Rajamanickam, MD, Saira Noor, MD, and Ali Usmani, MD

Does a carotid bruit predict cerebrovascular complications following noncardiac surgery in asymptomatic patients?
Robert Mayock, MD

What risks does a history of pulmonary hypertension present for patients undergoing noncardiac surgery?
Roop Kaw, MD, Priyanka Sharma, MD, and Omar A. Minai, MD

Does a systolic murmur heard in the aortic area need to be further evaluated prior to elective surgery?
Thadeo Catacutan, MD, Ali Usmani, MD, and Ashish Aneja, MD

Abstracts

Oral Abstracts
Preoperative electrocardiograms: Patient factors predictive of abnormalities
Darin Correll, David Hepner, Lawrence Tsen, Candace Chang, Angela Bader

Impact of combination medical therapy on mortality in vascular surgery patients
Thomas Barrett, Motomi Mori, Caroline Koudelka

Do large electronic medical record databases permit collection of reliable and valid data for quality improvement purposes?
Ashish Aneja, Eric Hixson, Brian Harte, Vesselin Dimov, Amir Jaffer

Poster Abstracts
Innovations in Perioperative Medicine
Abstract 1: PONV: 'An ounce of prevention is worth a pound of cure'
Catherine Capitula, Shari Duguay

Abstract 2: Optimization of perioperative processes through innovation and technology for the orthopaedic operating room of the future
J.H. James Choi, Jennifer Blueter, Barbara Fahey, James Leonard, Ted Omilanowski, Vincent Riley, Mark Schauer, Timothy Sullivan, Viktor Krebs, Jonathan Schaffer

Abstract 3: A systematic approach to interpreting electrocardiograms by using two mnemonics
Vesselin Dimov, Kalina Uzunova-Dimova, Ajay Kumar, Ashish Aneja

Abstract 4: Improving and standardizing medicine consultation
Benny Gavi, Lisa Shieh, Keith Posley, Shahram Sepehri, Phil Pang

Abstract 5: Medical students' assessment of a required rotation in perioperative medicine and pain
Amir Jaffer, Samuel Irefin, John Tetzlaff, J. Harry Isaacson

Abstract 6: Improving safety for adult surgical patients with obstructive sleep apnea
Karen Watkins

Abstract 7: A multidisciplinary approach to improving the safety of high-risk spine surgery: The complex spine protocol
Peter Kallas, Anjali Desai, Andrew Naidech, Tyler Koski, Steve Ondra, Mary Lou Green

Abstract 8: The nurse practitioner role in evidence-based medication strategies
Patricia Kidik, Kathleen Holbrook

Abstract 9: Use of the motivator/hygiene theory of motivation to guide quality efforts
Ronald Kratz

Abstract 10: A novel care model coordinating inpatient and outpatient perioperative care, utilizing a computerized patient tracking system
Diane Levitan, Dominic Reilly, Christopher Wong, Kara Mitchell, Philip Vedovatti, Nason Hamlin

Abstract 11: The development of an admitting team
Kathleen McGrath, Janet Piatek, Jeanne Lanchester

Abstract 12: Improve communication among caregivers: Eliminating unauthorized abbreviations on hospital medical records
Magdalena G. Smith, Maura Walsh, Laurie Walsh, Marjorie Guglin, Dio Sumaygaysay, Evangelina Sapalasan, Frances Haug, Olivia Voellmicke, Mahin Sanjari, Nancy Cimitile, Mariya Chernyatskaya

Abstract 13: Improve preadmission testing process
Magdalena G. Smith, Tak Tam, Rita Medrozo, Maura Walsh, Laurie Walsh, Marjorie Guglin

Perioperative Clinical Vignettes
Abstract 14: Chronic renal insufficiency: An oft-forgotten component of the revised cardiac risk index
Vesselin Dimov, Ashish Aneja, Kalina Uzunova-Dimova

Abstract 15: When is a stress test indicated in patients with chronic kidney disease evaluated for noncardiac surgery?
Vesselin Dimov, Kalina Uzunova-Dimova, Mitko Badov, Saira Noor

Abstract 16: When to correct hyperkalemia in patients with chronic kidney disease prior to noncardiac surgery?
Vesselin Dimov, Kalina Uzunova-Dimova, Ajay Kumar, Anitha Rajamanickam, Mitko Badov

Abstract 17: What is the optimal time frame for performing hemodialysis in patients with end-stage renal disease prior to surgery?
Vesselin Dimov, Kalina Uzunova-Dimova, Mitko Badov, Ajay Kumar

Abstract 18: A recent vascular graft in a patient with end-stage renal disease on hemodialysis and the need for preoperative antibiotic prophylaxis
Vesselin Dimov, Kalina Uzunova-Dimova, Mitko Badov, Ajay Kumar

Abstract 19: Postoperative risk of acute kidney injury in patients with chronic kidney disease
Vesselin Dimov, Kalina Uzunova-Dimova, Ali Usmani, Ajay Kumar

Abstract 20: Preoperative hypoglycemia in a patient on detemir insulin
Ronad P. Olson, M. Angelyn Bethel, Lillian F. Lien

Abstract 21: Evaluation of Mobitz I atrioventricular block in a preoperative patient
Margaret Pothier

Abstract 22: Perioperative cardiac arrest in a patient with aortic stenosis: Is it preventable?
Zdravka Zafirova, Bobbie Sweitzer

Abstract 23: Antiplatelet therapy interruption and perioperative stent thrombosis: Too much, too early
Zdravka Zafirova, Bobbie Sweitzer

Research in Perioperative Medicine
Abstract 24: Use of an at-home internet-based patient evaluation tool for preoperative assessment
Margaret Pothier, David Hepner, Darrin Correll, Thomas Ho, Alina Lazar, Angela Bader

Abstract 25: The utility of a preoperative clinic questionnaire to predict postoperative delirium risk
David Hepner, Darin Correll, Thomas Ho, Juergen Bludau, Jhoanna Santos, Angela Bader

Abstract 26: A drug by any other name: Preoperative insulin regimens
Carlee Clark, Vivek Moitra, Bobbie Jean Sweitzer

Abstract 27: Preoperative cardiovascular risk factor assessment in morbidly obese patients with an abnormal electrocardiogram
Girish Mood, Roomana Akhtar, Rajagopal Reddy Edula, Gunjana Bhandari, Vishal Gupta, Michael Koch

Abstract 28: Cardiac testing prior to nonvascular surgery: The results from a newly formed preoperative clinic
Sheela Pai, Giang Tran, Alvin Blaustein, Prasad Atluri, Salwa Shenaq

Abstract 29: Which is better—half-dose or no insulin on day of surgery?
Kirk Smith, Vivek Moitra, Melinda Drum, Bobbie Jean Sweitzer

Index of Authors

Supplement Co-Editors and Supplement Co-Directors:
Amir K. Jaffer, MD, and Franklin A. Michota, Jr., MD

Summit Co-Directors:
Angela M. Bader, MD, MPH, and Raymond Borkowski, MD

Contents

Forword: New topics, returning features, tools for enduring challenges
Amir K. Jaffer, MD, and Franklin A. Michota, Jr., MD

Summit Faculty

Summit Program

IMPACT Consults

Are routine preoperative chest radiographs necessary in asymptomatic patients undergoing noncardiothoracic surgery?
Anitha Rajamanickam, MD, Preethi Patel, MD, and Ali Usmani, MD

Do preoperative nutritional interventions improve outcomes in malnourished patients undergoing elective surgery?
Ramnath Hebbar, MD, and Brian Harte, MD

Do all patients undergoing bariatric surgery need polysomnography to evaluate for obstructive sleep apnea?
Roop Kaw, MD, Vesselin Dimov, MD, and Charles Bae, MD

Can brain natriuretic peptide identify noncardiac surgery patients at high risk for cardiac events?
Ali Usmani, MD, Priyanka Sharma, MD, and Ashish Aneja, MD

What is the significance of an isolated elevated activated partial thromboplastin time in the preoperative setting?
William H. Morris, MD, and Ajay Kumar, MD

Does unrecognized diabetes in the preoperative period worsen postoperative outcomes?
Krista Andersen-Harris, DO, and Christopher Whinney, MD

Should an asymptomatic patient with an abnormal urinalysis (bacteriuria or pyuria) be treated with antibiotics prior to major joint replacement surgery?
Anitha Rajamanickam, MD, Saira Noor, MD, and Ali Usmani, MD

Does a carotid bruit predict cerebrovascular complications following noncardiac surgery in asymptomatic patients?
Robert Mayock, MD

What risks does a history of pulmonary hypertension present for patients undergoing noncardiac surgery?
Roop Kaw, MD, Priyanka Sharma, MD, and Omar A. Minai, MD

Does a systolic murmur heard in the aortic area need to be further evaluated prior to elective surgery?
Thadeo Catacutan, MD, Ali Usmani, MD, and Ashish Aneja, MD

Abstracts

Oral Abstracts
Preoperative electrocardiograms: Patient factors predictive of abnormalities
Darin Correll, David Hepner, Lawrence Tsen, Candace Chang, Angela Bader

Impact of combination medical therapy on mortality in vascular surgery patients
Thomas Barrett, Motomi Mori, Caroline Koudelka

Do large electronic medical record databases permit collection of reliable and valid data for quality improvement purposes?
Ashish Aneja, Eric Hixson, Brian Harte, Vesselin Dimov, Amir Jaffer

Poster Abstracts
Innovations in Perioperative Medicine
Abstract 1: PONV: 'An ounce of prevention is worth a pound of cure'
Catherine Capitula, Shari Duguay

Abstract 2: Optimization of perioperative processes through innovation and technology for the orthopaedic operating room of the future
J.H. James Choi, Jennifer Blueter, Barbara Fahey, James Leonard, Ted Omilanowski, Vincent Riley, Mark Schauer, Timothy Sullivan, Viktor Krebs, Jonathan Schaffer

Abstract 3: A systematic approach to interpreting electrocardiograms by using two mnemonics
Vesselin Dimov, Kalina Uzunova-Dimova, Ajay Kumar, Ashish Aneja

Abstract 4: Improving and standardizing medicine consultation
Benny Gavi, Lisa Shieh, Keith Posley, Shahram Sepehri, Phil Pang

Abstract 5: Medical students' assessment of a required rotation in perioperative medicine and pain
Amir Jaffer, Samuel Irefin, John Tetzlaff, J. Harry Isaacson

Abstract 6: Improving safety for adult surgical patients with obstructive sleep apnea
Karen Watkins

Abstract 7: A multidisciplinary approach to improving the safety of high-risk spine surgery: The complex spine protocol
Peter Kallas, Anjali Desai, Andrew Naidech, Tyler Koski, Steve Ondra, Mary Lou Green

Abstract 8: The nurse practitioner role in evidence-based medication strategies
Patricia Kidik, Kathleen Holbrook

Abstract 9: Use of the motivator/hygiene theory of motivation to guide quality efforts
Ronald Kratz

Abstract 10: A novel care model coordinating inpatient and outpatient perioperative care, utilizing a computerized patient tracking system
Diane Levitan, Dominic Reilly, Christopher Wong, Kara Mitchell, Philip Vedovatti, Nason Hamlin

Abstract 11: The development of an admitting team
Kathleen McGrath, Janet Piatek, Jeanne Lanchester

Abstract 12: Improve communication among caregivers: Eliminating unauthorized abbreviations on hospital medical records
Magdalena G. Smith, Maura Walsh, Laurie Walsh, Marjorie Guglin, Dio Sumaygaysay, Evangelina Sapalasan, Frances Haug, Olivia Voellmicke, Mahin Sanjari, Nancy Cimitile, Mariya Chernyatskaya

Abstract 13: Improve preadmission testing process
Magdalena G. Smith, Tak Tam, Rita Medrozo, Maura Walsh, Laurie Walsh, Marjorie Guglin

Perioperative Clinical Vignettes
Abstract 14: Chronic renal insufficiency: An oft-forgotten component of the revised cardiac risk index
Vesselin Dimov, Ashish Aneja, Kalina Uzunova-Dimova

Abstract 15: When is a stress test indicated in patients with chronic kidney disease evaluated for noncardiac surgery?
Vesselin Dimov, Kalina Uzunova-Dimova, Mitko Badov, Saira Noor

Abstract 16: When to correct hyperkalemia in patients with chronic kidney disease prior to noncardiac surgery?
Vesselin Dimov, Kalina Uzunova-Dimova, Ajay Kumar, Anitha Rajamanickam, Mitko Badov

Abstract 17: What is the optimal time frame for performing hemodialysis in patients with end-stage renal disease prior to surgery?
Vesselin Dimov, Kalina Uzunova-Dimova, Mitko Badov, Ajay Kumar

Abstract 18: A recent vascular graft in a patient with end-stage renal disease on hemodialysis and the need for preoperative antibiotic prophylaxis
Vesselin Dimov, Kalina Uzunova-Dimova, Mitko Badov, Ajay Kumar

Abstract 19: Postoperative risk of acute kidney injury in patients with chronic kidney disease
Vesselin Dimov, Kalina Uzunova-Dimova, Ali Usmani, Ajay Kumar

Abstract 20: Preoperative hypoglycemia in a patient on detemir insulin
Ronad P. Olson, M. Angelyn Bethel, Lillian F. Lien

Abstract 21: Evaluation of Mobitz I atrioventricular block in a preoperative patient
Margaret Pothier

Abstract 22: Perioperative cardiac arrest in a patient with aortic stenosis: Is it preventable?
Zdravka Zafirova, Bobbie Sweitzer

Abstract 23: Antiplatelet therapy interruption and perioperative stent thrombosis: Too much, too early
Zdravka Zafirova, Bobbie Sweitzer

Research in Perioperative Medicine
Abstract 24: Use of an at-home internet-based patient evaluation tool for preoperative assessment
Margaret Pothier, David Hepner, Darrin Correll, Thomas Ho, Alina Lazar, Angela Bader

Abstract 25: The utility of a preoperative clinic questionnaire to predict postoperative delirium risk
David Hepner, Darin Correll, Thomas Ho, Juergen Bludau, Jhoanna Santos, Angela Bader

Abstract 26: A drug by any other name: Preoperative insulin regimens
Carlee Clark, Vivek Moitra, Bobbie Jean Sweitzer

Abstract 27: Preoperative cardiovascular risk factor assessment in morbidly obese patients with an abnormal electrocardiogram
Girish Mood, Roomana Akhtar, Rajagopal Reddy Edula, Gunjana Bhandari, Vishal Gupta, Michael Koch

Abstract 28: Cardiac testing prior to nonvascular surgery: The results from a newly formed preoperative clinic
Sheela Pai, Giang Tran, Alvin Blaustein, Prasad Atluri, Salwa Shenaq

Abstract 29: Which is better—half-dose or no insulin on day of surgery?
Kirk Smith, Vivek Moitra, Melinda Drum, Bobbie Jean Sweitzer

Index of Authors

Proper sleep hygiene can help your patients fall and stay asleep consistently. Patients with insomnia are at a higher risk of developing or experiencing a recurrence of a mood disorder, and poor sleep can worsen psychiatric symptoms such as depression or mania.¹ Data about combining behavioral approaches and hypnotic medications to treat insomnia are inconclusive;² however, using the 2 together may help patients who do not respond to a single approach.

First rule out other causes of insomnia, such as sleep apnea, other medical conditions, or medications. Patients may improve after these factors are addressed.

Teaching sleep hygiene principles (Box) does not mean patients will adopt these habits, but employing the following suggestions could improve adherence:

Obtain a detailed sleep history to identify specific behaviors to be changed. For example, a patient might only have to stop watching television in bed to get a good night’s sleep, although some may find a brief exposure to television or radio facilitates relaxation.

Explain the rationale for changing a behavior. For example, when telling patients to limit caffeine or alcohol at night, list these substances’ negative effects on sleep. Similarly, when instructing patients to avoid watching television in bed, tell them that using the bedroom only for sleep or sex will help condition them for sleep at bedtime.

Box

Discuss sleep regularly. A patient might not disclose poor sleeping habits during the first session.

Give your patient handouts on sleep hygiene principles and highlight the most pertinent information. Ask the patient to place the handout where he or she will see it regularly.

Involve the family to help identify a patient’s poor sleep habits and find ways to implement sleep hygiene principles.

Encourage patients to keep a sleep diary. Ask the patient to note how many hours and at what time he or she slept for at least 2 weeks, then bring this information to the next appointment. This record allows you to examine patients’ sleep patterns and recommend appropriate changes.

Ask patients for creative ideas to improve their sleep. This dialogue will facilitate the therapeutic alliance and encourage positive changes in patients’ lives.

Proper sleep hygiene can help your patients fall and stay asleep consistently. Patients with insomnia are at a higher risk of developing or experiencing a recurrence of a mood disorder, and poor sleep can worsen psychiatric symptoms such as depression or mania.¹ Data about combining behavioral approaches and hypnotic medications to treat insomnia are inconclusive;² however, using the 2 together may help patients who do not respond to a single approach.

First rule out other causes of insomnia, such as sleep apnea, other medical conditions, or medications. Patients may improve after these factors are addressed.

Teaching sleep hygiene principles (Box) does not mean patients will adopt these habits, but employing the following suggestions could improve adherence:

Obtain a detailed sleep history to identify specific behaviors to be changed. For example, a patient might only have to stop watching television in bed to get a good night’s sleep, although some may find a brief exposure to television or radio facilitates relaxation.

Explain the rationale for changing a behavior. For example, when telling patients to limit caffeine or alcohol at night, list these substances’ negative effects on sleep. Similarly, when instructing patients to avoid watching television in bed, tell them that using the bedroom only for sleep or sex will help condition them for sleep at bedtime.

Box

Discuss sleep regularly. A patient might not disclose poor sleeping habits during the first session.

Give your patient handouts on sleep hygiene principles and highlight the most pertinent information. Ask the patient to place the handout where he or she will see it regularly.

Involve the family to help identify a patient’s poor sleep habits and find ways to implement sleep hygiene principles.

Encourage patients to keep a sleep diary. Ask the patient to note how many hours and at what time he or she slept for at least 2 weeks, then bring this information to the next appointment. This record allows you to examine patients’ sleep patterns and recommend appropriate changes.

Ask patients for creative ideas to improve their sleep. This dialogue will facilitate the therapeutic alliance and encourage positive changes in patients’ lives.

Proper sleep hygiene can help your patients fall and stay asleep consistently. Patients with insomnia are at a higher risk of developing or experiencing a recurrence of a mood disorder, and poor sleep can worsen psychiatric symptoms such as depression or mania.¹ Data about combining behavioral approaches and hypnotic medications to treat insomnia are inconclusive;² however, using the 2 together may help patients who do not respond to a single approach.

First rule out other causes of insomnia, such as sleep apnea, other medical conditions, or medications. Patients may improve after these factors are addressed.

Teaching sleep hygiene principles (Box) does not mean patients will adopt these habits, but employing the following suggestions could improve adherence:

Obtain a detailed sleep history to identify specific behaviors to be changed. For example, a patient might only have to stop watching television in bed to get a good night’s sleep, although some may find a brief exposure to television or radio facilitates relaxation.

Explain the rationale for changing a behavior. For example, when telling patients to limit caffeine or alcohol at night, list these substances’ negative effects on sleep. Similarly, when instructing patients to avoid watching television in bed, tell them that using the bedroom only for sleep or sex will help condition them for sleep at bedtime.

Box

Discuss sleep regularly. A patient might not disclose poor sleeping habits during the first session.

Give your patient handouts on sleep hygiene principles and highlight the most pertinent information. Ask the patient to place the handout where he or she will see it regularly.

Involve the family to help identify a patient’s poor sleep habits and find ways to implement sleep hygiene principles.

Encourage patients to keep a sleep diary. Ask the patient to note how many hours and at what time he or she slept for at least 2 weeks, then bring this information to the next appointment. This record allows you to examine patients’ sleep patterns and recommend appropriate changes.

Ask patients for creative ideas to improve their sleep. This dialogue will facilitate the therapeutic alliance and encourage positive changes in patients’ lives.

Posttraumatic stress disorder (PTSD) is a preventable mental illness—without trauma, the illness does not occur. Primary prevention (such as eliminating war, rape, physical assaults, child abuse, or motor vehicle accidents) would be effective but is an unrealistic goal. Secondary prevention (such as preventing PTSD after individuals have been exposed to trauma) may be attainable.

No medication is FDA-approved to prevent PTSD, but patients recently exposed to trauma might benefit from drugs approved for other indications. Possibilities include noradrenergics such as propranolol, corticosteroids that affect the hypothalamic-pituitary-adrenal (HPA) axis, opioids, benzodiazepines, and antidepressants. Some investigational agents also might block the process that turns a traumatic experience into PTSD.

This article discusses these intriguing ideas and suggests which trauma victims might benefit now from acute pharmacologic PTSD prevention.

Who might be treated?

An estimated 8% to 10% of the U.S. population experiences PTSD at some point in life (Box 1).^1,2 A person’s risk of developing PTSD after a traumatic event depends on the type of trauma. For example, 10% of motor vehicle accident survivors develop PTSD, compared with 60% of rape survivors.¹

Targeting anyone who has experienced trauma for secondary PTSD prevention would expose large groups of people to medications they do not need. Targeting selected persons who are at the highest risk would be more efficient and cost-effective. In a group of acute trauma-exposed persons, 2 selection criteria could be considered simultaneously:

• Which patients may be most predisposed to PTSD?
• Which patients are showing early symptoms that may predict PTSD?

Box 1

Risk factors and resiliency. Certain factors have been shown to increase a person’s vulnerability for PTSD (Table 1).³ Other proposed risk factors include:

• personality types⁴
• psychophysiologic factors such as reactivity, conditionability, and resistance to extinction/habituation.⁵

Strong evidence also indicates that acute trauma-related symptoms—including excessive arousal and fear,⁶ peritraumatic dissociation, and depression—predict the later development of PTSD.

Once identified, individuals predisposed to developing PTSD could be given treatment to increase their resiliency after they have been exposed to trauma. Early evidence suggests that you also could consider giving these patients medications as secondary prevention (Table 2).

Table 1

Who develops PTSD? Risk and resiliency factors

Table 2

Medications being studied for PTSD prevention

Targeting noradrenergic activity

Increased noradrenergic activity has been associated with persistent memories and PTSD. Therefore, medications that reduce noradrenergic tone by blocking receptors or reduce norepinephrine release are being explored for PTSD prevention.

Propranolol. Three small studies have examined whether the beta-noradrenergic receptor blocker propranolol can prevent PTSD.

In a randomized, double-blind, placebo-controlled trial,⁷ 41 emergency department patients who had a heart rate of ≥ 80 bpm within 6 hours of a traumatic accident received propranolol, 40 mg qid, or placebo for 10 days. After 1 month, the 11 patients who completed propranolol treatment showed a nonsignificant trend toward lower scores on the Clinician-Administered PTSD Scale (CAPS), compared with 20 patients taking placebo. At 3 months, the propranolol group had less physiologic reactivity (as measured by heart rate and skin conductance) to trauma-related cues than the placebo group.

In a nonrandomized study,⁸ PTSD developed within 2 months in 1 of 11 trauma victims who agreed to take propranolol, 40 mg tid, immediately after the trauma, compared with 3 of 8 victims who refused the medication.

In an unpublished randomized, double-blind trial,⁹ 48 patients admitted to a level I trauma center received propranolol, 40 mg tid; gabapentin, 400 mg tid; or placebo for PTSD prevention. Gabapentin was chosen because it has few side effects or metabolic interactions and preliminary evidence of anxiolytic efficacy.

Neither propranolol nor gabapentin showed statistically significant benefit in preventing PTSD compared with placebo. Effect sizes with the 2 treatments were too small to suggest that larger samples would produce a statistically significant result.

Prazosin—an alpha-1 adrenergic receptor antagonist—has been evaluated in 3 controlled studies and found to reduce intrusive nightmares typical of chronic PTSD.

Ten combat veterans with chronic PTSD showed significantly improved sleep, fewer severe nightmares, and improved global clinical status after receiving prazosin (mean dose 9.5 mg at bedtime) in a 20-week, placebo-controlled, double-blind, crossover study.¹⁰

In a larger randomized, parallel group trial,¹¹ the same authors compared prazosin with placebo in 40 combat veterans (mean age 56) with chronic PTSD. After 8 weeks, veterans taking prazosin (mean 13.3 ± 3 mg) had significantly fewer trauma nightmares, improved sleep (including return of normal dreams), and improved global clinical status vs placebo. Overall CAP scores did not decline significantly, however.

In a third placebo-controlled study,¹² a midmorning dose of prazosin was added to the regimens of 11 civilian trauma patients already taking the drug at bedtime to suppress trauma-related nightmares. Their daytime PTSD symptoms improved, as shown by reduced psychological distress in response to verbal trauma cues.

Prazosin can reduce chronic PTSD manifestations of nightmares and disturbed sleep, but it has not been shown to ameliorate the full PTSD syndrome. Prazosin has not been studied as an early PTSD intervention.

Other antiadrenergics that reduce the release of norepinephrine—including clonidine and guanfacine—have been studied in open trials as treatment for PTSD. The only controlled study¹³ showed no benefit from guanfacine for PTSD prevention.

De-stressing the HPA axis

Hydrocortisone has been proposed to prevent PTSD by reducing HPA axis activation, acting as a countermeasure to elevated corticotropin-releasing factor found in patients with chronic PTSD.

IV hydrocortisone’s effect on the development of PTSD was compared with placebo in 20 septic shock survivors after discharge from intensive care.¹⁴ One of 9 patients (11%) in the hydrocortisone group was diagnosed with PTSD at follow-up (mean 31 months), compared with 7 of 11 (64%) in the placebo group.

In a similar study, the same researchers gave patients hydrocortisone before, during, and after cardiac surgery. Follow-up interviews revealed significantly lower PTSD and chronic stress symptom scores in the treatment group vs the placebo group.¹⁵

These studies—although provocative—are limited by the narrow range of trauma related to severe medical illness or extensive medical procedures.

Norepinephrine-blocking opioids

When the noradrenergic system is activated, one physiologic response is the activation of endogenous opioid systems, which may promote recovery by inhibiting the HPA axis. Opioid systems might be involved in PTSD, as suggested by:

• preclinical evidence that opioids modulate memory¹⁶
• studies showing low pain thresholds¹⁷ and abnormal beta-endorphin (an opioid peptide neurotransmitter)¹⁸ and methionine enkephalin (an opioid peptide)¹⁹ levels in PTSD patients.

In theory, opioid administration immediately after trauma may attenuate norepinephrine release, thus thwarting arousal-charged memory consolidation, hyperarousal, and re-experiencing.

One uncontrolled report of pediatric burn victims found a significant association between the morphine dose given for pain during hospitalization and reduced PTSD symptoms 6 months later.²⁰ Decreased pain did not explain the reduction in PTSD, as no significant correlation was seen between pain symptoms and PTSD outcome measures. Similarly, a longitudinal study of substance use among Vietnam War veterans with PTSD found decreased hyperarousal symptoms in heroin users.²¹

Using opioids to prevent PTSD would be feasible and efficient in acute care settings because 80% to 90% of traumatically-injured patients are discharged on opioid analgesics (compared with <10% on beta blockers or corticosteroids).²² However, 20% to 40% of physically injured inpatients are diagnosed with a substance use disorder at some point in life, making the use of opioid analgesics a practical concern.²³

GABA-benzodiazepine paradox

The GABA-benzodiazepine system plays an important role in mediating anxiety, which is consistent with the potent anxiolytic effects of benzodiazepines. Even so, trials of benzodiazepines have found these drugs surprisingly unhelpful—and perhaps harmful—in patients with acute trauma.

Alprazolam did not reduce PTSD symptoms in a small randomized, double-blind study.²⁴ Another trial found that receiving benzodiazepines shortly after trauma exposure was associated with increased PTSD risk in trauma survivors. Nine of 13 patients (69%) who received alprazolam or clonazepam met PTSD diagnostic criteria 6 months after the trauma, compared with 3 of 13 controls (15%).²⁵

Similarly, in a randomized controlled trial, 22 patients were given temazepam for 7 nights, starting approximately 14 days after exposure to a traumatic event. Six weeks later, 55% of those receiving temazepam and 27% of those receiving placebo met criteria for PTSD.²⁶

In summary, benzodiazepines might be helpful when given for a few days after traumatization to control overwhelming anxiety but could be harmful over a longer term.

Other agents for PTSD

Antidepressants. Early trauma-related symptoms of depression predict later development of PTSD.²⁷ Thus, antidepressants have been proposed for early intervention in addition to their well-established role as first-line treatment of PTSD.²⁸

One study supports this idea: a 7-day randomized double-blind trial that compared the tricyclic antidepressant imipramine with chloral hydrate in pediatric burn patients with acute stress disorder (ASD). Imipramine was more effective (83% response) than chloral hydrate (38% response) in reducing ASD symptoms.²⁹

Drugs in development. Three new medications being explored for treating anxiety and depression also might be useful for PTSD prevention. Neuropeptide Y (NPY) agonists,³⁰ substance P antagonists,³¹ and CRH-antagonists³² are thought to hold promise because of their more proximate roles—compared with monoamine neurotransmitters such as dopamine, norepinephrine and serotonin—in mediating the stress response.

Box 2

Analyzing the evidence

Insufficient evidence exists to determine which strategies might be most effective to prevent PTSD, what optimal dosing might be, and which traumatized individuals might be best targeted with these approaches.

• Beta-blockers and corticosteroids—the most theoretically compelling strategies—are the most difficult agents to use for PTSD prevention because they have the most medical contraindications. In addition, evidence supporting their ability to prevent PTSD is meager at best.
• Prazosin is intriguing but has contra-indications similar to those of beta blockers, no studies of secondary prevention, and no clear indication that it works for the overall PTSD syndrome.
• Opioids are restricted agents with substantial contraindications.
• Evidence is limited but points most strongly toward earlier use of antidepressants. Early trauma-related symptoms of depression predict later development of PTSD,²⁷ and a number of selective serotonin reuptake inhibitors—such as citalopram, fluoxetine, paroxetine, and sertraline—are FDA-approved or used off-label for treating PTSD.³³

Prescribing recommendations. Consider practicality, ease of use, and safety of the proposed medication when choosing a drug for PTSD prevention (Table 3).²² Based on the evidence, the most reasonable posttrauma approach (Box 2) might be to consider starting an approved antidepressant for individuals thought to be particularly vulnerable to PTSD because of:

• past history of PTSD, depression, or anxiety disorder
• severity of the trauma (such as in cases of sexual assault or torture)
• pain (antidepressants with analgesic properties—such as venlafaxine or duloxetine—might be useful in patients whose trauma is associated with physical injury, although neither is FDA-approved to treat PTSD).

Table 3

4 considerations when choosing a drug for PTSD prevention

Related resources

• Mental health and mass violence: Evidence-based early psychological intervention for victims/survivors of mass violence. A workshop to reach consensus on best practices. Rockland, MD: National Institute of Mental Health; 2002. www.nimh.nih.gov.
• Post-traumatic stress disorder: the management of PTSD in adults and children in primary and secondary care (clinical guideline 26). London, UK: National Institute for Clinical Excellence; 2005. www.nice.org.uk.
• Ursano RJ, Bell C, Eth S, et al. Practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder. Am J Psychiatry 2004;161(suppl 11):3-31.

Drug brand names

• Alprazolam • Xanax
• Amitriptyline • Elavil
• Citalopram • Celexa
• Clonazepam • Klonopin
• Clonidine • Catapres
• Duloxetine • Cymbalta
• Fluoxetine • Prozac
• Gabapentin • Neurontin
• Guanfacine • Tenex
• Imipramine • Tofranil
• Lamotrigine • Lamictal
• Paroxetine • Paxil
• Prazosin • Minipress
• Propranolol • Inderal
• Sertraline • Zoloft
• Temazepam • Restoril
• Venlafaxine • Effexor

Disclosure

Dr. Bennett and Dr. Zatzick report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Roy-Byrne is a consultant to Jazz Pharmaceuticals and Solvay and has received speaker honoraria from Wyeth and Forrest Pharmaceuticals.

Posttraumatic stress disorder (PTSD) is a preventable mental illness—without trauma, the illness does not occur. Primary prevention (such as eliminating war, rape, physical assaults, child abuse, or motor vehicle accidents) would be effective but is an unrealistic goal. Secondary prevention (such as preventing PTSD after individuals have been exposed to trauma) may be attainable.

No medication is FDA-approved to prevent PTSD, but patients recently exposed to trauma might benefit from drugs approved for other indications. Possibilities include noradrenergics such as propranolol, corticosteroids that affect the hypothalamic-pituitary-adrenal (HPA) axis, opioids, benzodiazepines, and antidepressants. Some investigational agents also might block the process that turns a traumatic experience into PTSD.

This article discusses these intriguing ideas and suggests which trauma victims might benefit now from acute pharmacologic PTSD prevention.

Who might be treated?

An estimated 8% to 10% of the U.S. population experiences PTSD at some point in life (Box 1).^1,2 A person’s risk of developing PTSD after a traumatic event depends on the type of trauma. For example, 10% of motor vehicle accident survivors develop PTSD, compared with 60% of rape survivors.¹

Targeting anyone who has experienced trauma for secondary PTSD prevention would expose large groups of people to medications they do not need. Targeting selected persons who are at the highest risk would be more efficient and cost-effective. In a group of acute trauma-exposed persons, 2 selection criteria could be considered simultaneously:

• Which patients may be most predisposed to PTSD?
• Which patients are showing early symptoms that may predict PTSD?

Box 1

Risk factors and resiliency. Certain factors have been shown to increase a person’s vulnerability for PTSD (Table 1).³ Other proposed risk factors include:

• personality types⁴
• psychophysiologic factors such as reactivity, conditionability, and resistance to extinction/habituation.⁵

Strong evidence also indicates that acute trauma-related symptoms—including excessive arousal and fear,⁶ peritraumatic dissociation, and depression—predict the later development of PTSD.

Once identified, individuals predisposed to developing PTSD could be given treatment to increase their resiliency after they have been exposed to trauma. Early evidence suggests that you also could consider giving these patients medications as secondary prevention (Table 2).

Table 1

Who develops PTSD? Risk and resiliency factors

Table 2

Medications being studied for PTSD prevention

Targeting noradrenergic activity

Increased noradrenergic activity has been associated with persistent memories and PTSD. Therefore, medications that reduce noradrenergic tone by blocking receptors or reduce norepinephrine release are being explored for PTSD prevention.

Propranolol. Three small studies have examined whether the beta-noradrenergic receptor blocker propranolol can prevent PTSD.

In a randomized, double-blind, placebo-controlled trial,⁷ 41 emergency department patients who had a heart rate of ≥ 80 bpm within 6 hours of a traumatic accident received propranolol, 40 mg qid, or placebo for 10 days. After 1 month, the 11 patients who completed propranolol treatment showed a nonsignificant trend toward lower scores on the Clinician-Administered PTSD Scale (CAPS), compared with 20 patients taking placebo. At 3 months, the propranolol group had less physiologic reactivity (as measured by heart rate and skin conductance) to trauma-related cues than the placebo group.

In a nonrandomized study,⁸ PTSD developed within 2 months in 1 of 11 trauma victims who agreed to take propranolol, 40 mg tid, immediately after the trauma, compared with 3 of 8 victims who refused the medication.

In an unpublished randomized, double-blind trial,⁹ 48 patients admitted to a level I trauma center received propranolol, 40 mg tid; gabapentin, 400 mg tid; or placebo for PTSD prevention. Gabapentin was chosen because it has few side effects or metabolic interactions and preliminary evidence of anxiolytic efficacy.

Neither propranolol nor gabapentin showed statistically significant benefit in preventing PTSD compared with placebo. Effect sizes with the 2 treatments were too small to suggest that larger samples would produce a statistically significant result.

Prazosin—an alpha-1 adrenergic receptor antagonist—has been evaluated in 3 controlled studies and found to reduce intrusive nightmares typical of chronic PTSD.

Ten combat veterans with chronic PTSD showed significantly improved sleep, fewer severe nightmares, and improved global clinical status after receiving prazosin (mean dose 9.5 mg at bedtime) in a 20-week, placebo-controlled, double-blind, crossover study.¹⁰

In a larger randomized, parallel group trial,¹¹ the same authors compared prazosin with placebo in 40 combat veterans (mean age 56) with chronic PTSD. After 8 weeks, veterans taking prazosin (mean 13.3 ± 3 mg) had significantly fewer trauma nightmares, improved sleep (including return of normal dreams), and improved global clinical status vs placebo. Overall CAP scores did not decline significantly, however.

In a third placebo-controlled study,¹² a midmorning dose of prazosin was added to the regimens of 11 civilian trauma patients already taking the drug at bedtime to suppress trauma-related nightmares. Their daytime PTSD symptoms improved, as shown by reduced psychological distress in response to verbal trauma cues.

Prazosin can reduce chronic PTSD manifestations of nightmares and disturbed sleep, but it has not been shown to ameliorate the full PTSD syndrome. Prazosin has not been studied as an early PTSD intervention.

Other antiadrenergics that reduce the release of norepinephrine—including clonidine and guanfacine—have been studied in open trials as treatment for PTSD. The only controlled study¹³ showed no benefit from guanfacine for PTSD prevention.

De-stressing the HPA axis

Hydrocortisone has been proposed to prevent PTSD by reducing HPA axis activation, acting as a countermeasure to elevated corticotropin-releasing factor found in patients with chronic PTSD.

IV hydrocortisone’s effect on the development of PTSD was compared with placebo in 20 septic shock survivors after discharge from intensive care.¹⁴ One of 9 patients (11%) in the hydrocortisone group was diagnosed with PTSD at follow-up (mean 31 months), compared with 7 of 11 (64%) in the placebo group.

In a similar study, the same researchers gave patients hydrocortisone before, during, and after cardiac surgery. Follow-up interviews revealed significantly lower PTSD and chronic stress symptom scores in the treatment group vs the placebo group.¹⁵

These studies—although provocative—are limited by the narrow range of trauma related to severe medical illness or extensive medical procedures.

Norepinephrine-blocking opioids

When the noradrenergic system is activated, one physiologic response is the activation of endogenous opioid systems, which may promote recovery by inhibiting the HPA axis. Opioid systems might be involved in PTSD, as suggested by:

• preclinical evidence that opioids modulate memory¹⁶
• studies showing low pain thresholds¹⁷ and abnormal beta-endorphin (an opioid peptide neurotransmitter)¹⁸ and methionine enkephalin (an opioid peptide)¹⁹ levels in PTSD patients.

In theory, opioid administration immediately after trauma may attenuate norepinephrine release, thus thwarting arousal-charged memory consolidation, hyperarousal, and re-experiencing.

One uncontrolled report of pediatric burn victims found a significant association between the morphine dose given for pain during hospitalization and reduced PTSD symptoms 6 months later.²⁰ Decreased pain did not explain the reduction in PTSD, as no significant correlation was seen between pain symptoms and PTSD outcome measures. Similarly, a longitudinal study of substance use among Vietnam War veterans with PTSD found decreased hyperarousal symptoms in heroin users.²¹

Using opioids to prevent PTSD would be feasible and efficient in acute care settings because 80% to 90% of traumatically-injured patients are discharged on opioid analgesics (compared with <10% on beta blockers or corticosteroids).²² However, 20% to 40% of physically injured inpatients are diagnosed with a substance use disorder at some point in life, making the use of opioid analgesics a practical concern.²³

GABA-benzodiazepine paradox

The GABA-benzodiazepine system plays an important role in mediating anxiety, which is consistent with the potent anxiolytic effects of benzodiazepines. Even so, trials of benzodiazepines have found these drugs surprisingly unhelpful—and perhaps harmful—in patients with acute trauma.

Alprazolam did not reduce PTSD symptoms in a small randomized, double-blind study.²⁴ Another trial found that receiving benzodiazepines shortly after trauma exposure was associated with increased PTSD risk in trauma survivors. Nine of 13 patients (69%) who received alprazolam or clonazepam met PTSD diagnostic criteria 6 months after the trauma, compared with 3 of 13 controls (15%).²⁵

Similarly, in a randomized controlled trial, 22 patients were given temazepam for 7 nights, starting approximately 14 days after exposure to a traumatic event. Six weeks later, 55% of those receiving temazepam and 27% of those receiving placebo met criteria for PTSD.²⁶

In summary, benzodiazepines might be helpful when given for a few days after traumatization to control overwhelming anxiety but could be harmful over a longer term.

Other agents for PTSD

Antidepressants. Early trauma-related symptoms of depression predict later development of PTSD.²⁷ Thus, antidepressants have been proposed for early intervention in addition to their well-established role as first-line treatment of PTSD.²⁸

One study supports this idea: a 7-day randomized double-blind trial that compared the tricyclic antidepressant imipramine with chloral hydrate in pediatric burn patients with acute stress disorder (ASD). Imipramine was more effective (83% response) than chloral hydrate (38% response) in reducing ASD symptoms.²⁹

Drugs in development. Three new medications being explored for treating anxiety and depression also might be useful for PTSD prevention. Neuropeptide Y (NPY) agonists,³⁰ substance P antagonists,³¹ and CRH-antagonists³² are thought to hold promise because of their more proximate roles—compared with monoamine neurotransmitters such as dopamine, norepinephrine and serotonin—in mediating the stress response.

Box 2

Analyzing the evidence

Insufficient evidence exists to determine which strategies might be most effective to prevent PTSD, what optimal dosing might be, and which traumatized individuals might be best targeted with these approaches.

• Beta-blockers and corticosteroids—the most theoretically compelling strategies—are the most difficult agents to use for PTSD prevention because they have the most medical contraindications. In addition, evidence supporting their ability to prevent PTSD is meager at best.
• Prazosin is intriguing but has contra-indications similar to those of beta blockers, no studies of secondary prevention, and no clear indication that it works for the overall PTSD syndrome.
• Opioids are restricted agents with substantial contraindications.
• Evidence is limited but points most strongly toward earlier use of antidepressants. Early trauma-related symptoms of depression predict later development of PTSD,²⁷ and a number of selective serotonin reuptake inhibitors—such as citalopram, fluoxetine, paroxetine, and sertraline—are FDA-approved or used off-label for treating PTSD.³³

Prescribing recommendations. Consider practicality, ease of use, and safety of the proposed medication when choosing a drug for PTSD prevention (Table 3).²² Based on the evidence, the most reasonable posttrauma approach (Box 2) might be to consider starting an approved antidepressant for individuals thought to be particularly vulnerable to PTSD because of:

• past history of PTSD, depression, or anxiety disorder
• severity of the trauma (such as in cases of sexual assault or torture)
• pain (antidepressants with analgesic properties—such as venlafaxine or duloxetine—might be useful in patients whose trauma is associated with physical injury, although neither is FDA-approved to treat PTSD).

Table 3

4 considerations when choosing a drug for PTSD prevention

Related resources

• Mental health and mass violence: Evidence-based early psychological intervention for victims/survivors of mass violence. A workshop to reach consensus on best practices. Rockland, MD: National Institute of Mental Health; 2002. www.nimh.nih.gov.
• Post-traumatic stress disorder: the management of PTSD in adults and children in primary and secondary care (clinical guideline 26). London, UK: National Institute for Clinical Excellence; 2005. www.nice.org.uk.
• Ursano RJ, Bell C, Eth S, et al. Practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder. Am J Psychiatry 2004;161(suppl 11):3-31.

Drug brand names

• Alprazolam • Xanax
• Amitriptyline • Elavil
• Citalopram • Celexa
• Clonazepam • Klonopin
• Clonidine • Catapres
• Duloxetine • Cymbalta
• Fluoxetine • Prozac
• Gabapentin • Neurontin
• Guanfacine • Tenex
• Imipramine • Tofranil
• Lamotrigine • Lamictal
• Paroxetine • Paxil
• Prazosin • Minipress
• Propranolol • Inderal
• Sertraline • Zoloft
• Temazepam • Restoril
• Venlafaxine • Effexor

Disclosure

Dr. Bennett and Dr. Zatzick report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Roy-Byrne is a consultant to Jazz Pharmaceuticals and Solvay and has received speaker honoraria from Wyeth and Forrest Pharmaceuticals.

Posttraumatic stress disorder (PTSD) is a preventable mental illness—without trauma, the illness does not occur. Primary prevention (such as eliminating war, rape, physical assaults, child abuse, or motor vehicle accidents) would be effective but is an unrealistic goal. Secondary prevention (such as preventing PTSD after individuals have been exposed to trauma) may be attainable.

No medication is FDA-approved to prevent PTSD, but patients recently exposed to trauma might benefit from drugs approved for other indications. Possibilities include noradrenergics such as propranolol, corticosteroids that affect the hypothalamic-pituitary-adrenal (HPA) axis, opioids, benzodiazepines, and antidepressants. Some investigational agents also might block the process that turns a traumatic experience into PTSD.

This article discusses these intriguing ideas and suggests which trauma victims might benefit now from acute pharmacologic PTSD prevention.

Who might be treated?

An estimated 8% to 10% of the U.S. population experiences PTSD at some point in life (Box 1).^1,2 A person’s risk of developing PTSD after a traumatic event depends on the type of trauma. For example, 10% of motor vehicle accident survivors develop PTSD, compared with 60% of rape survivors.¹

Targeting anyone who has experienced trauma for secondary PTSD prevention would expose large groups of people to medications they do not need. Targeting selected persons who are at the highest risk would be more efficient and cost-effective. In a group of acute trauma-exposed persons, 2 selection criteria could be considered simultaneously:

• Which patients may be most predisposed to PTSD?
• Which patients are showing early symptoms that may predict PTSD?

Box 1

Risk factors and resiliency. Certain factors have been shown to increase a person’s vulnerability for PTSD (Table 1).³ Other proposed risk factors include:

• personality types⁴
• psychophysiologic factors such as reactivity, conditionability, and resistance to extinction/habituation.⁵

Strong evidence also indicates that acute trauma-related symptoms—including excessive arousal and fear,⁶ peritraumatic dissociation, and depression—predict the later development of PTSD.

Once identified, individuals predisposed to developing PTSD could be given treatment to increase their resiliency after they have been exposed to trauma. Early evidence suggests that you also could consider giving these patients medications as secondary prevention (Table 2).

Table 1

Who develops PTSD? Risk and resiliency factors

Table 2

Medications being studied for PTSD prevention

Targeting noradrenergic activity

Increased noradrenergic activity has been associated with persistent memories and PTSD. Therefore, medications that reduce noradrenergic tone by blocking receptors or reduce norepinephrine release are being explored for PTSD prevention.

Propranolol. Three small studies have examined whether the beta-noradrenergic receptor blocker propranolol can prevent PTSD.

In a randomized, double-blind, placebo-controlled trial,⁷ 41 emergency department patients who had a heart rate of ≥ 80 bpm within 6 hours of a traumatic accident received propranolol, 40 mg qid, or placebo for 10 days. After 1 month, the 11 patients who completed propranolol treatment showed a nonsignificant trend toward lower scores on the Clinician-Administered PTSD Scale (CAPS), compared with 20 patients taking placebo. At 3 months, the propranolol group had less physiologic reactivity (as measured by heart rate and skin conductance) to trauma-related cues than the placebo group.

In a nonrandomized study,⁸ PTSD developed within 2 months in 1 of 11 trauma victims who agreed to take propranolol, 40 mg tid, immediately after the trauma, compared with 3 of 8 victims who refused the medication.

In an unpublished randomized, double-blind trial,⁹ 48 patients admitted to a level I trauma center received propranolol, 40 mg tid; gabapentin, 400 mg tid; or placebo for PTSD prevention. Gabapentin was chosen because it has few side effects or metabolic interactions and preliminary evidence of anxiolytic efficacy.

Neither propranolol nor gabapentin showed statistically significant benefit in preventing PTSD compared with placebo. Effect sizes with the 2 treatments were too small to suggest that larger samples would produce a statistically significant result.

Prazosin—an alpha-1 adrenergic receptor antagonist—has been evaluated in 3 controlled studies and found to reduce intrusive nightmares typical of chronic PTSD.

Ten combat veterans with chronic PTSD showed significantly improved sleep, fewer severe nightmares, and improved global clinical status after receiving prazosin (mean dose 9.5 mg at bedtime) in a 20-week, placebo-controlled, double-blind, crossover study.¹⁰

In a larger randomized, parallel group trial,¹¹ the same authors compared prazosin with placebo in 40 combat veterans (mean age 56) with chronic PTSD. After 8 weeks, veterans taking prazosin (mean 13.3 ± 3 mg) had significantly fewer trauma nightmares, improved sleep (including return of normal dreams), and improved global clinical status vs placebo. Overall CAP scores did not decline significantly, however.

In a third placebo-controlled study,¹² a midmorning dose of prazosin was added to the regimens of 11 civilian trauma patients already taking the drug at bedtime to suppress trauma-related nightmares. Their daytime PTSD symptoms improved, as shown by reduced psychological distress in response to verbal trauma cues.

Prazosin can reduce chronic PTSD manifestations of nightmares and disturbed sleep, but it has not been shown to ameliorate the full PTSD syndrome. Prazosin has not been studied as an early PTSD intervention.

Other antiadrenergics that reduce the release of norepinephrine—including clonidine and guanfacine—have been studied in open trials as treatment for PTSD. The only controlled study¹³ showed no benefit from guanfacine for PTSD prevention.

De-stressing the HPA axis

Hydrocortisone has been proposed to prevent PTSD by reducing HPA axis activation, acting as a countermeasure to elevated corticotropin-releasing factor found in patients with chronic PTSD.

IV hydrocortisone’s effect on the development of PTSD was compared with placebo in 20 septic shock survivors after discharge from intensive care.¹⁴ One of 9 patients (11%) in the hydrocortisone group was diagnosed with PTSD at follow-up (mean 31 months), compared with 7 of 11 (64%) in the placebo group.

In a similar study, the same researchers gave patients hydrocortisone before, during, and after cardiac surgery. Follow-up interviews revealed significantly lower PTSD and chronic stress symptom scores in the treatment group vs the placebo group.¹⁵

These studies—although provocative—are limited by the narrow range of trauma related to severe medical illness or extensive medical procedures.

Norepinephrine-blocking opioids

When the noradrenergic system is activated, one physiologic response is the activation of endogenous opioid systems, which may promote recovery by inhibiting the HPA axis. Opioid systems might be involved in PTSD, as suggested by:

• preclinical evidence that opioids modulate memory¹⁶
• studies showing low pain thresholds¹⁷ and abnormal beta-endorphin (an opioid peptide neurotransmitter)¹⁸ and methionine enkephalin (an opioid peptide)¹⁹ levels in PTSD patients.

In theory, opioid administration immediately after trauma may attenuate norepinephrine release, thus thwarting arousal-charged memory consolidation, hyperarousal, and re-experiencing.

One uncontrolled report of pediatric burn victims found a significant association between the morphine dose given for pain during hospitalization and reduced PTSD symptoms 6 months later.²⁰ Decreased pain did not explain the reduction in PTSD, as no significant correlation was seen between pain symptoms and PTSD outcome measures. Similarly, a longitudinal study of substance use among Vietnam War veterans with PTSD found decreased hyperarousal symptoms in heroin users.²¹

Using opioids to prevent PTSD would be feasible and efficient in acute care settings because 80% to 90% of traumatically-injured patients are discharged on opioid analgesics (compared with <10% on beta blockers or corticosteroids).²² However, 20% to 40% of physically injured inpatients are diagnosed with a substance use disorder at some point in life, making the use of opioid analgesics a practical concern.²³

GABA-benzodiazepine paradox

The GABA-benzodiazepine system plays an important role in mediating anxiety, which is consistent with the potent anxiolytic effects of benzodiazepines. Even so, trials of benzodiazepines have found these drugs surprisingly unhelpful—and perhaps harmful—in patients with acute trauma.

Alprazolam did not reduce PTSD symptoms in a small randomized, double-blind study.²⁴ Another trial found that receiving benzodiazepines shortly after trauma exposure was associated with increased PTSD risk in trauma survivors. Nine of 13 patients (69%) who received alprazolam or clonazepam met PTSD diagnostic criteria 6 months after the trauma, compared with 3 of 13 controls (15%).²⁵

Similarly, in a randomized controlled trial, 22 patients were given temazepam for 7 nights, starting approximately 14 days after exposure to a traumatic event. Six weeks later, 55% of those receiving temazepam and 27% of those receiving placebo met criteria for PTSD.²⁶

In summary, benzodiazepines might be helpful when given for a few days after traumatization to control overwhelming anxiety but could be harmful over a longer term.

Other agents for PTSD

Antidepressants. Early trauma-related symptoms of depression predict later development of PTSD.²⁷ Thus, antidepressants have been proposed for early intervention in addition to their well-established role as first-line treatment of PTSD.²⁸

One study supports this idea: a 7-day randomized double-blind trial that compared the tricyclic antidepressant imipramine with chloral hydrate in pediatric burn patients with acute stress disorder (ASD). Imipramine was more effective (83% response) than chloral hydrate (38% response) in reducing ASD symptoms.²⁹

Drugs in development. Three new medications being explored for treating anxiety and depression also might be useful for PTSD prevention. Neuropeptide Y (NPY) agonists,³⁰ substance P antagonists,³¹ and CRH-antagonists³² are thought to hold promise because of their more proximate roles—compared with monoamine neurotransmitters such as dopamine, norepinephrine and serotonin—in mediating the stress response.

Box 2

Analyzing the evidence

Insufficient evidence exists to determine which strategies might be most effective to prevent PTSD, what optimal dosing might be, and which traumatized individuals might be best targeted with these approaches.

• Beta-blockers and corticosteroids—the most theoretically compelling strategies—are the most difficult agents to use for PTSD prevention because they have the most medical contraindications. In addition, evidence supporting their ability to prevent PTSD is meager at best.
• Prazosin is intriguing but has contra-indications similar to those of beta blockers, no studies of secondary prevention, and no clear indication that it works for the overall PTSD syndrome.
• Opioids are restricted agents with substantial contraindications.
• Evidence is limited but points most strongly toward earlier use of antidepressants. Early trauma-related symptoms of depression predict later development of PTSD,²⁷ and a number of selective serotonin reuptake inhibitors—such as citalopram, fluoxetine, paroxetine, and sertraline—are FDA-approved or used off-label for treating PTSD.³³

Prescribing recommendations. Consider practicality, ease of use, and safety of the proposed medication when choosing a drug for PTSD prevention (Table 3).²² Based on the evidence, the most reasonable posttrauma approach (Box 2) might be to consider starting an approved antidepressant for individuals thought to be particularly vulnerable to PTSD because of:

• past history of PTSD, depression, or anxiety disorder
• severity of the trauma (such as in cases of sexual assault or torture)
• pain (antidepressants with analgesic properties—such as venlafaxine or duloxetine—might be useful in patients whose trauma is associated with physical injury, although neither is FDA-approved to treat PTSD).

Table 3

4 considerations when choosing a drug for PTSD prevention

Related resources

• Mental health and mass violence: Evidence-based early psychological intervention for victims/survivors of mass violence. A workshop to reach consensus on best practices. Rockland, MD: National Institute of Mental Health; 2002. www.nimh.nih.gov.
• Post-traumatic stress disorder: the management of PTSD in adults and children in primary and secondary care (clinical guideline 26). London, UK: National Institute for Clinical Excellence; 2005. www.nice.org.uk.
• Ursano RJ, Bell C, Eth S, et al. Practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder. Am J Psychiatry 2004;161(suppl 11):3-31.

Drug brand names

• Alprazolam • Xanax
• Amitriptyline • Elavil
• Citalopram • Celexa
• Clonazepam • Klonopin
• Clonidine • Catapres
• Duloxetine • Cymbalta
• Fluoxetine • Prozac
• Gabapentin • Neurontin
• Guanfacine • Tenex
• Imipramine • Tofranil
• Lamotrigine • Lamictal
• Paroxetine • Paxil
• Prazosin • Minipress
• Propranolol • Inderal
• Sertraline • Zoloft
• Temazepam • Restoril
• Venlafaxine • Effexor

Disclosure

Dr. Bennett and Dr. Zatzick report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Roy-Byrne is a consultant to Jazz Pharmaceuticals and Solvay and has received speaker honoraria from Wyeth and Forrest Pharmaceuticals.