Medicolegal Issues

Complementary and alterative medicine (CAM) is defined as any product, including herbal remedies/foods/teas, vitamins, minerals, and natural products, that can be purchased without a prescription at a health food store, supermarket, from a magazine/newspaper or online, for self-treatment.1

Taylor et al. evaluated CAM perceptions of emergency department patients in Australia. They determined 44% of patients felt that by using CAM they were “drug free,” with 29% of patients agreeing (or strongly agreeing) CAM use is always safe to take with prescription medications. In an earlier study, Eisenberg et al. evaluated CAM use perceptions in the United States and found 79% of patients felt that, combined with prescription drugs, CAM was superior to either modality alone.2 They also found 63% to 72% of CAM-using patients that had seen a medical doctor in the prior year did not disclose the therapy.

The two most common reasons cited by patients were “they felt it wasn’t important for the doctor to know (61%)” and “the doctor didn’t ask (60%).” Overall, national CAM-use surveys have revealed that about 80% of adults typically do not disclose CAM use to medical doctors.

It is, therefore, imperative that physicians ask patients about their CAM use. It also is important to remember there are more foods and beverages that contain some of these “natural” ingredients, and patients need to be queried about the use of these products. CAM products can complicate traditional patient management, either when used alone or in combination with prescription drugs.

A clinically significant drug interaction that bears its own warning is that of warfarin and chondroitin/glucosamine. Patients might not tell you that they are taking chondroitin/glucosamine, so you have to ask. Functional foods and beverages that include “natural” ingredients, such as glucosamine and chondroitin, and other CAM abound. Examples include Joint Juice (1,500 mg glucosamine), Vitamin Water, and others.3

Two case reports, and a report from the World Health Organization (WHO) Collaborating Center for International Drug Monitoring, and the MedWatch database point to a potentially serious drug interaction between glucosamine and warfarin.4-7 Although not FDA approved for joint supplementation, the usual daily dose should generally not exceed 1.5 grams of glucosamine and 1.2 grams of chondroitin. Chondroitin may have anti-coagulant activity, which would explain the increase in International Normalized Ratio (INR) seen in patients using it in combination with warfarin. The WHO database identified at least 34 cases of concomitant use, with most cases of increased INR resolving upon glucosamine discontinuation. Nine cases required physician intervention, and in one case a positive rechallenge was documented. In June 2007, there were 81 cases of a possible interaction from the MedWatch database, of these, 61 cases had potential alternate etiologies. Of the 20 possibly-related cases, five led to patient hospitalization due to bleeding complications; the median patient age was 62 years and there were no deaths reported.

Ramsay et al. reported from a United Kingdom survey that 92% of patients admitted to taking herbal medicines while receiving warfarin, noting that significant numbers of patients are in need of close monitoring. They also note that other CAM can interact with warfarin to increase bleeding time or act as anti-platelet agents (e.g., high dose vitamin E [> 400 IU], fish oils, garlic, St. John’s Wort, etc.) They particularly note that all patients receiving warfarin or that will be commencing warfarin be specifically asked about their use of CAM. The mechanism for this interaction still is unclear, but may be due to the inhibition of warfarin metabolism by the CYP2C9 or CYP3A4 enzymes, or a pharmacodynamic interaction between glucosamine and warfarin.

It is critical all patients, particularly those taking warfarin, have a full drug history at all hospitalizations. Make sure you inquire about vitamins and other supplements/CAM. If someone else is doing the intake medication history, make sure they get this information. A nurse might not think to ask. TH

Michele B. Kaufman, PharmD, BSc, RPh, is a registered pharmacist based in New York City.

References

1. Taylor DM, Walsham N, Taylor SE, Wong LF. Complementary and alternative medicines versus prescription drugs: perceptions of emergency department patients. Emerg Med J. 2006;23:266-268.

2. Eisenberg DM, Kessler RC, Van Rompay MI, et al.. Perceptions about complementary therapies relative to conventional therapies among adults how use both: results from a national survey. Ann Intern Med. 2001;135:344-351.

3. What is Joint Juice? Joint Juice, Inc. www.jointjuice.com/jointjuice.php. Published 1997. Accessed August 1, 2008.

4. Rozenfeld V, Crain JL, Callahan AK. Possible augmentation of warfarin effect by glucosamine-chondroitin. Am J Health-Syst Pharm. 2004;61:306-307.

5. Knudsen JF, Sokol GH. Potential glucosamine-warfarin interaction resulting in increased international normalized ratio: case report and review of the literature and medwatch database. Pharmacother. 2008;28(4):540-548.

6. Ramsay NA, Kenny MW, Davies G, Patel JP. Complimentary and alternative medicine use among patients starting warfarin. Br J Haematology. 2005;130:777-780.

7. Yue Q-Y, Strandell J, Myrberg O. Concomitant use of glucosamine may potentiate the effect of warfarin. The Uppsalla Monitoring Centre Web site. www.who-umc.org/graphics/9722.pdf; Accessed August 1, 2008.

Complementary and alterative medicine (CAM) is defined as any product, including herbal remedies/foods/teas, vitamins, minerals, and natural products, that can be purchased without a prescription at a health food store, supermarket, from a magazine/newspaper or online, for self-treatment.1

Taylor et al. evaluated CAM perceptions of emergency department patients in Australia. They determined 44% of patients felt that by using CAM they were “drug free,” with 29% of patients agreeing (or strongly agreeing) CAM use is always safe to take with prescription medications. In an earlier study, Eisenberg et al. evaluated CAM use perceptions in the United States and found 79% of patients felt that, combined with prescription drugs, CAM was superior to either modality alone.2 They also found 63% to 72% of CAM-using patients that had seen a medical doctor in the prior year did not disclose the therapy.

The two most common reasons cited by patients were “they felt it wasn’t important for the doctor to know (61%)” and “the doctor didn’t ask (60%).” Overall, national CAM-use surveys have revealed that about 80% of adults typically do not disclose CAM use to medical doctors.

It is, therefore, imperative that physicians ask patients about their CAM use. It also is important to remember there are more foods and beverages that contain some of these “natural” ingredients, and patients need to be queried about the use of these products. CAM products can complicate traditional patient management, either when used alone or in combination with prescription drugs.

A clinically significant drug interaction that bears its own warning is that of warfarin and chondroitin/glucosamine. Patients might not tell you that they are taking chondroitin/glucosamine, so you have to ask. Functional foods and beverages that include “natural” ingredients, such as glucosamine and chondroitin, and other CAM abound. Examples include Joint Juice (1,500 mg glucosamine), Vitamin Water, and others.3

Two case reports, and a report from the World Health Organization (WHO) Collaborating Center for International Drug Monitoring, and the MedWatch database point to a potentially serious drug interaction between glucosamine and warfarin.4-7 Although not FDA approved for joint supplementation, the usual daily dose should generally not exceed 1.5 grams of glucosamine and 1.2 grams of chondroitin. Chondroitin may have anti-coagulant activity, which would explain the increase in International Normalized Ratio (INR) seen in patients using it in combination with warfarin. The WHO database identified at least 34 cases of concomitant use, with most cases of increased INR resolving upon glucosamine discontinuation. Nine cases required physician intervention, and in one case a positive rechallenge was documented. In June 2007, there were 81 cases of a possible interaction from the MedWatch database, of these, 61 cases had potential alternate etiologies. Of the 20 possibly-related cases, five led to patient hospitalization due to bleeding complications; the median patient age was 62 years and there were no deaths reported.

Ramsay et al. reported from a United Kingdom survey that 92% of patients admitted to taking herbal medicines while receiving warfarin, noting that significant numbers of patients are in need of close monitoring. They also note that other CAM can interact with warfarin to increase bleeding time or act as anti-platelet agents (e.g., high dose vitamin E [> 400 IU], fish oils, garlic, St. John’s Wort, etc.) They particularly note that all patients receiving warfarin or that will be commencing warfarin be specifically asked about their use of CAM. The mechanism for this interaction still is unclear, but may be due to the inhibition of warfarin metabolism by the CYP2C9 or CYP3A4 enzymes, or a pharmacodynamic interaction between glucosamine and warfarin.

It is critical all patients, particularly those taking warfarin, have a full drug history at all hospitalizations. Make sure you inquire about vitamins and other supplements/CAM. If someone else is doing the intake medication history, make sure they get this information. A nurse might not think to ask. TH

Michele B. Kaufman, PharmD, BSc, RPh, is a registered pharmacist based in New York City.

References

1. Taylor DM, Walsham N, Taylor SE, Wong LF. Complementary and alternative medicines versus prescription drugs: perceptions of emergency department patients. Emerg Med J. 2006;23:266-268.

2. Eisenberg DM, Kessler RC, Van Rompay MI, et al.. Perceptions about complementary therapies relative to conventional therapies among adults how use both: results from a national survey. Ann Intern Med. 2001;135:344-351.

3. What is Joint Juice? Joint Juice, Inc. www.jointjuice.com/jointjuice.php. Published 1997. Accessed August 1, 2008.

4. Rozenfeld V, Crain JL, Callahan AK. Possible augmentation of warfarin effect by glucosamine-chondroitin. Am J Health-Syst Pharm. 2004;61:306-307.

5. Knudsen JF, Sokol GH. Potential glucosamine-warfarin interaction resulting in increased international normalized ratio: case report and review of the literature and medwatch database. Pharmacother. 2008;28(4):540-548.

6. Ramsay NA, Kenny MW, Davies G, Patel JP. Complimentary and alternative medicine use among patients starting warfarin. Br J Haematology. 2005;130:777-780.

7. Yue Q-Y, Strandell J, Myrberg O. Concomitant use of glucosamine may potentiate the effect of warfarin. The Uppsalla Monitoring Centre Web site. www.who-umc.org/graphics/9722.pdf; Accessed August 1, 2008.

Complementary and alterative medicine (CAM) is defined as any product, including herbal remedies/foods/teas, vitamins, minerals, and natural products, that can be purchased without a prescription at a health food store, supermarket, from a magazine/newspaper or online, for self-treatment.1

Taylor et al. evaluated CAM perceptions of emergency department patients in Australia. They determined 44% of patients felt that by using CAM they were “drug free,” with 29% of patients agreeing (or strongly agreeing) CAM use is always safe to take with prescription medications. In an earlier study, Eisenberg et al. evaluated CAM use perceptions in the United States and found 79% of patients felt that, combined with prescription drugs, CAM was superior to either modality alone.2 They also found 63% to 72% of CAM-using patients that had seen a medical doctor in the prior year did not disclose the therapy.

The two most common reasons cited by patients were “they felt it wasn’t important for the doctor to know (61%)” and “the doctor didn’t ask (60%).” Overall, national CAM-use surveys have revealed that about 80% of adults typically do not disclose CAM use to medical doctors.

It is, therefore, imperative that physicians ask patients about their CAM use. It also is important to remember there are more foods and beverages that contain some of these “natural” ingredients, and patients need to be queried about the use of these products. CAM products can complicate traditional patient management, either when used alone or in combination with prescription drugs.

A clinically significant drug interaction that bears its own warning is that of warfarin and chondroitin/glucosamine. Patients might not tell you that they are taking chondroitin/glucosamine, so you have to ask. Functional foods and beverages that include “natural” ingredients, such as glucosamine and chondroitin, and other CAM abound. Examples include Joint Juice (1,500 mg glucosamine), Vitamin Water, and others.3

Two case reports, and a report from the World Health Organization (WHO) Collaborating Center for International Drug Monitoring, and the MedWatch database point to a potentially serious drug interaction between glucosamine and warfarin.4-7 Although not FDA approved for joint supplementation, the usual daily dose should generally not exceed 1.5 grams of glucosamine and 1.2 grams of chondroitin. Chondroitin may have anti-coagulant activity, which would explain the increase in International Normalized Ratio (INR) seen in patients using it in combination with warfarin. The WHO database identified at least 34 cases of concomitant use, with most cases of increased INR resolving upon glucosamine discontinuation. Nine cases required physician intervention, and in one case a positive rechallenge was documented. In June 2007, there were 81 cases of a possible interaction from the MedWatch database, of these, 61 cases had potential alternate etiologies. Of the 20 possibly-related cases, five led to patient hospitalization due to bleeding complications; the median patient age was 62 years and there were no deaths reported.

Ramsay et al. reported from a United Kingdom survey that 92% of patients admitted to taking herbal medicines while receiving warfarin, noting that significant numbers of patients are in need of close monitoring. They also note that other CAM can interact with warfarin to increase bleeding time or act as anti-platelet agents (e.g., high dose vitamin E [> 400 IU], fish oils, garlic, St. John’s Wort, etc.) They particularly note that all patients receiving warfarin or that will be commencing warfarin be specifically asked about their use of CAM. The mechanism for this interaction still is unclear, but may be due to the inhibition of warfarin metabolism by the CYP2C9 or CYP3A4 enzymes, or a pharmacodynamic interaction between glucosamine and warfarin.

It is critical all patients, particularly those taking warfarin, have a full drug history at all hospitalizations. Make sure you inquire about vitamins and other supplements/CAM. If someone else is doing the intake medication history, make sure they get this information. A nurse might not think to ask. TH

Michele B. Kaufman, PharmD, BSc, RPh, is a registered pharmacist based in New York City.

References

1. Taylor DM, Walsham N, Taylor SE, Wong LF. Complementary and alternative medicines versus prescription drugs: perceptions of emergency department patients. Emerg Med J. 2006;23:266-268.

2. Eisenberg DM, Kessler RC, Van Rompay MI, et al.. Perceptions about complementary therapies relative to conventional therapies among adults how use both: results from a national survey. Ann Intern Med. 2001;135:344-351.

3. What is Joint Juice? Joint Juice, Inc. www.jointjuice.com/jointjuice.php. Published 1997. Accessed August 1, 2008.

4. Rozenfeld V, Crain JL, Callahan AK. Possible augmentation of warfarin effect by glucosamine-chondroitin. Am J Health-Syst Pharm. 2004;61:306-307.

5. Knudsen JF, Sokol GH. Potential glucosamine-warfarin interaction resulting in increased international normalized ratio: case report and review of the literature and medwatch database. Pharmacother. 2008;28(4):540-548.

6. Ramsay NA, Kenny MW, Davies G, Patel JP. Complimentary and alternative medicine use among patients starting warfarin. Br J Haematology. 2005;130:777-780.

7. Yue Q-Y, Strandell J, Myrberg O. Concomitant use of glucosamine may potentiate the effect of warfarin. The Uppsalla Monitoring Centre Web site. www.who-umc.org/graphics/9722.pdf; Accessed August 1, 2008.

Literature at a Glance

• Postoperative prophylactic LMWH should be considered for arthroscopic knee surgery patients.
• Individualized therapy is required for DVT prophylaxis in the neurosurgical patient.
• SMART-COP is a reasonable screening tool for ICU admission.
• Mediterranean and low-carb diets are safe and effective alternatives to low-fat diets.
• Admissions for ACS in both smokers and non-smokers decrease after implementation of smoking ban.
• Beta-blockers should be continued whenever possible in patients hospitalized for heart failure with LVSD.
• Non-invasive ventilation improved dyspnea, but did not improve short-term mortality rates in patients with acute cardiogenic pulmonary edema.
• COX-2 inhibitors should be used with caution in patients with increased cerebrovascular disease risk.

LMWH after Arthroscopic Knee Surgery May Prevent VTE Compared to Graduated Compression Stockings

Clinical question: Does low molecular weight heparin (LMWH) prevent venous thromboembolism (VTE) compared to compression stockings without increasing bleeding complications in arthroscopic knee surgery?

Background: Knee arthroscopy is a common orthopedic surgery and postoperative venous thromboprophylaxis is not routinely recommended.

Study design: Randomized, controlled trial with blinding of the investigators.

Setting: Single orthopedic clinic in Italy, with followup at a university hospital.

Synopsis: 1,761 consecutive patients undergoing knee arthroscopy were randomly assigned to full-length graduated compression stockings (CS) for seven days postoperatively, subcutaneous LMWH (nadoparin 3800 units daily) for seven or 14 days postoperatively. The primary outcome of asymptomatic proximal deep venous thrombosis (DVT), symptomatic VTE, and all-cause mortality within three months of surgery was higher with CS (3.2%) than with LMWH for seven or 14 days (0.9% in each group) (P=0.005). There was no significant difference in bleeding events between groups.

The study was underpowered to detect differences in bleeding risk. Furthermore, almost half the events making up the primary outcome were distal DVTs of uncertain clinical significance. Notably, the 14-day LMWH group was discontinued early because of unspecified safety concerns related to longer exposure to LMWH.

Bottom line: Postoperative prophylactic LMWH for seven days may prevent some thromboses after knee surgery and should be considered in higher-risk patients.

Citation: Camporese G, Bernardi E, Prandoni P, et al. Low-molecular-weight heparin versus compression stockings for thrombophylaxis after knee arthroscopy. Ann Intern Med. 2008;14(9):73-82.

Heparins and Compression Devices are Effective in Preventing VTE in a Mixed Neurosurgical Population

Clinical question: What is the efficacy and safety of LMWH, unfractionated heparin, and mechanical devices in preventing VTE in neurosurgical patients?

Background: Neurosurgical patients are at high risk for VTE, but concerns remain regarding the risk of bleeding complications with the use of LMWH or unfractionated heparin (UFH).

Study design: Meta-analysis of 18 randomized trials and 12 cohort studies.

Setting: Patients undergoing spinal surgery or craniotomy.

Synopsis: Among all patients, the pooled DVT rate was 15.5/100. Use of sequential compression devices (SCD) significantly reduced the risk of DVT compared with placebo (relative risk [RR] 0.41, 95% confidence interval [CI] 0.21-0.78). Subcutaneous LMWH was associated with a significantly reduced risk of DVT compared with CS (RR 0.60, 95% CI 0.44-0.81). No other head-to-head comparisons were associated with significant reductions in VTE risk. After adjusting for potential risk factors for DVT and study design, use of heparins or SCDs was associated with a lower risk of DVT. Intracranial hemorrhage (ICH), minor bleeding, major bleeding, or death was not statistically different between any of the groups, although, after adjustment, LMWH was associated with a slightly increased risk of ICH.

The quality of included studies varied considerably and inter-rater agreement on study quality was low, raising the possibility of study selection bias. Potential publication bias was not addressed. Bleeding complications were rare, so the estimates of risk may be imprecise.

Bottom line: Individualized therapy is required for DVT prophylaxis in the neurosurgical patient; SCDs reduce VTE risk and both pharmacologic and mechanical prophylaxis may be indicated in patients with increased VTE risk.

Citation: Collen JF, Jackson JL, Shorr AF, Moores LK. Prevention of venous thromboembolism in neurosurgery: A metaanalysis. Chest. 2008;13(4):237-249.

SMART-COP Predicts Need for ICU Care in CAP

Clinical question: Can a clinical tool predict the need for critical care in community acquired pneumonia (CAP)?

Background: Clinical tools predicting 30-day mortality in community acquired pneumonia (CAP) exist, but do not accurately identify who will require intensive care unit-level care, such as intensive respiratory or vasosuppressor support (IRVS).

Study design: Prospective multi-center observational study.

Setting: Six hospitals in Australia participating in the Australian Community Acquired Pneumonia Study (ACAPS).

Synopsis: Multivariate analysis of a dataset of 882 episodes of CAP identified eight factors that were associated with the need for IRVS, summarized by the mnemonic “SMART-COP” (Systolic blood pressure, Multilobar chest radiography involvement, low Albumin level, high Respiratory rate, Tachycardia, Confusion, poor Oxygenation, and low arterial pH). Assigning one point for five factors and two points for three factors (systolic blood pressure, poor oxygenation, and low arterial pH) a SMART-COP score >3 identified 92.3% (95% CI 84.8-96.9%) of patients who required IRVS, including 84% who did not initially require ICU care. Specificity was 62.3% (CI 58.8-65.7%). Test characteristics for predicting IRVS were superior to existing prediction rules (PSI and CURB-65).

Most patients were drawn from large, urban teaching hospitals in Australia, so the results may not be generalizable. The authors also presented a modification of SMART-COP, using pulse oximetry rather than blood gas results; this may be even more useful in the pre-hospital setting.

Bottom line: SMART-COP is a reasonable screening tool for predicting need for ICU-level care in patients admitted with CAP.

Citation: Charles PGP, Wolfe, R, Whitby, M, et. al. SMART-COP: a tool for predicting the need for intensive respiratory or vasopressor support in community-acquired pneumonia. Clin Infect Dis. 2008;47(3):375-384.

Mediterranean and Low-Carbohydrate Diets are Effective for Weight Loss

Clinical question: Are dietary intervention with low-fat, Mediterranean or low-carbohydrate diets effective?

Background: Obesity is a growing, worldwide problem. Past trials comparing the effectiveness and safety of various dietary interventions have been limited by short follow up and high dropout rates.

Study design: Prospective randomized trial.

Setting: Employees of a research center in Israel.

Synopsis: 322 subjects (average BMI 31) were randomized to a low-fat/restricted-calorie, Mediterranean/ restricted-calorie, or a low-carbohydrate/non-restricted calorie diet. Diet adherence was 84.6% at two years and all groups lost significant amounts of weight. The Mediterranean and low-carbohydrate diets showed similar aver∆age weight loss of 4.4 kg and 4.7 kg, respectively. The low-fat diet group on average lost 2.9 kg. Diabetic patients had improved glycemic control and lower insulin levels with the Mediterranean diet. Subjects assigned to the low-carbohydrate diet had the greatest improvement in lipid profile (20% relative decrease of total cholesterol to HDL ratio).

The trial took place at a single site (a scientific research center in Israel) and included only 14% women, so its generalization is uncertain. The study was based on self-reported dietary intake and may be subject to reporting bias.

Bottom line: Mediterranean and low-carbohydrate diets are safe and effective alternatives to low-fat diets with favorable effects on glycemic control in diabetics and lipid metabolism, respectively.

Citation: Shai I, Schwarz-fuchs D, Henkin Y, et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. NEJM. 2008;359(3):229-241.

Admissions for Acute Coronary Syndrome Decreased after Implementation of Smoke-free Legislation

Clinical question: Is there a reduction in admissions for acute coronary syndrome (ACS) after enactment of smoke-free legislation?

Background: Multiple, small, retrospective studies have shown a decrease in ACS after implementation of smoke-free legislation.

Study design: Prospective observational multi-center cohort study.

Setting: Nine hospitals in Scotland.

Synopsis: Data was collected on all patients admitted with ACS 10 months before and after implementation of smoke-free legislation, which prohibited smoking in all enclosed public and work places in Scotland. After the smoking ban, the number of ACS admissions fell by 17% (95% CI 16-18) in Scotland as a whole, compared with a 4% reduction in England during the same period (England does not have similar smoke-free legislation). Among smokers, former smokers and non-smokers, the number of ACS admissions decreased by 14% (95% CI 12-16), 19% (95% CI 17-21), and 21% (95% CI 18-24), respectively. Among non-smokers, self-reported exposure to second-hand smoke decreased significantly; these reductions were confirmed by measured reductions in serum cotinine levels, even among those who never smoked.

Results were limited by the observational nature of the study, although the authors did attempt to carefully match comparison cohorts by season and geography. Also, secular trends other than legislation may have reduced prevalent smoking in Scotland during the study period.

Bottom line: Admissions for ACS for both smokers and non-smokers decreased after implementation of smoke-free legislation.

Citation: Pell JP, Haw S, Cobbe S, et al. Smoke-free legislation and hospitalizations for acute coronary syndrome. NEJM. 2008;359(5):482-491.

Continuation of Beta-blockers in Patients Hospitalized for Heart Failure Improves Mortality

Clinical question: Does the withdrawal or continuation of beta-blockers in patients hospitalized with decompensated heart failure have any effect on clinical outcomes?

Background: Previous clinical trials have demonstrated mortality benefit with the use of beta-blockers in patients with symptomatic chronic heart failure and left ventricular systolic dysfunction (LVSD), however, controversy exists whether to continue these medications in acute decompensated heart failure.

Study design: Prospective cohort analysis from the OPTIMIZE-HF registry (Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure).

Setting: 91 academic and community hospitals in the United States.

Synopsis: Data was analyzed on 2,373 registry patients with documented LVSD (EF <40) eligible for beta-blocker therapy. During hospitalization, 1,350 patients were continued on beta-blockers, 79 had therapy withdrawn, 303 were not started, and 632 had beta-blockade initiated. Compared with no beta-blocker treatment, adjusted hazard ratio (HR) for death at 60 and 90 days following discharge was lower in patients who were continued on beta-blockade (HR 0.60, 95% CI 0.37–0.99). Compared with continuation of beta-blockade, withdrawal of beta-blockade increased the risk of death (HR 2.3, 95% CI 1.2–4.6).

Results were limited by the observational nature of the study and short follow up. The reason for discontinuation or not starting beta-blockade was not captured in the database, so it is possible sicker patients had beta-blockers discontinued during hospitalization (although the authors attempted to control for this).

Bottom line: Beta-blockers should be continued whenever possible in patients hospitalized for heart failure with LVSD.

Citation: Fonarow GC, Abraham WT, Albert NM, et al. Influence of beta-blocker continuation or withdrawal on outcomes in patients hospitalized with heart failure. J Am Coll Cardiol. 2008;52(3):190-199.

Non-invasive Ventilation Does Not Improve Short-term Mortality in Acute Cardiogenic Pulmonary Edema

Clinical question: Does non-invasive ventilation reduce mortality in patients with acute cardiogenic pulmonary edema and are there differences in outcome between use of continuous positive airway pressure (CPAP) or non-invasive positive pressure ventilation (NIPPV)?

Background: In patients with acute cardiogenic pulmonary edema, noninvasive ventilation improves physiologic variables and symptoms, decreases rates of invasive ventilation, and may improve mortality.

Study design: Randomized multi center controlled trial.

Setting: 26 district and regional hospitals in the United Kingdom.

Synopsis: 1,156 patients admitted with acute cardiogenic pulmonary edema between July 2003 and April 2007 were randomized to standard oxygen therapy, versus CPAP or NIPPV. There were no significant differences in seven- or 30-day mortality rates between the standard oxygen therapy versus noninvasive ventilation. Mortality at seven days was 9.8% in the standard oxygen group versus 9.5% in the noninvasive ventilation group (P=0.87); 30-day mortality was 16% in the standard oxygen group and 15% in the non-invasive ventilation group (P=0.64). There were no major differences in treatment outcome with NIPPV compared to CPAP.

Although mortality was not decreased, non-invasive ventilation did improve dyspnea and tachycardia within one hour of therapy.

Bottom line: In patients admitted with acute cardiogenic pulmonary edema, noninvasive ventilation improved dyspnea and some physiological parameters, but did not improve short-term mortality rates.

Citation: Gray A, Goodacre S, Newby D, Masson M, Sampson F, Nicholl J. Noninvasive ventilation in acute cardiogenic pulmonary edema. NEJM. 2008;359(2):142-151. 

Cyclooxygenase 2 Inhibitors May Increase the Risk of Ischemic Stroke

Clinical question: Do NSAIDs and COX-2 inhibitors increase the risk of ischemic or hemorrhagic stroke?

Background: Selected cyclooxygenase 2 (COX-2) inhibitors have been shown to increase cardiovascular morbidity in a dose-dependent manner and are now used with caution in patients at risk for cardiovascular disease. Little is known about the safety of these medications and non-aspirin, non-steroidal anti-inflammatory drugs (NSAIDS) in those at risk for cerebrovascular disease.

Study design: Retrospective observational cohort study.

Setting: Tennessee Medicaid Program enrollees.

Synopsis: Data was collected from the medical records of 336,906 subjects. Non-users had a baseline stroke rate of 4.51 strokes/1000 person-years. The rate increased to 5.15/1,000 person-years and 5.95/1,000 person-years for rofecoxib and valdecoxib, respectively. Celecoxib and other NSAIDs did not significantly increase the risk of stroke. Analysis of new users of rofexocib and valdecoxib yielded a similarly increased risk of stroke. Most strokes were ischemic.

Limitations include the ready availability of NSAIDs raising the possibility that some patients classified as non-users were actually users of NSAIDs. Other potential confounders may not have been measured and, therefore, not available for analysis.

Bottom line: COX-2 inhibitors should be used with caution in patients with increased cerebrovascular disease risk.

Citation: Roumie CL, Mitchel EF, Kaltenback L, Arbogast PG, Gideon P Griffen MR. Nonaspirin NSAIDs, cyclooxygenase 2 inhibitors, and the risk for stroke. Stroke. 2008;39:1037-2045.

Literature at a Glance

• Postoperative prophylactic LMWH should be considered for arthroscopic knee surgery patients.
• Individualized therapy is required for DVT prophylaxis in the neurosurgical patient.
• SMART-COP is a reasonable screening tool for ICU admission.
• Mediterranean and low-carb diets are safe and effective alternatives to low-fat diets.
• Admissions for ACS in both smokers and non-smokers decrease after implementation of smoking ban.
• Beta-blockers should be continued whenever possible in patients hospitalized for heart failure with LVSD.
• Non-invasive ventilation improved dyspnea, but did not improve short-term mortality rates in patients with acute cardiogenic pulmonary edema.
• COX-2 inhibitors should be used with caution in patients with increased cerebrovascular disease risk.

LMWH after Arthroscopic Knee Surgery May Prevent VTE Compared to Graduated Compression Stockings

Clinical question: Does low molecular weight heparin (LMWH) prevent venous thromboembolism (VTE) compared to compression stockings without increasing bleeding complications in arthroscopic knee surgery?

Background: Knee arthroscopy is a common orthopedic surgery and postoperative venous thromboprophylaxis is not routinely recommended.

Study design: Randomized, controlled trial with blinding of the investigators.

Setting: Single orthopedic clinic in Italy, with followup at a university hospital.

Synopsis: 1,761 consecutive patients undergoing knee arthroscopy were randomly assigned to full-length graduated compression stockings (CS) for seven days postoperatively, subcutaneous LMWH (nadoparin 3800 units daily) for seven or 14 days postoperatively. The primary outcome of asymptomatic proximal deep venous thrombosis (DVT), symptomatic VTE, and all-cause mortality within three months of surgery was higher with CS (3.2%) than with LMWH for seven or 14 days (0.9% in each group) (P=0.005). There was no significant difference in bleeding events between groups.

The study was underpowered to detect differences in bleeding risk. Furthermore, almost half the events making up the primary outcome were distal DVTs of uncertain clinical significance. Notably, the 14-day LMWH group was discontinued early because of unspecified safety concerns related to longer exposure to LMWH.

Bottom line: Postoperative prophylactic LMWH for seven days may prevent some thromboses after knee surgery and should be considered in higher-risk patients.

Citation: Camporese G, Bernardi E, Prandoni P, et al. Low-molecular-weight heparin versus compression stockings for thrombophylaxis after knee arthroscopy. Ann Intern Med. 2008;14(9):73-82.

Heparins and Compression Devices are Effective in Preventing VTE in a Mixed Neurosurgical Population

Clinical question: What is the efficacy and safety of LMWH, unfractionated heparin, and mechanical devices in preventing VTE in neurosurgical patients?

Background: Neurosurgical patients are at high risk for VTE, but concerns remain regarding the risk of bleeding complications with the use of LMWH or unfractionated heparin (UFH).

Study design: Meta-analysis of 18 randomized trials and 12 cohort studies.

Setting: Patients undergoing spinal surgery or craniotomy.

Synopsis: Among all patients, the pooled DVT rate was 15.5/100. Use of sequential compression devices (SCD) significantly reduced the risk of DVT compared with placebo (relative risk [RR] 0.41, 95% confidence interval [CI] 0.21-0.78). Subcutaneous LMWH was associated with a significantly reduced risk of DVT compared with CS (RR 0.60, 95% CI 0.44-0.81). No other head-to-head comparisons were associated with significant reductions in VTE risk. After adjusting for potential risk factors for DVT and study design, use of heparins or SCDs was associated with a lower risk of DVT. Intracranial hemorrhage (ICH), minor bleeding, major bleeding, or death was not statistically different between any of the groups, although, after adjustment, LMWH was associated with a slightly increased risk of ICH.

The quality of included studies varied considerably and inter-rater agreement on study quality was low, raising the possibility of study selection bias. Potential publication bias was not addressed. Bleeding complications were rare, so the estimates of risk may be imprecise.

Bottom line: Individualized therapy is required for DVT prophylaxis in the neurosurgical patient; SCDs reduce VTE risk and both pharmacologic and mechanical prophylaxis may be indicated in patients with increased VTE risk.

Citation: Collen JF, Jackson JL, Shorr AF, Moores LK. Prevention of venous thromboembolism in neurosurgery: A metaanalysis. Chest. 2008;13(4):237-249.

SMART-COP Predicts Need for ICU Care in CAP

Clinical question: Can a clinical tool predict the need for critical care in community acquired pneumonia (CAP)?

Background: Clinical tools predicting 30-day mortality in community acquired pneumonia (CAP) exist, but do not accurately identify who will require intensive care unit-level care, such as intensive respiratory or vasosuppressor support (IRVS).

Study design: Prospective multi-center observational study.

Setting: Six hospitals in Australia participating in the Australian Community Acquired Pneumonia Study (ACAPS).

Synopsis: Multivariate analysis of a dataset of 882 episodes of CAP identified eight factors that were associated with the need for IRVS, summarized by the mnemonic “SMART-COP” (Systolic blood pressure, Multilobar chest radiography involvement, low Albumin level, high Respiratory rate, Tachycardia, Confusion, poor Oxygenation, and low arterial pH). Assigning one point for five factors and two points for three factors (systolic blood pressure, poor oxygenation, and low arterial pH) a SMART-COP score >3 identified 92.3% (95% CI 84.8-96.9%) of patients who required IRVS, including 84% who did not initially require ICU care. Specificity was 62.3% (CI 58.8-65.7%). Test characteristics for predicting IRVS were superior to existing prediction rules (PSI and CURB-65).

Most patients were drawn from large, urban teaching hospitals in Australia, so the results may not be generalizable. The authors also presented a modification of SMART-COP, using pulse oximetry rather than blood gas results; this may be even more useful in the pre-hospital setting.

Bottom line: SMART-COP is a reasonable screening tool for predicting need for ICU-level care in patients admitted with CAP.

Citation: Charles PGP, Wolfe, R, Whitby, M, et. al. SMART-COP: a tool for predicting the need for intensive respiratory or vasopressor support in community-acquired pneumonia. Clin Infect Dis. 2008;47(3):375-384.

Mediterranean and Low-Carbohydrate Diets are Effective for Weight Loss

Clinical question: Are dietary intervention with low-fat, Mediterranean or low-carbohydrate diets effective?

Background: Obesity is a growing, worldwide problem. Past trials comparing the effectiveness and safety of various dietary interventions have been limited by short follow up and high dropout rates.

Study design: Prospective randomized trial.

Setting: Employees of a research center in Israel.

Synopsis: 322 subjects (average BMI 31) were randomized to a low-fat/restricted-calorie, Mediterranean/ restricted-calorie, or a low-carbohydrate/non-restricted calorie diet. Diet adherence was 84.6% at two years and all groups lost significant amounts of weight. The Mediterranean and low-carbohydrate diets showed similar aver∆age weight loss of 4.4 kg and 4.7 kg, respectively. The low-fat diet group on average lost 2.9 kg. Diabetic patients had improved glycemic control and lower insulin levels with the Mediterranean diet. Subjects assigned to the low-carbohydrate diet had the greatest improvement in lipid profile (20% relative decrease of total cholesterol to HDL ratio).

The trial took place at a single site (a scientific research center in Israel) and included only 14% women, so its generalization is uncertain. The study was based on self-reported dietary intake and may be subject to reporting bias.

Bottom line: Mediterranean and low-carbohydrate diets are safe and effective alternatives to low-fat diets with favorable effects on glycemic control in diabetics and lipid metabolism, respectively.

Citation: Shai I, Schwarz-fuchs D, Henkin Y, et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. NEJM. 2008;359(3):229-241.

Admissions for Acute Coronary Syndrome Decreased after Implementation of Smoke-free Legislation

Clinical question: Is there a reduction in admissions for acute coronary syndrome (ACS) after enactment of smoke-free legislation?

Background: Multiple, small, retrospective studies have shown a decrease in ACS after implementation of smoke-free legislation.

Study design: Prospective observational multi-center cohort study.

Setting: Nine hospitals in Scotland.

Synopsis: Data was collected on all patients admitted with ACS 10 months before and after implementation of smoke-free legislation, which prohibited smoking in all enclosed public and work places in Scotland. After the smoking ban, the number of ACS admissions fell by 17% (95% CI 16-18) in Scotland as a whole, compared with a 4% reduction in England during the same period (England does not have similar smoke-free legislation). Among smokers, former smokers and non-smokers, the number of ACS admissions decreased by 14% (95% CI 12-16), 19% (95% CI 17-21), and 21% (95% CI 18-24), respectively. Among non-smokers, self-reported exposure to second-hand smoke decreased significantly; these reductions were confirmed by measured reductions in serum cotinine levels, even among those who never smoked.

Results were limited by the observational nature of the study, although the authors did attempt to carefully match comparison cohorts by season and geography. Also, secular trends other than legislation may have reduced prevalent smoking in Scotland during the study period.

Bottom line: Admissions for ACS for both smokers and non-smokers decreased after implementation of smoke-free legislation.

Citation: Pell JP, Haw S, Cobbe S, et al. Smoke-free legislation and hospitalizations for acute coronary syndrome. NEJM. 2008;359(5):482-491.

Continuation of Beta-blockers in Patients Hospitalized for Heart Failure Improves Mortality

Clinical question: Does the withdrawal or continuation of beta-blockers in patients hospitalized with decompensated heart failure have any effect on clinical outcomes?

Background: Previous clinical trials have demonstrated mortality benefit with the use of beta-blockers in patients with symptomatic chronic heart failure and left ventricular systolic dysfunction (LVSD), however, controversy exists whether to continue these medications in acute decompensated heart failure.

Study design: Prospective cohort analysis from the OPTIMIZE-HF registry (Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure).

Setting: 91 academic and community hospitals in the United States.

Synopsis: Data was analyzed on 2,373 registry patients with documented LVSD (EF <40) eligible for beta-blocker therapy. During hospitalization, 1,350 patients were continued on beta-blockers, 79 had therapy withdrawn, 303 were not started, and 632 had beta-blockade initiated. Compared with no beta-blocker treatment, adjusted hazard ratio (HR) for death at 60 and 90 days following discharge was lower in patients who were continued on beta-blockade (HR 0.60, 95% CI 0.37–0.99). Compared with continuation of beta-blockade, withdrawal of beta-blockade increased the risk of death (HR 2.3, 95% CI 1.2–4.6).

Results were limited by the observational nature of the study and short follow up. The reason for discontinuation or not starting beta-blockade was not captured in the database, so it is possible sicker patients had beta-blockers discontinued during hospitalization (although the authors attempted to control for this).

Bottom line: Beta-blockers should be continued whenever possible in patients hospitalized for heart failure with LVSD.

Citation: Fonarow GC, Abraham WT, Albert NM, et al. Influence of beta-blocker continuation or withdrawal on outcomes in patients hospitalized with heart failure. J Am Coll Cardiol. 2008;52(3):190-199.

Non-invasive Ventilation Does Not Improve Short-term Mortality in Acute Cardiogenic Pulmonary Edema

Clinical question: Does non-invasive ventilation reduce mortality in patients with acute cardiogenic pulmonary edema and are there differences in outcome between use of continuous positive airway pressure (CPAP) or non-invasive positive pressure ventilation (NIPPV)?

Background: In patients with acute cardiogenic pulmonary edema, noninvasive ventilation improves physiologic variables and symptoms, decreases rates of invasive ventilation, and may improve mortality.

Study design: Randomized multi center controlled trial.

Setting: 26 district and regional hospitals in the United Kingdom.

Synopsis: 1,156 patients admitted with acute cardiogenic pulmonary edema between July 2003 and April 2007 were randomized to standard oxygen therapy, versus CPAP or NIPPV. There were no significant differences in seven- or 30-day mortality rates between the standard oxygen therapy versus noninvasive ventilation. Mortality at seven days was 9.8% in the standard oxygen group versus 9.5% in the noninvasive ventilation group (P=0.87); 30-day mortality was 16% in the standard oxygen group and 15% in the non-invasive ventilation group (P=0.64). There were no major differences in treatment outcome with NIPPV compared to CPAP.

Although mortality was not decreased, non-invasive ventilation did improve dyspnea and tachycardia within one hour of therapy.

Bottom line: In patients admitted with acute cardiogenic pulmonary edema, noninvasive ventilation improved dyspnea and some physiological parameters, but did not improve short-term mortality rates.

Citation: Gray A, Goodacre S, Newby D, Masson M, Sampson F, Nicholl J. Noninvasive ventilation in acute cardiogenic pulmonary edema. NEJM. 2008;359(2):142-151. 

Cyclooxygenase 2 Inhibitors May Increase the Risk of Ischemic Stroke

Clinical question: Do NSAIDs and COX-2 inhibitors increase the risk of ischemic or hemorrhagic stroke?

Background: Selected cyclooxygenase 2 (COX-2) inhibitors have been shown to increase cardiovascular morbidity in a dose-dependent manner and are now used with caution in patients at risk for cardiovascular disease. Little is known about the safety of these medications and non-aspirin, non-steroidal anti-inflammatory drugs (NSAIDS) in those at risk for cerebrovascular disease.

Study design: Retrospective observational cohort study.

Setting: Tennessee Medicaid Program enrollees.

Synopsis: Data was collected from the medical records of 336,906 subjects. Non-users had a baseline stroke rate of 4.51 strokes/1000 person-years. The rate increased to 5.15/1,000 person-years and 5.95/1,000 person-years for rofecoxib and valdecoxib, respectively. Celecoxib and other NSAIDs did not significantly increase the risk of stroke. Analysis of new users of rofexocib and valdecoxib yielded a similarly increased risk of stroke. Most strokes were ischemic.

Limitations include the ready availability of NSAIDs raising the possibility that some patients classified as non-users were actually users of NSAIDs. Other potential confounders may not have been measured and, therefore, not available for analysis.

Bottom line: COX-2 inhibitors should be used with caution in patients with increased cerebrovascular disease risk.

Citation: Roumie CL, Mitchel EF, Kaltenback L, Arbogast PG, Gideon P Griffen MR. Nonaspirin NSAIDs, cyclooxygenase 2 inhibitors, and the risk for stroke. Stroke. 2008;39:1037-2045.

Literature at a Glance

• Postoperative prophylactic LMWH should be considered for arthroscopic knee surgery patients.
• Individualized therapy is required for DVT prophylaxis in the neurosurgical patient.
• SMART-COP is a reasonable screening tool for ICU admission.
• Mediterranean and low-carb diets are safe and effective alternatives to low-fat diets.
• Admissions for ACS in both smokers and non-smokers decrease after implementation of smoking ban.
• Beta-blockers should be continued whenever possible in patients hospitalized for heart failure with LVSD.
• Non-invasive ventilation improved dyspnea, but did not improve short-term mortality rates in patients with acute cardiogenic pulmonary edema.
• COX-2 inhibitors should be used with caution in patients with increased cerebrovascular disease risk.

LMWH after Arthroscopic Knee Surgery May Prevent VTE Compared to Graduated Compression Stockings

Clinical question: Does low molecular weight heparin (LMWH) prevent venous thromboembolism (VTE) compared to compression stockings without increasing bleeding complications in arthroscopic knee surgery?

Background: Knee arthroscopy is a common orthopedic surgery and postoperative venous thromboprophylaxis is not routinely recommended.

Study design: Randomized, controlled trial with blinding of the investigators.

Setting: Single orthopedic clinic in Italy, with followup at a university hospital.

Synopsis: 1,761 consecutive patients undergoing knee arthroscopy were randomly assigned to full-length graduated compression stockings (CS) for seven days postoperatively, subcutaneous LMWH (nadoparin 3800 units daily) for seven or 14 days postoperatively. The primary outcome of asymptomatic proximal deep venous thrombosis (DVT), symptomatic VTE, and all-cause mortality within three months of surgery was higher with CS (3.2%) than with LMWH for seven or 14 days (0.9% in each group) (P=0.005). There was no significant difference in bleeding events between groups.

The study was underpowered to detect differences in bleeding risk. Furthermore, almost half the events making up the primary outcome were distal DVTs of uncertain clinical significance. Notably, the 14-day LMWH group was discontinued early because of unspecified safety concerns related to longer exposure to LMWH.

Bottom line: Postoperative prophylactic LMWH for seven days may prevent some thromboses after knee surgery and should be considered in higher-risk patients.

Citation: Camporese G, Bernardi E, Prandoni P, et al. Low-molecular-weight heparin versus compression stockings for thrombophylaxis after knee arthroscopy. Ann Intern Med. 2008;14(9):73-82.

Heparins and Compression Devices are Effective in Preventing VTE in a Mixed Neurosurgical Population

Clinical question: What is the efficacy and safety of LMWH, unfractionated heparin, and mechanical devices in preventing VTE in neurosurgical patients?

Background: Neurosurgical patients are at high risk for VTE, but concerns remain regarding the risk of bleeding complications with the use of LMWH or unfractionated heparin (UFH).

Study design: Meta-analysis of 18 randomized trials and 12 cohort studies.

Setting: Patients undergoing spinal surgery or craniotomy.

Synopsis: Among all patients, the pooled DVT rate was 15.5/100. Use of sequential compression devices (SCD) significantly reduced the risk of DVT compared with placebo (relative risk [RR] 0.41, 95% confidence interval [CI] 0.21-0.78). Subcutaneous LMWH was associated with a significantly reduced risk of DVT compared with CS (RR 0.60, 95% CI 0.44-0.81). No other head-to-head comparisons were associated with significant reductions in VTE risk. After adjusting for potential risk factors for DVT and study design, use of heparins or SCDs was associated with a lower risk of DVT. Intracranial hemorrhage (ICH), minor bleeding, major bleeding, or death was not statistically different between any of the groups, although, after adjustment, LMWH was associated with a slightly increased risk of ICH.

The quality of included studies varied considerably and inter-rater agreement on study quality was low, raising the possibility of study selection bias. Potential publication bias was not addressed. Bleeding complications were rare, so the estimates of risk may be imprecise.

Bottom line: Individualized therapy is required for DVT prophylaxis in the neurosurgical patient; SCDs reduce VTE risk and both pharmacologic and mechanical prophylaxis may be indicated in patients with increased VTE risk.

Citation: Collen JF, Jackson JL, Shorr AF, Moores LK. Prevention of venous thromboembolism in neurosurgery: A metaanalysis. Chest. 2008;13(4):237-249.

SMART-COP Predicts Need for ICU Care in CAP

Clinical question: Can a clinical tool predict the need for critical care in community acquired pneumonia (CAP)?

Background: Clinical tools predicting 30-day mortality in community acquired pneumonia (CAP) exist, but do not accurately identify who will require intensive care unit-level care, such as intensive respiratory or vasosuppressor support (IRVS).

Study design: Prospective multi-center observational study.

Setting: Six hospitals in Australia participating in the Australian Community Acquired Pneumonia Study (ACAPS).

Synopsis: Multivariate analysis of a dataset of 882 episodes of CAP identified eight factors that were associated with the need for IRVS, summarized by the mnemonic “SMART-COP” (Systolic blood pressure, Multilobar chest radiography involvement, low Albumin level, high Respiratory rate, Tachycardia, Confusion, poor Oxygenation, and low arterial pH). Assigning one point for five factors and two points for three factors (systolic blood pressure, poor oxygenation, and low arterial pH) a SMART-COP score >3 identified 92.3% (95% CI 84.8-96.9%) of patients who required IRVS, including 84% who did not initially require ICU care. Specificity was 62.3% (CI 58.8-65.7%). Test characteristics for predicting IRVS were superior to existing prediction rules (PSI and CURB-65).

Most patients were drawn from large, urban teaching hospitals in Australia, so the results may not be generalizable. The authors also presented a modification of SMART-COP, using pulse oximetry rather than blood gas results; this may be even more useful in the pre-hospital setting.

Bottom line: SMART-COP is a reasonable screening tool for predicting need for ICU-level care in patients admitted with CAP.

Citation: Charles PGP, Wolfe, R, Whitby, M, et. al. SMART-COP: a tool for predicting the need for intensive respiratory or vasopressor support in community-acquired pneumonia. Clin Infect Dis. 2008;47(3):375-384.

Mediterranean and Low-Carbohydrate Diets are Effective for Weight Loss

Clinical question: Are dietary intervention with low-fat, Mediterranean or low-carbohydrate diets effective?

Background: Obesity is a growing, worldwide problem. Past trials comparing the effectiveness and safety of various dietary interventions have been limited by short follow up and high dropout rates.

Study design: Prospective randomized trial.

Setting: Employees of a research center in Israel.

Synopsis: 322 subjects (average BMI 31) were randomized to a low-fat/restricted-calorie, Mediterranean/ restricted-calorie, or a low-carbohydrate/non-restricted calorie diet. Diet adherence was 84.6% at two years and all groups lost significant amounts of weight. The Mediterranean and low-carbohydrate diets showed similar aver∆age weight loss of 4.4 kg and 4.7 kg, respectively. The low-fat diet group on average lost 2.9 kg. Diabetic patients had improved glycemic control and lower insulin levels with the Mediterranean diet. Subjects assigned to the low-carbohydrate diet had the greatest improvement in lipid profile (20% relative decrease of total cholesterol to HDL ratio).

The trial took place at a single site (a scientific research center in Israel) and included only 14% women, so its generalization is uncertain. The study was based on self-reported dietary intake and may be subject to reporting bias.

Bottom line: Mediterranean and low-carbohydrate diets are safe and effective alternatives to low-fat diets with favorable effects on glycemic control in diabetics and lipid metabolism, respectively.

Citation: Shai I, Schwarz-fuchs D, Henkin Y, et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. NEJM. 2008;359(3):229-241.

Admissions for Acute Coronary Syndrome Decreased after Implementation of Smoke-free Legislation

Clinical question: Is there a reduction in admissions for acute coronary syndrome (ACS) after enactment of smoke-free legislation?

Background: Multiple, small, retrospective studies have shown a decrease in ACS after implementation of smoke-free legislation.

Study design: Prospective observational multi-center cohort study.

Setting: Nine hospitals in Scotland.

Synopsis: Data was collected on all patients admitted with ACS 10 months before and after implementation of smoke-free legislation, which prohibited smoking in all enclosed public and work places in Scotland. After the smoking ban, the number of ACS admissions fell by 17% (95% CI 16-18) in Scotland as a whole, compared with a 4% reduction in England during the same period (England does not have similar smoke-free legislation). Among smokers, former smokers and non-smokers, the number of ACS admissions decreased by 14% (95% CI 12-16), 19% (95% CI 17-21), and 21% (95% CI 18-24), respectively. Among non-smokers, self-reported exposure to second-hand smoke decreased significantly; these reductions were confirmed by measured reductions in serum cotinine levels, even among those who never smoked.

Results were limited by the observational nature of the study, although the authors did attempt to carefully match comparison cohorts by season and geography. Also, secular trends other than legislation may have reduced prevalent smoking in Scotland during the study period.

Bottom line: Admissions for ACS for both smokers and non-smokers decreased after implementation of smoke-free legislation.

Citation: Pell JP, Haw S, Cobbe S, et al. Smoke-free legislation and hospitalizations for acute coronary syndrome. NEJM. 2008;359(5):482-491.

Continuation of Beta-blockers in Patients Hospitalized for Heart Failure Improves Mortality

Clinical question: Does the withdrawal or continuation of beta-blockers in patients hospitalized with decompensated heart failure have any effect on clinical outcomes?

Background: Previous clinical trials have demonstrated mortality benefit with the use of beta-blockers in patients with symptomatic chronic heart failure and left ventricular systolic dysfunction (LVSD), however, controversy exists whether to continue these medications in acute decompensated heart failure.

Study design: Prospective cohort analysis from the OPTIMIZE-HF registry (Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure).

Setting: 91 academic and community hospitals in the United States.

Synopsis: Data was analyzed on 2,373 registry patients with documented LVSD (EF <40) eligible for beta-blocker therapy. During hospitalization, 1,350 patients were continued on beta-blockers, 79 had therapy withdrawn, 303 were not started, and 632 had beta-blockade initiated. Compared with no beta-blocker treatment, adjusted hazard ratio (HR) for death at 60 and 90 days following discharge was lower in patients who were continued on beta-blockade (HR 0.60, 95% CI 0.37–0.99). Compared with continuation of beta-blockade, withdrawal of beta-blockade increased the risk of death (HR 2.3, 95% CI 1.2–4.6).

Results were limited by the observational nature of the study and short follow up. The reason for discontinuation or not starting beta-blockade was not captured in the database, so it is possible sicker patients had beta-blockers discontinued during hospitalization (although the authors attempted to control for this).

Bottom line: Beta-blockers should be continued whenever possible in patients hospitalized for heart failure with LVSD.

Citation: Fonarow GC, Abraham WT, Albert NM, et al. Influence of beta-blocker continuation or withdrawal on outcomes in patients hospitalized with heart failure. J Am Coll Cardiol. 2008;52(3):190-199.

Non-invasive Ventilation Does Not Improve Short-term Mortality in Acute Cardiogenic Pulmonary Edema

Clinical question: Does non-invasive ventilation reduce mortality in patients with acute cardiogenic pulmonary edema and are there differences in outcome between use of continuous positive airway pressure (CPAP) or non-invasive positive pressure ventilation (NIPPV)?

Background: In patients with acute cardiogenic pulmonary edema, noninvasive ventilation improves physiologic variables and symptoms, decreases rates of invasive ventilation, and may improve mortality.

Study design: Randomized multi center controlled trial.

Setting: 26 district and regional hospitals in the United Kingdom.

Synopsis: 1,156 patients admitted with acute cardiogenic pulmonary edema between July 2003 and April 2007 were randomized to standard oxygen therapy, versus CPAP or NIPPV. There were no significant differences in seven- or 30-day mortality rates between the standard oxygen therapy versus noninvasive ventilation. Mortality at seven days was 9.8% in the standard oxygen group versus 9.5% in the noninvasive ventilation group (P=0.87); 30-day mortality was 16% in the standard oxygen group and 15% in the non-invasive ventilation group (P=0.64). There were no major differences in treatment outcome with NIPPV compared to CPAP.

Although mortality was not decreased, non-invasive ventilation did improve dyspnea and tachycardia within one hour of therapy.

Bottom line: In patients admitted with acute cardiogenic pulmonary edema, noninvasive ventilation improved dyspnea and some physiological parameters, but did not improve short-term mortality rates.

Citation: Gray A, Goodacre S, Newby D, Masson M, Sampson F, Nicholl J. Noninvasive ventilation in acute cardiogenic pulmonary edema. NEJM. 2008;359(2):142-151. 

Cyclooxygenase 2 Inhibitors May Increase the Risk of Ischemic Stroke

Clinical question: Do NSAIDs and COX-2 inhibitors increase the risk of ischemic or hemorrhagic stroke?

Background: Selected cyclooxygenase 2 (COX-2) inhibitors have been shown to increase cardiovascular morbidity in a dose-dependent manner and are now used with caution in patients at risk for cardiovascular disease. Little is known about the safety of these medications and non-aspirin, non-steroidal anti-inflammatory drugs (NSAIDS) in those at risk for cerebrovascular disease.

Study design: Retrospective observational cohort study.

Setting: Tennessee Medicaid Program enrollees.

Synopsis: Data was collected from the medical records of 336,906 subjects. Non-users had a baseline stroke rate of 4.51 strokes/1000 person-years. The rate increased to 5.15/1,000 person-years and 5.95/1,000 person-years for rofecoxib and valdecoxib, respectively. Celecoxib and other NSAIDs did not significantly increase the risk of stroke. Analysis of new users of rofexocib and valdecoxib yielded a similarly increased risk of stroke. Most strokes were ischemic.

Limitations include the ready availability of NSAIDs raising the possibility that some patients classified as non-users were actually users of NSAIDs. Other potential confounders may not have been measured and, therefore, not available for analysis.

Bottom line: COX-2 inhibitors should be used with caution in patients with increased cerebrovascular disease risk.

Citation: Roumie CL, Mitchel EF, Kaltenback L, Arbogast PG, Gideon P Griffen MR. Nonaspirin NSAIDs, cyclooxygenase 2 inhibitors, and the risk for stroke. Stroke. 2008;39:1037-2045.

SHM is growing, changing, evolving and advancing. If you have been a member or been engaged with the society for the past few years, this isn’t news to you. Our membership is growing; the products, publications and services we offer are expanding; attendance at our annual meeting is increasing; and we are continuing to create new and valuable online resources. These are tangible signs of growth that many of you see and touch on a regular basis. On a day-to-day basis, I see the same things, but because I work for SHM, I have the opportunity to see the growth and change from within the organization.

When I signed on with SHM more than three years ago, I walked through the door and into a small office, approximately 3,000 square feet in size with about 13 full-time staff members. Since then, we have grown steadily, consistently adding new faces to the SHM team and expanding into new places by breaking through a wall into an adjacent space. Flash forward to the present day. Between April and July 2008, SHM has added 13 new faces to the staff. At the end of September 2008, we broke ground on construction of our new corporate headquarters, a 16,000-square-foot office in downtown Philadelphia.

Since its inception 12 years ago, SHM has called 190 Independence Mall home, but just as the hospital medicine movement has grown, so has SHM and the staff supporting the society. This winter, SHM will be moving our corporate headquarters to the new facility at 1500 Spring Garden. The process to find our new headquarters has been an extensive one. We began the search for a new office approximately one year ago, and as I am writing this, final construction documents have been sent to a list of general contractors.

During the past six months, SHM has been working with projects managers, architects, engineers, and consultants to take our new office from a “blank slate” to a finished and fully operational office before the end of 2008. As you read this article, construction on the new headquarters is fully underway. Workers are putting up drywall, running cables, laying carpet, and installing equipment that will be the supporting foundation for the staff and society for the next decade.

So, by now you are probably asking, “What does this mean to me? I don’t see these people on a daily basis, and I don’t work at SHM headquarters.” At a very basic level it means SHM will have a new address and new phone numbers. Your letters, applications, registrations, and anything addressed to SHM will be routed to our new home. Additionally, as part of our move, SHM will implement a new phone system. Our toll-free, 1-800 number will remain the same, however, all of the people who work for SHM will have new office phone numbers.

It is important you know how to reach SHM in our new home, but even more important is to know that this move is a significant milestone in the evolution of the society and the next step in providing you, our members, with ever-improving and enhanced levels of service and support. In creating a new facility, we are further equipping staff with the tools they need to serve you, creating technical capacities to meet current and future needs, and setting a stage for SHM’s continued growth in support of the growing hospital medicine movement.

During the weeks and months ahead, the SHM team will be preparing for the launch of the new One Day Hospitalist University, opening of the new Fellowship in Hospital Medicine and[Add Another New Program Here. In addition to all of these new and exciting initiatives, we will be organizing files, packing boxes and preparing for our move. As we transition to new desks, new phones, new commutes and a new environment, we would like to take a moment to thank you for your support and understanding while we take another significant step in the history of the Society of Hospital Medicine.

Behind the Scenes

Change is in the air

By Geri Barnes

It’s autumn and there is a bite to the air. Every year around this time, I vacillate between being depressed about the pending winter and energized by the change of season. This year, I definitely am excited and energized.

As weather is one of those environmental dynamics that impacts daily life, so do changes in the healthcare arena impact on SHM and its life. We’ve seen “never events” come into being, an expansion of CMS’ Hospitals Compare, and an increasing focus on pay-for-performance. All of these factors are designed to improve patient care, particularly care of the hospitalized patient. SHM staff needs to be ready to support the hospital medicine community.

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SHM long has been focused on defining and providing hospitalists with the education and resources needed for every day practice, as well as for imple- menting cutting-edge quality improvement interventions. To support these focus areas, our staff members were organized in one department, Education and Quality Initiatives. During the last year, we decided our efforts would be better served by creating two departments: Education and Meetings and Quality Initiatives. Last summer, we hired two new staff members to lead the department and move the quality efforts forward. Jane Kelly-Cummings, RN, CPHQ, senior director, Quality Initiatives, has more than 20 years of experience in clinical practice, quality improvement, patient safety, healthcare informatics and quality improvement education. Linda Boclair, MT (ASCP), MEd, MBA, brings to SHM 25 years of management in the healthcare industry and serves as the Quality Initiatives Department director. You will be hearing more about the Quality Initiatives Department in the near future.

I am heading up the newly organized Education and Meetings Department. I am joined by Erica Pearson, director, Meetings; Theresa Jones, education project manager; Meghan Pitzer, meetings coordinator; and Carolyn Brennan, director, Research Program Development. We are charged with managing SHM’s Education Enterprise, which includes meetings and all other educational activities that support our members.

For meetings, we focus on leading our volunteers in the development of relevant program and educational content, ensuring we meet the requirements for continuing medical education (CME) programs. We design and implement meeting logistics with a common goal: the attendees leave the meeting feeling nothing could have been better organized. The Education and Meetings staff has focused their energies on the following meetings:

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• The cornerstone of our meetings is the SHM annual meeting. Hospital Medicine 2009 will take place May 14-17, 2009, in Chicago at the Hyatt Regency. The planning of the program and logistics began in March 2008, and the organizational effort will continue through the end of the meeting. This comprehensive program includes annual meeting education sessions over the course of two and a half days and another full day of seven concurrent pre-courses.
• An important educational event is SHM’s Leadership Academy. Established in 2005, the Level I Academy has been presented semi-annually, with the eighth event taking place in Los Angeles this past September. Based on a need for the next level of leadership skills, Level II started in 2006 and recently presented for the third time. All events have basically sold out, and their popularity continues to grow.
• SHM instituted the One-Day Hospitalist University (ODHU) series this year, presenting four of our best pre-courses on a regional basis. The goal is to present ODHU in four different locations during the course of the year. The first ODHU takes place this month in Baltimore; the next is Feb. 3-4 in Atlanta.
• Pediatric Hospital Medicine 2009 was held in July in Denver. As the lead sponsor, SHM organized this successful conference, which was co-sponsored by the American Pediatric Association and the American Academy of Pediatrics.
• Expert Training Sessions is a new series of educational events that provide the opportunity to learn quality improvement strategies for glycemic control, VTE prevention, or transitions of care directly from an expert and interact on a personal basis. Presented in Boston and Nashville and planned for St. Louis, this initiative already is proving successful and we are hoping to expand in the near future.

The other major focus area for the Education and Meetings Department lies in meeting the educational needs of the hospital medicine community. Staff, working with the Education Committee, are exploring new and exciting ways to identify needs and define strategies to deliver relevant programming. The efforts, which will lead to a comprehensive education plan that will drive the activities the next few years, are focused on the following:

• Life-long learning has become the standard for physicians in general and hospitalists in particular. SHM is in the early stages of identifying and developing resources that will be readily accessible on the SHM Web site, such as a hospital medicine reading list on clinical and healthcare-systems topics based on the Core Competencies.
• The Education Committee is exploring the possibility of developing an evidence-based medicine (EBM) primer, which can be used to practice and teach EBM. It will be designed for the practicing hospitalist in a community hospital setting and will define how to research, read, and use EBM journal articles.
• SHM is exploring the use of Web 2.0 to continually assess needs, deliver educational programs, and communicate with members and faculty.
• The needs of academic hospitalists are unique and SHM is dedicated to support this important segment of our constituency. Joining with the Society of General Internal Medicine (SGIM), SHM is planning an Academic Boot Camp that will focus on education skills, research, mentoring, and career pathways.
• SHM is developing a comprehensive communication and education program to become the main resource for hospitalists as they engage in Maintenance of Certification.

So, the welcome winds of change blow, bringing the energy and organization needed to accomplish our education and quality goals. We are confident our internal changes will result in moving our agenda forward in ways previously only imagined.

Volunteer Search

Interested in being a part of an SHM Committee or Task Force? Now is your chance! Nominations are open for SHM Committees and Task Forces. This is your opportunity to shape the future of SHM and the hospital medicine movement.

To nominate yourself, visit www.hospitalmedicine.org and click on “About SHM,” then click on “Committees.” Here, you will see a full list of committees, as well as task forces and current members. For each committee you would like to serve on, please submit your name and a one- to two-paragraph statement about why you are qualified and interested. E-mail this information to Joi Seabrooks at [email protected] by Dec. 5. Appointments will be made in February, take affect in May and last one year. TH

SHM is growing, changing, evolving and advancing. If you have been a member or been engaged with the society for the past few years, this isn’t news to you. Our membership is growing; the products, publications and services we offer are expanding; attendance at our annual meeting is increasing; and we are continuing to create new and valuable online resources. These are tangible signs of growth that many of you see and touch on a regular basis. On a day-to-day basis, I see the same things, but because I work for SHM, I have the opportunity to see the growth and change from within the organization.

When I signed on with SHM more than three years ago, I walked through the door and into a small office, approximately 3,000 square feet in size with about 13 full-time staff members. Since then, we have grown steadily, consistently adding new faces to the SHM team and expanding into new places by breaking through a wall into an adjacent space. Flash forward to the present day. Between April and July 2008, SHM has added 13 new faces to the staff. At the end of September 2008, we broke ground on construction of our new corporate headquarters, a 16,000-square-foot office in downtown Philadelphia.

Since its inception 12 years ago, SHM has called 190 Independence Mall home, but just as the hospital medicine movement has grown, so has SHM and the staff supporting the society. This winter, SHM will be moving our corporate headquarters to the new facility at 1500 Spring Garden. The process to find our new headquarters has been an extensive one. We began the search for a new office approximately one year ago, and as I am writing this, final construction documents have been sent to a list of general contractors.

During the past six months, SHM has been working with projects managers, architects, engineers, and consultants to take our new office from a “blank slate” to a finished and fully operational office before the end of 2008. As you read this article, construction on the new headquarters is fully underway. Workers are putting up drywall, running cables, laying carpet, and installing equipment that will be the supporting foundation for the staff and society for the next decade.

So, by now you are probably asking, “What does this mean to me? I don’t see these people on a daily basis, and I don’t work at SHM headquarters.” At a very basic level it means SHM will have a new address and new phone numbers. Your letters, applications, registrations, and anything addressed to SHM will be routed to our new home. Additionally, as part of our move, SHM will implement a new phone system. Our toll-free, 1-800 number will remain the same, however, all of the people who work for SHM will have new office phone numbers.

It is important you know how to reach SHM in our new home, but even more important is to know that this move is a significant milestone in the evolution of the society and the next step in providing you, our members, with ever-improving and enhanced levels of service and support. In creating a new facility, we are further equipping staff with the tools they need to serve you, creating technical capacities to meet current and future needs, and setting a stage for SHM’s continued growth in support of the growing hospital medicine movement.

During the weeks and months ahead, the SHM team will be preparing for the launch of the new One Day Hospitalist University, opening of the new Fellowship in Hospital Medicine and[Add Another New Program Here. In addition to all of these new and exciting initiatives, we will be organizing files, packing boxes and preparing for our move. As we transition to new desks, new phones, new commutes and a new environment, we would like to take a moment to thank you for your support and understanding while we take another significant step in the history of the Society of Hospital Medicine.

Behind the Scenes

Change is in the air

By Geri Barnes

It’s autumn and there is a bite to the air. Every year around this time, I vacillate between being depressed about the pending winter and energized by the change of season. This year, I definitely am excited and energized.

As weather is one of those environmental dynamics that impacts daily life, so do changes in the healthcare arena impact on SHM and its life. We’ve seen “never events” come into being, an expansion of CMS’ Hospitals Compare, and an increasing focus on pay-for-performance. All of these factors are designed to improve patient care, particularly care of the hospitalized patient. SHM staff needs to be ready to support the hospital medicine community.

click for large version

click for large version

SHM long has been focused on defining and providing hospitalists with the education and resources needed for every day practice, as well as for imple- menting cutting-edge quality improvement interventions. To support these focus areas, our staff members were organized in one department, Education and Quality Initiatives. During the last year, we decided our efforts would be better served by creating two departments: Education and Meetings and Quality Initiatives. Last summer, we hired two new staff members to lead the department and move the quality efforts forward. Jane Kelly-Cummings, RN, CPHQ, senior director, Quality Initiatives, has more than 20 years of experience in clinical practice, quality improvement, patient safety, healthcare informatics and quality improvement education. Linda Boclair, MT (ASCP), MEd, MBA, brings to SHM 25 years of management in the healthcare industry and serves as the Quality Initiatives Department director. You will be hearing more about the Quality Initiatives Department in the near future.

I am heading up the newly organized Education and Meetings Department. I am joined by Erica Pearson, director, Meetings; Theresa Jones, education project manager; Meghan Pitzer, meetings coordinator; and Carolyn Brennan, director, Research Program Development. We are charged with managing SHM’s Education Enterprise, which includes meetings and all other educational activities that support our members.

For meetings, we focus on leading our volunteers in the development of relevant program and educational content, ensuring we meet the requirements for continuing medical education (CME) programs. We design and implement meeting logistics with a common goal: the attendees leave the meeting feeling nothing could have been better organized. The Education and Meetings staff has focused their energies on the following meetings:

click for large version

• The cornerstone of our meetings is the SHM annual meeting. Hospital Medicine 2009 will take place May 14-17, 2009, in Chicago at the Hyatt Regency. The planning of the program and logistics began in March 2008, and the organizational effort will continue through the end of the meeting. This comprehensive program includes annual meeting education sessions over the course of two and a half days and another full day of seven concurrent pre-courses.
• An important educational event is SHM’s Leadership Academy. Established in 2005, the Level I Academy has been presented semi-annually, with the eighth event taking place in Los Angeles this past September. Based on a need for the next level of leadership skills, Level II started in 2006 and recently presented for the third time. All events have basically sold out, and their popularity continues to grow.
• SHM instituted the One-Day Hospitalist University (ODHU) series this year, presenting four of our best pre-courses on a regional basis. The goal is to present ODHU in four different locations during the course of the year. The first ODHU takes place this month in Baltimore; the next is Feb. 3-4 in Atlanta.
• Pediatric Hospital Medicine 2009 was held in July in Denver. As the lead sponsor, SHM organized this successful conference, which was co-sponsored by the American Pediatric Association and the American Academy of Pediatrics.
• Expert Training Sessions is a new series of educational events that provide the opportunity to learn quality improvement strategies for glycemic control, VTE prevention, or transitions of care directly from an expert and interact on a personal basis. Presented in Boston and Nashville and planned for St. Louis, this initiative already is proving successful and we are hoping to expand in the near future.

The other major focus area for the Education and Meetings Department lies in meeting the educational needs of the hospital medicine community. Staff, working with the Education Committee, are exploring new and exciting ways to identify needs and define strategies to deliver relevant programming. The efforts, which will lead to a comprehensive education plan that will drive the activities the next few years, are focused on the following:

• Life-long learning has become the standard for physicians in general and hospitalists in particular. SHM is in the early stages of identifying and developing resources that will be readily accessible on the SHM Web site, such as a hospital medicine reading list on clinical and healthcare-systems topics based on the Core Competencies.
• The Education Committee is exploring the possibility of developing an evidence-based medicine (EBM) primer, which can be used to practice and teach EBM. It will be designed for the practicing hospitalist in a community hospital setting and will define how to research, read, and use EBM journal articles.
• SHM is exploring the use of Web 2.0 to continually assess needs, deliver educational programs, and communicate with members and faculty.
• The needs of academic hospitalists are unique and SHM is dedicated to support this important segment of our constituency. Joining with the Society of General Internal Medicine (SGIM), SHM is planning an Academic Boot Camp that will focus on education skills, research, mentoring, and career pathways.
• SHM is developing a comprehensive communication and education program to become the main resource for hospitalists as they engage in Maintenance of Certification.

So, the welcome winds of change blow, bringing the energy and organization needed to accomplish our education and quality goals. We are confident our internal changes will result in moving our agenda forward in ways previously only imagined.

Volunteer Search

Interested in being a part of an SHM Committee or Task Force? Now is your chance! Nominations are open for SHM Committees and Task Forces. This is your opportunity to shape the future of SHM and the hospital medicine movement.

To nominate yourself, visit www.hospitalmedicine.org and click on “About SHM,” then click on “Committees.” Here, you will see a full list of committees, as well as task forces and current members. For each committee you would like to serve on, please submit your name and a one- to two-paragraph statement about why you are qualified and interested. E-mail this information to Joi Seabrooks at [email protected] by Dec. 5. Appointments will be made in February, take affect in May and last one year. TH

SHM is growing, changing, evolving and advancing. If you have been a member or been engaged with the society for the past few years, this isn’t news to you. Our membership is growing; the products, publications and services we offer are expanding; attendance at our annual meeting is increasing; and we are continuing to create new and valuable online resources. These are tangible signs of growth that many of you see and touch on a regular basis. On a day-to-day basis, I see the same things, but because I work for SHM, I have the opportunity to see the growth and change from within the organization.

When I signed on with SHM more than three years ago, I walked through the door and into a small office, approximately 3,000 square feet in size with about 13 full-time staff members. Since then, we have grown steadily, consistently adding new faces to the SHM team and expanding into new places by breaking through a wall into an adjacent space. Flash forward to the present day. Between April and July 2008, SHM has added 13 new faces to the staff. At the end of September 2008, we broke ground on construction of our new corporate headquarters, a 16,000-square-foot office in downtown Philadelphia.

Since its inception 12 years ago, SHM has called 190 Independence Mall home, but just as the hospital medicine movement has grown, so has SHM and the staff supporting the society. This winter, SHM will be moving our corporate headquarters to the new facility at 1500 Spring Garden. The process to find our new headquarters has been an extensive one. We began the search for a new office approximately one year ago, and as I am writing this, final construction documents have been sent to a list of general contractors.

During the past six months, SHM has been working with projects managers, architects, engineers, and consultants to take our new office from a “blank slate” to a finished and fully operational office before the end of 2008. As you read this article, construction on the new headquarters is fully underway. Workers are putting up drywall, running cables, laying carpet, and installing equipment that will be the supporting foundation for the staff and society for the next decade.

So, by now you are probably asking, “What does this mean to me? I don’t see these people on a daily basis, and I don’t work at SHM headquarters.” At a very basic level it means SHM will have a new address and new phone numbers. Your letters, applications, registrations, and anything addressed to SHM will be routed to our new home. Additionally, as part of our move, SHM will implement a new phone system. Our toll-free, 1-800 number will remain the same, however, all of the people who work for SHM will have new office phone numbers.

It is important you know how to reach SHM in our new home, but even more important is to know that this move is a significant milestone in the evolution of the society and the next step in providing you, our members, with ever-improving and enhanced levels of service and support. In creating a new facility, we are further equipping staff with the tools they need to serve you, creating technical capacities to meet current and future needs, and setting a stage for SHM’s continued growth in support of the growing hospital medicine movement.

During the weeks and months ahead, the SHM team will be preparing for the launch of the new One Day Hospitalist University, opening of the new Fellowship in Hospital Medicine and[Add Another New Program Here. In addition to all of these new and exciting initiatives, we will be organizing files, packing boxes and preparing for our move. As we transition to new desks, new phones, new commutes and a new environment, we would like to take a moment to thank you for your support and understanding while we take another significant step in the history of the Society of Hospital Medicine.

Behind the Scenes

Change is in the air

By Geri Barnes

It’s autumn and there is a bite to the air. Every year around this time, I vacillate between being depressed about the pending winter and energized by the change of season. This year, I definitely am excited and energized.

As weather is one of those environmental dynamics that impacts daily life, so do changes in the healthcare arena impact on SHM and its life. We’ve seen “never events” come into being, an expansion of CMS’ Hospitals Compare, and an increasing focus on pay-for-performance. All of these factors are designed to improve patient care, particularly care of the hospitalized patient. SHM staff needs to be ready to support the hospital medicine community.

click for large version

click for large version

SHM long has been focused on defining and providing hospitalists with the education and resources needed for every day practice, as well as for imple- menting cutting-edge quality improvement interventions. To support these focus areas, our staff members were organized in one department, Education and Quality Initiatives. During the last year, we decided our efforts would be better served by creating two departments: Education and Meetings and Quality Initiatives. Last summer, we hired two new staff members to lead the department and move the quality efforts forward. Jane Kelly-Cummings, RN, CPHQ, senior director, Quality Initiatives, has more than 20 years of experience in clinical practice, quality improvement, patient safety, healthcare informatics and quality improvement education. Linda Boclair, MT (ASCP), MEd, MBA, brings to SHM 25 years of management in the healthcare industry and serves as the Quality Initiatives Department director. You will be hearing more about the Quality Initiatives Department in the near future.

I am heading up the newly organized Education and Meetings Department. I am joined by Erica Pearson, director, Meetings; Theresa Jones, education project manager; Meghan Pitzer, meetings coordinator; and Carolyn Brennan, director, Research Program Development. We are charged with managing SHM’s Education Enterprise, which includes meetings and all other educational activities that support our members.

For meetings, we focus on leading our volunteers in the development of relevant program and educational content, ensuring we meet the requirements for continuing medical education (CME) programs. We design and implement meeting logistics with a common goal: the attendees leave the meeting feeling nothing could have been better organized. The Education and Meetings staff has focused their energies on the following meetings:

click for large version

• The cornerstone of our meetings is the SHM annual meeting. Hospital Medicine 2009 will take place May 14-17, 2009, in Chicago at the Hyatt Regency. The planning of the program and logistics began in March 2008, and the organizational effort will continue through the end of the meeting. This comprehensive program includes annual meeting education sessions over the course of two and a half days and another full day of seven concurrent pre-courses.
• An important educational event is SHM’s Leadership Academy. Established in 2005, the Level I Academy has been presented semi-annually, with the eighth event taking place in Los Angeles this past September. Based on a need for the next level of leadership skills, Level II started in 2006 and recently presented for the third time. All events have basically sold out, and their popularity continues to grow.
• SHM instituted the One-Day Hospitalist University (ODHU) series this year, presenting four of our best pre-courses on a regional basis. The goal is to present ODHU in four different locations during the course of the year. The first ODHU takes place this month in Baltimore; the next is Feb. 3-4 in Atlanta.
• Pediatric Hospital Medicine 2009 was held in July in Denver. As the lead sponsor, SHM organized this successful conference, which was co-sponsored by the American Pediatric Association and the American Academy of Pediatrics.
• Expert Training Sessions is a new series of educational events that provide the opportunity to learn quality improvement strategies for glycemic control, VTE prevention, or transitions of care directly from an expert and interact on a personal basis. Presented in Boston and Nashville and planned for St. Louis, this initiative already is proving successful and we are hoping to expand in the near future.

The other major focus area for the Education and Meetings Department lies in meeting the educational needs of the hospital medicine community. Staff, working with the Education Committee, are exploring new and exciting ways to identify needs and define strategies to deliver relevant programming. The efforts, which will lead to a comprehensive education plan that will drive the activities the next few years, are focused on the following:

• Life-long learning has become the standard for physicians in general and hospitalists in particular. SHM is in the early stages of identifying and developing resources that will be readily accessible on the SHM Web site, such as a hospital medicine reading list on clinical and healthcare-systems topics based on the Core Competencies.
• The Education Committee is exploring the possibility of developing an evidence-based medicine (EBM) primer, which can be used to practice and teach EBM. It will be designed for the practicing hospitalist in a community hospital setting and will define how to research, read, and use EBM journal articles.
• SHM is exploring the use of Web 2.0 to continually assess needs, deliver educational programs, and communicate with members and faculty.
• The needs of academic hospitalists are unique and SHM is dedicated to support this important segment of our constituency. Joining with the Society of General Internal Medicine (SGIM), SHM is planning an Academic Boot Camp that will focus on education skills, research, mentoring, and career pathways.
• SHM is developing a comprehensive communication and education program to become the main resource for hospitalists as they engage in Maintenance of Certification.

So, the welcome winds of change blow, bringing the energy and organization needed to accomplish our education and quality goals. We are confident our internal changes will result in moving our agenda forward in ways previously only imagined.

Volunteer Search

Interested in being a part of an SHM Committee or Task Force? Now is your chance! Nominations are open for SHM Committees and Task Forces. This is your opportunity to shape the future of SHM and the hospital medicine movement.

To nominate yourself, visit www.hospitalmedicine.org and click on “About SHM,” then click on “Committees.” Here, you will see a full list of committees, as well as task forces and current members. For each committee you would like to serve on, please submit your name and a one- to two-paragraph statement about why you are qualified and interested. E-mail this information to Joi Seabrooks at [email protected] by Dec. 5. Appointments will be made in February, take affect in May and last one year. TH

Case

A 72-year-old retired nurse with known nonischemic dilated cardiomyopathy with an ejection fraction of approximately 20% and status-post cardiac resynchronization therapy presents to the emergency department with dyspnea with minimal activity, three-pillow orthopnea, and paroxysmal nocturnal dyspnea.

She had been hospitalized twice during the past 60 days for similar symptoms. Her medications included losartan (20 mg po q daily), carvedilol (3.125 mg twice daily), spironolactone (25 mg daily), digoxin (0.125 mg daily), and furosemide (80 mg twice daily). Vital signs are notable for a blood pressure of 90/50 mmHg and an irregular pulse of 90 beats per minute. Physical examination is notable for marked jugular venous distension, lungs clear to auscultation bilaterally, biventricular heaves, a markedly displaced left ventricular point of maximal impulse, and a prominent S3 gallop.

Despite treatment with intravenous furosemide and temporary withdrawal of carvedilol, the patient remains symptomatic with persistent jugular venous distension.

Should she be given a vasoactive agent?

Overview

Acute heart failure syndrome (AHFS), defined as a gradual or rapid change in heart failure signs and symptoms, is the most common cause of hospitalization in the United States1. It is associated with an average in-hospital mortality of 4% to 5%, a 30-day mortality of 7% to11%, and a one-year mortality of 33%2.

In patients with previously established myocardial dysfunction, AHFS commonly reflects exacerbation of symptoms after a period of stability. The clinical presentation and severity of AHFS may range from mild volume overload to life-threatening cardiogenic shock and multi-organ failure unresponsive to pharmacologic therapy.2

Initial management of AHFS depends on definition of the patient’s hemodynamic profile. To guide initial therapy, classify patients into one of four hemodynamic profiles during a brief bedside assessment that relies on evaluation of filling pressures (wet or dry) and adequacy of perfusion (hot or cold) (see figure 1).3

Treating volume overload or elevated filling pressures generally begins with diuretics. Diuretics have been shown to provide symptomatic relief, though they have not yet been proven safe.4 Initial treatment can include a loop diuretic at a dose higher than the patient’s chronic dose, with intravenous dosing offering greater bio-absorption and rapidity in onset of action.5 If perfusion is inadequate, escalate therapy beyond diuretics to include vasoactive agents.

Review of the Data

The use of vasoactive medications is largely based on anecdotal experiences and physiologic assumptions rather than on adequately powered prospective randomized controlled trials.6 Vasoactive therapy includes vasodilator and inotropic support and is generally limited for use in patients with advanced disease not responding to standard medical treatment and diuresis. The physiologic premise rests in the expected improvement in ventricular filling pressures and cardiac output with reduction in afterload and/or preload. Vasodilators counteract vascular constriction, reducing both preload and afterload. Positive inotropic agents amplify cardiac output by increasing the strength of myocardial contraction.

Vasodilators

The Heart Failure Society of America (HFSA) 2006 Comprehensive Heart Failure Practice Guidelines state, “In the absence of symptomatic hypotension, intravenous vasodilators (nitroglycerin, nitroprusside, or nesiritide) may be considered as an addition to diuretic therapy for rapid improvement of congestive symptoms.”7 The clinical utility of nesiritide remains in question with clinical and hemodynamic improvement demonstrated in three randomized trials 8-10; but tempered against meta-analyses 11-12 of selected trials, demonstrating a non-significant trend toward increased kidney dysfunction and death within 30 days (35/485 [7.2%] vs. 15/377 [4.0%] patients; risk ratio from meta-analyses, 1.74; 95% confidence interval, 0.97-3.12; p=0.059). In a randomized trial of 489 in-patients with dyspnea at rest from AHFS, treatment with three hours of intravenous nesiritide resulted in a significant improvement in dyspnea compared with placebo (p=0.03). Similar improvement was observed with intravenous nitroglycerin and did not differ statistically from that observed with nesiritide.8 Nitroprusside, an attractive option among those with hypertension and cardiogenic pulmonary edema, is limited by the need for invasive hemodynamic monitoring and potential for either cyanide toxicity or worsening myocardial ischemia.

click for large version

Inotropes

Again, there is little evidence from adequately powered randomized controlled trials guiding the use of inotropes. Their use is generally limited to the following indications (see figure 2): (1) Short-term treatment for AHFS that is unresponsive to adequate doses of diuretics and especially when associated with systemic hypotension, (2) Bridge to recovery (as following myocarditis) or to definitive treatment (as with transplant), or (3) For palliation when symptomatic relief is the agreed upon goal.13 The HFSA 2006 guideline states: “Intravenous inotropes may be considered to relieve symptoms and improve end-organ function in patients with advanced HF characterized by left ventricle dilation, reduced left ventricular ejection fraction, and diminished peripheral perfusion or end-organ dysfunction, particularly if these patients have marginal systolic blood pressure, have symptomatic hypotension despite adequate filling pressures, or are unresponsive to, or intolerant of, intravenous vasodilators.”7

Dobutamine and milrinone are the most commonly used IV inotropes for the treatment of AHFS and increase contractility by increasing intracellular levels of cyclic adenylate monophosphate (cAMP). Dobutamine is a catechlamine agonist that increases cAMP production through stimulation of adenylate cyclase. Milrinone selectively inhibits phosphodiesterase III, which catalyzes the breakdown of cAMP.

Despite their frequent use when traditional treatments have failed, the data supporting the use of dobutamine and milrinone is limited. The largest registry of patients with AHFS to date associated excess mortality with intravenous inotrope use compared to nitroglycerin or nesiritide.14 In a study population of 255 patients randomized to receive either intravenous nesiritide or intravenous dobutamine, Burger et al.15 demonstrated that dobutamine significantly increased the mean number of ventricular tachycardia events per 24 hours (p=0.001), suggesting increased arrhythmogenicity associated with inotrope use. Nonetheless, in a randomized trial of 15 patients admitted with AHFS, functional class improved in six of eight dobutamine-treated patients, but in only two of seven patients treated with placebo, suggesting clinical improvement as a consequence of inotropic stimulation.16 Unverferth et al. demonstrated a similar sustained functional improvement up to 10 weeks following a 72-hour infusion of intravenous dobutamine. 17

The Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure trial (OPTIME-CHF), randomized 951 patients with AHFS to receive either intravenous milrinone or placebo within 48 hours of hospitalization.18 Compared to placebo, milrinone was associated with a significant increase in sustained hypotension requiring intervention (10.7% vs. 3.2%; p<.001) and new atrial arrhythmias (4.6% vs. 1.5%; p=0.004), along with a non-significant trend toward increased mortality (3.8% vs. 2.3%; p=0.19). However, as measured by a visual analog scale, milrinone-treated patients reported feeling better than those treated with placebo at 30 days post-randomization (p=0.02).

Although there are not randomized data comparing the efficacy of milrinone and dobutamine in AHFS, a retrospective analysis of 329 patients compared the hemodynamic and clinical effects of these two inotropes.19 Milrinone consistently was associated with a more favorable hemodynamic response, including lower systemic vascular resistance (p=0.01); lower pulmonary artery wedge pressure (p<0.001); larger percentage increase in cardiac index (p=0.03); and larger percentage decrease in pulmonary vascular resistance (p=0.0001). In-hospital mortality (dobutamine 7.8% vs. milrinone 10%) was not significantly different.

Conclusion

Clearly, vasoactive and inotropic agents are available when AHFS is refractory to traditional diuresis and may offer short-term symptomatic relief, palliation in the context of end-of-life care, or bridge to recovery or more definitive treatment. Unfortunately, sufficient and robust evidence that supports the safety and efficacy of such agents is lacking and their use is largely guided by historical practices, clinical experience, and anticipation of theoretic physiologic changes. While adequately powered prospective randomized data emerge, newer agents such as vasopressin receptor antagonists, cardiac myosin activators, calcium sensitizers, and adenosine-receptor antagonists will offer additional pharmacologic options.20 When continued pharmacologic support becomes ineffective, device therapy is available to aid in the treatment of AHFS and includes ultrafiltration to reduce filling pressures and intra-aortic balloon pump counterpulsation or left ventricular assist device placement for pharmacologically resistant cardiogenic shock.21

Back to the Case

Despite maximal medical therapy for her chronic heart failure and biventricular pacing, the patient continued to have markedly limited functional status and repeated hospitalizations for AHFS. Given her advanced age and poor nutritional status, she was not a candidate for cardiac transplantation or placement of a left ventricular assist device. To allow for palliative tailored therapy, right heart catheterization was performed. Right heart catheterization revealed elevated filling pressures, as follows: right atrium, 20 mmHg; pulmonary artery, 63/34 mmHg (mean 47 mmHg); and pulmonary capillary wedge, 29 mmHg. Her mixed venous oxygen saturation was only 41% with a calculated cardiac output of 2.9 liters per minute and cardiac index of 2 liters per minute per meter squared.

As she expressed symptomatic relief as her goal, she was started on intravenous milrinone at 0.2 micrograms per kilogram per minute. This was done with the understanding her symptoms would likely would improve, at the expense of worsening longevity and prognosis. With uptitration of her intravenous milrinone and a continuous infusion of furosemide, she demonstrated the following filling pressures within 24 hours: right atrium, 18 mmHg; pulmonary artery, 63/33 mmHg (mean 43 mmHg); and pulmonary capillary wedge, 24. Importantly, her mixed venous oxygen saturation improved to 68% with a calculated cardiac output of 3.4 liters per minute and cardiac index of 2.4 liters per minute per meter squared. These favorable hemodynamic changes were accompanied by modest improvement in symptoms. After continued intravenous diuresis, she was transitioned back to an oral diuretic regimen and was ultimately discharged to home with a continuous infusion of milrinone for palliation. TH

Drs. Vaishnava, McKean, Nohria, and Baughman are from Brigham and Women’s Hospital and Harvard Medical School in Boston, Mass.

REFERENCES:

1. Thom T, Haase N, Rosamond W, et al. Heart disease and stroke statistics – 2006 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2006;113:85-151.
2. Iong P, Vowinckel E, Liu PP, Gong Y, Tu JV. Prognosis and determinants of survival in patients newly hospitalized for heart failure: a population-based study. Arch Intern Med. 2002;162:1689-94.
3. Nohria A, Lewis EF, Stevenson LW. Medical management of advanced heart failure. JAMA. 2002;287;628-40.
4. Faris R, Flather MD, Purcell H, et al. Diuretics for heart failure. Cochrane Database Syst Rev. 2006;1;CD003838.
5. Wang DJ and Gottlieb SS. Diuretics: Still the mainstay of treatment. Crit Care Med. 2008;36(Suppl.):S89-S94.
6. Fares WH. Management of acute decompensated heart failure in an evidence-based era: What is the evidence behind the current standard of care? Heart & Lung. 2008;37(3):173-8.
7. Adams KF, Lindenfield J, Arnold J, et al. Executive summary: HFSA 2006 comprehensive heart failure practice guidelines. J Card Fail. 2006;12:10-38.
8. Publication Committee for the VMAC Investigators (Vasodilatation in the Management of Acute CHF). Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: a randomized controlled trial. JAMA. 2002;297:1531-40.
9. Peacock WF, Enerman CL, Silver MA, on behalf of the PROACTION Study Group. Am J Emerg Med. 2005;23:327-31.
10. Cotter G, Metzkor E, Kaluski E, et al. Randomized trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary edema. Lancet. 1998;351:389-93.
11. Sackner-Bernstein JD, Kowalski M, Fox M, Aaronson K. Short-term risk of death after treatment with nesiritide for decompensated heart failure: a pooled analysis of randomized controlled trials. JAMA. 2005;293:1900-5.
12. Sackner-Bernstein JD, Skopicki HA, Aaronson K. Risk of worsening renal function with nesiritide in patients with acutely decompensated heart failure. Circulation. 2005;111:1487-91.
13. Felker GM and O’Connor CM. Inotropic therapy for heart failure: An evidence-based approach. American Heart Journal. 2001; 142:393-401.
14. Abrahm WT, Adams KF, Fonarow GC, et al. In-hospital mortality in patients with acute decompensated heart failure requiring intravenous vasoactive medications: an analysis from the Acute Decompensated Heart Failure National Registry (ADHERE). J Am Coll Cardiol. 2005;46:57-64.
15. Burger AJ, Houton DP, LeJemtel T, et al. Effect of nesiritide and dobutamine on ventricular arrhythmias in the treatment of patients with acutely decompensated congestive heart failure: the PRECEDENT study. American Heart Journal. 2002;144:1102-8.
16. Liang CS, Sherman LG, Doherty JU, et al. Sustained improvement of cardiac function in patients with congestive heart failure after short-term infusion of dobutamine. Circulation. 1984;69:113-9.
17. Unverferth DV, Magorien RD, Lewis RP, et al. Long-term benefit of dobutamine in patients with congestive cardiomyopathy. American Heart Journal. 1980;100:622-30.
18. Cuffe MS, Califf RM, Adams KF Jr, et al. Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) Investigators. Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial. JAMA. 2002;287:1541-7.
19. Yamani MH, Haji SA, Starling RC, et al. Comparison of dobutamine-based and milrinone-based therapy for advanced decompensated congestive heart failure: Hemodynamic efficacy, clinical outcome, and economic impact. American Heart Journal. 2001;142:998-1002.
20. Shin, DD, Brandimarte F, De Luca L, et al. Review of current and investigational pharmacologic agents for acute heart failure syndromes. Am J Cardiol. 2007;99(suppl):4A-23A.
21. Kale P and Fang JC. Devices in acute heart failure. Crit Care Med. 2008;36(Suppl.):S121-128.

Case

A 72-year-old retired nurse with known nonischemic dilated cardiomyopathy with an ejection fraction of approximately 20% and status-post cardiac resynchronization therapy presents to the emergency department with dyspnea with minimal activity, three-pillow orthopnea, and paroxysmal nocturnal dyspnea.

She had been hospitalized twice during the past 60 days for similar symptoms. Her medications included losartan (20 mg po q daily), carvedilol (3.125 mg twice daily), spironolactone (25 mg daily), digoxin (0.125 mg daily), and furosemide (80 mg twice daily). Vital signs are notable for a blood pressure of 90/50 mmHg and an irregular pulse of 90 beats per minute. Physical examination is notable for marked jugular venous distension, lungs clear to auscultation bilaterally, biventricular heaves, a markedly displaced left ventricular point of maximal impulse, and a prominent S3 gallop.

Despite treatment with intravenous furosemide and temporary withdrawal of carvedilol, the patient remains symptomatic with persistent jugular venous distension.

Should she be given a vasoactive agent?

Overview

Acute heart failure syndrome (AHFS), defined as a gradual or rapid change in heart failure signs and symptoms, is the most common cause of hospitalization in the United States1. It is associated with an average in-hospital mortality of 4% to 5%, a 30-day mortality of 7% to11%, and a one-year mortality of 33%2.

In patients with previously established myocardial dysfunction, AHFS commonly reflects exacerbation of symptoms after a period of stability. The clinical presentation and severity of AHFS may range from mild volume overload to life-threatening cardiogenic shock and multi-organ failure unresponsive to pharmacologic therapy.2

Initial management of AHFS depends on definition of the patient’s hemodynamic profile. To guide initial therapy, classify patients into one of four hemodynamic profiles during a brief bedside assessment that relies on evaluation of filling pressures (wet or dry) and adequacy of perfusion (hot or cold) (see figure 1).3

Treating volume overload or elevated filling pressures generally begins with diuretics. Diuretics have been shown to provide symptomatic relief, though they have not yet been proven safe.4 Initial treatment can include a loop diuretic at a dose higher than the patient’s chronic dose, with intravenous dosing offering greater bio-absorption and rapidity in onset of action.5 If perfusion is inadequate, escalate therapy beyond diuretics to include vasoactive agents.

Review of the Data

The use of vasoactive medications is largely based on anecdotal experiences and physiologic assumptions rather than on adequately powered prospective randomized controlled trials.6 Vasoactive therapy includes vasodilator and inotropic support and is generally limited for use in patients with advanced disease not responding to standard medical treatment and diuresis. The physiologic premise rests in the expected improvement in ventricular filling pressures and cardiac output with reduction in afterload and/or preload. Vasodilators counteract vascular constriction, reducing both preload and afterload. Positive inotropic agents amplify cardiac output by increasing the strength of myocardial contraction.

Vasodilators

The Heart Failure Society of America (HFSA) 2006 Comprehensive Heart Failure Practice Guidelines state, “In the absence of symptomatic hypotension, intravenous vasodilators (nitroglycerin, nitroprusside, or nesiritide) may be considered as an addition to diuretic therapy for rapid improvement of congestive symptoms.”7 The clinical utility of nesiritide remains in question with clinical and hemodynamic improvement demonstrated in three randomized trials 8-10; but tempered against meta-analyses 11-12 of selected trials, demonstrating a non-significant trend toward increased kidney dysfunction and death within 30 days (35/485 [7.2%] vs. 15/377 [4.0%] patients; risk ratio from meta-analyses, 1.74; 95% confidence interval, 0.97-3.12; p=0.059). In a randomized trial of 489 in-patients with dyspnea at rest from AHFS, treatment with three hours of intravenous nesiritide resulted in a significant improvement in dyspnea compared with placebo (p=0.03). Similar improvement was observed with intravenous nitroglycerin and did not differ statistically from that observed with nesiritide.8 Nitroprusside, an attractive option among those with hypertension and cardiogenic pulmonary edema, is limited by the need for invasive hemodynamic monitoring and potential for either cyanide toxicity or worsening myocardial ischemia.

click for large version

Inotropes

Again, there is little evidence from adequately powered randomized controlled trials guiding the use of inotropes. Their use is generally limited to the following indications (see figure 2): (1) Short-term treatment for AHFS that is unresponsive to adequate doses of diuretics and especially when associated with systemic hypotension, (2) Bridge to recovery (as following myocarditis) or to definitive treatment (as with transplant), or (3) For palliation when symptomatic relief is the agreed upon goal.13 The HFSA 2006 guideline states: “Intravenous inotropes may be considered to relieve symptoms and improve end-organ function in patients with advanced HF characterized by left ventricle dilation, reduced left ventricular ejection fraction, and diminished peripheral perfusion or end-organ dysfunction, particularly if these patients have marginal systolic blood pressure, have symptomatic hypotension despite adequate filling pressures, or are unresponsive to, or intolerant of, intravenous vasodilators.”7

Dobutamine and milrinone are the most commonly used IV inotropes for the treatment of AHFS and increase contractility by increasing intracellular levels of cyclic adenylate monophosphate (cAMP). Dobutamine is a catechlamine agonist that increases cAMP production through stimulation of adenylate cyclase. Milrinone selectively inhibits phosphodiesterase III, which catalyzes the breakdown of cAMP.

Despite their frequent use when traditional treatments have failed, the data supporting the use of dobutamine and milrinone is limited. The largest registry of patients with AHFS to date associated excess mortality with intravenous inotrope use compared to nitroglycerin or nesiritide.14 In a study population of 255 patients randomized to receive either intravenous nesiritide or intravenous dobutamine, Burger et al.15 demonstrated that dobutamine significantly increased the mean number of ventricular tachycardia events per 24 hours (p=0.001), suggesting increased arrhythmogenicity associated with inotrope use. Nonetheless, in a randomized trial of 15 patients admitted with AHFS, functional class improved in six of eight dobutamine-treated patients, but in only two of seven patients treated with placebo, suggesting clinical improvement as a consequence of inotropic stimulation.16 Unverferth et al. demonstrated a similar sustained functional improvement up to 10 weeks following a 72-hour infusion of intravenous dobutamine. 17

The Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure trial (OPTIME-CHF), randomized 951 patients with AHFS to receive either intravenous milrinone or placebo within 48 hours of hospitalization.18 Compared to placebo, milrinone was associated with a significant increase in sustained hypotension requiring intervention (10.7% vs. 3.2%; p<.001) and new atrial arrhythmias (4.6% vs. 1.5%; p=0.004), along with a non-significant trend toward increased mortality (3.8% vs. 2.3%; p=0.19). However, as measured by a visual analog scale, milrinone-treated patients reported feeling better than those treated with placebo at 30 days post-randomization (p=0.02).

Although there are not randomized data comparing the efficacy of milrinone and dobutamine in AHFS, a retrospective analysis of 329 patients compared the hemodynamic and clinical effects of these two inotropes.19 Milrinone consistently was associated with a more favorable hemodynamic response, including lower systemic vascular resistance (p=0.01); lower pulmonary artery wedge pressure (p<0.001); larger percentage increase in cardiac index (p=0.03); and larger percentage decrease in pulmonary vascular resistance (p=0.0001). In-hospital mortality (dobutamine 7.8% vs. milrinone 10%) was not significantly different.

Conclusion

Clearly, vasoactive and inotropic agents are available when AHFS is refractory to traditional diuresis and may offer short-term symptomatic relief, palliation in the context of end-of-life care, or bridge to recovery or more definitive treatment. Unfortunately, sufficient and robust evidence that supports the safety and efficacy of such agents is lacking and their use is largely guided by historical practices, clinical experience, and anticipation of theoretic physiologic changes. While adequately powered prospective randomized data emerge, newer agents such as vasopressin receptor antagonists, cardiac myosin activators, calcium sensitizers, and adenosine-receptor antagonists will offer additional pharmacologic options.20 When continued pharmacologic support becomes ineffective, device therapy is available to aid in the treatment of AHFS and includes ultrafiltration to reduce filling pressures and intra-aortic balloon pump counterpulsation or left ventricular assist device placement for pharmacologically resistant cardiogenic shock.21

Back to the Case

Despite maximal medical therapy for her chronic heart failure and biventricular pacing, the patient continued to have markedly limited functional status and repeated hospitalizations for AHFS. Given her advanced age and poor nutritional status, she was not a candidate for cardiac transplantation or placement of a left ventricular assist device. To allow for palliative tailored therapy, right heart catheterization was performed. Right heart catheterization revealed elevated filling pressures, as follows: right atrium, 20 mmHg; pulmonary artery, 63/34 mmHg (mean 47 mmHg); and pulmonary capillary wedge, 29 mmHg. Her mixed venous oxygen saturation was only 41% with a calculated cardiac output of 2.9 liters per minute and cardiac index of 2 liters per minute per meter squared.

As she expressed symptomatic relief as her goal, she was started on intravenous milrinone at 0.2 micrograms per kilogram per minute. This was done with the understanding her symptoms would likely would improve, at the expense of worsening longevity and prognosis. With uptitration of her intravenous milrinone and a continuous infusion of furosemide, she demonstrated the following filling pressures within 24 hours: right atrium, 18 mmHg; pulmonary artery, 63/33 mmHg (mean 43 mmHg); and pulmonary capillary wedge, 24. Importantly, her mixed venous oxygen saturation improved to 68% with a calculated cardiac output of 3.4 liters per minute and cardiac index of 2.4 liters per minute per meter squared. These favorable hemodynamic changes were accompanied by modest improvement in symptoms. After continued intravenous diuresis, she was transitioned back to an oral diuretic regimen and was ultimately discharged to home with a continuous infusion of milrinone for palliation. TH

Drs. Vaishnava, McKean, Nohria, and Baughman are from Brigham and Women’s Hospital and Harvard Medical School in Boston, Mass.

REFERENCES:

1. Thom T, Haase N, Rosamond W, et al. Heart disease and stroke statistics – 2006 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2006;113:85-151.
2. Iong P, Vowinckel E, Liu PP, Gong Y, Tu JV. Prognosis and determinants of survival in patients newly hospitalized for heart failure: a population-based study. Arch Intern Med. 2002;162:1689-94.
3. Nohria A, Lewis EF, Stevenson LW. Medical management of advanced heart failure. JAMA. 2002;287;628-40.
4. Faris R, Flather MD, Purcell H, et al. Diuretics for heart failure. Cochrane Database Syst Rev. 2006;1;CD003838.
5. Wang DJ and Gottlieb SS. Diuretics: Still the mainstay of treatment. Crit Care Med. 2008;36(Suppl.):S89-S94.
6. Fares WH. Management of acute decompensated heart failure in an evidence-based era: What is the evidence behind the current standard of care? Heart & Lung. 2008;37(3):173-8.
7. Adams KF, Lindenfield J, Arnold J, et al. Executive summary: HFSA 2006 comprehensive heart failure practice guidelines. J Card Fail. 2006;12:10-38.
8. Publication Committee for the VMAC Investigators (Vasodilatation in the Management of Acute CHF). Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: a randomized controlled trial. JAMA. 2002;297:1531-40.
9. Peacock WF, Enerman CL, Silver MA, on behalf of the PROACTION Study Group. Am J Emerg Med. 2005;23:327-31.
10. Cotter G, Metzkor E, Kaluski E, et al. Randomized trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary edema. Lancet. 1998;351:389-93.
11. Sackner-Bernstein JD, Kowalski M, Fox M, Aaronson K. Short-term risk of death after treatment with nesiritide for decompensated heart failure: a pooled analysis of randomized controlled trials. JAMA. 2005;293:1900-5.
12. Sackner-Bernstein JD, Skopicki HA, Aaronson K. Risk of worsening renal function with nesiritide in patients with acutely decompensated heart failure. Circulation. 2005;111:1487-91.
13. Felker GM and O’Connor CM. Inotropic therapy for heart failure: An evidence-based approach. American Heart Journal. 2001; 142:393-401.
14. Abrahm WT, Adams KF, Fonarow GC, et al. In-hospital mortality in patients with acute decompensated heart failure requiring intravenous vasoactive medications: an analysis from the Acute Decompensated Heart Failure National Registry (ADHERE). J Am Coll Cardiol. 2005;46:57-64.
15. Burger AJ, Houton DP, LeJemtel T, et al. Effect of nesiritide and dobutamine on ventricular arrhythmias in the treatment of patients with acutely decompensated congestive heart failure: the PRECEDENT study. American Heart Journal. 2002;144:1102-8.
16. Liang CS, Sherman LG, Doherty JU, et al. Sustained improvement of cardiac function in patients with congestive heart failure after short-term infusion of dobutamine. Circulation. 1984;69:113-9.
17. Unverferth DV, Magorien RD, Lewis RP, et al. Long-term benefit of dobutamine in patients with congestive cardiomyopathy. American Heart Journal. 1980;100:622-30.
18. Cuffe MS, Califf RM, Adams KF Jr, et al. Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) Investigators. Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial. JAMA. 2002;287:1541-7.
19. Yamani MH, Haji SA, Starling RC, et al. Comparison of dobutamine-based and milrinone-based therapy for advanced decompensated congestive heart failure: Hemodynamic efficacy, clinical outcome, and economic impact. American Heart Journal. 2001;142:998-1002.
20. Shin, DD, Brandimarte F, De Luca L, et al. Review of current and investigational pharmacologic agents for acute heart failure syndromes. Am J Cardiol. 2007;99(suppl):4A-23A.
21. Kale P and Fang JC. Devices in acute heart failure. Crit Care Med. 2008;36(Suppl.):S121-128.

Case

A 72-year-old retired nurse with known nonischemic dilated cardiomyopathy with an ejection fraction of approximately 20% and status-post cardiac resynchronization therapy presents to the emergency department with dyspnea with minimal activity, three-pillow orthopnea, and paroxysmal nocturnal dyspnea.

She had been hospitalized twice during the past 60 days for similar symptoms. Her medications included losartan (20 mg po q daily), carvedilol (3.125 mg twice daily), spironolactone (25 mg daily), digoxin (0.125 mg daily), and furosemide (80 mg twice daily). Vital signs are notable for a blood pressure of 90/50 mmHg and an irregular pulse of 90 beats per minute. Physical examination is notable for marked jugular venous distension, lungs clear to auscultation bilaterally, biventricular heaves, a markedly displaced left ventricular point of maximal impulse, and a prominent S3 gallop.

Despite treatment with intravenous furosemide and temporary withdrawal of carvedilol, the patient remains symptomatic with persistent jugular venous distension.

Should she be given a vasoactive agent?

Overview

Acute heart failure syndrome (AHFS), defined as a gradual or rapid change in heart failure signs and symptoms, is the most common cause of hospitalization in the United States1. It is associated with an average in-hospital mortality of 4% to 5%, a 30-day mortality of 7% to11%, and a one-year mortality of 33%2.

In patients with previously established myocardial dysfunction, AHFS commonly reflects exacerbation of symptoms after a period of stability. The clinical presentation and severity of AHFS may range from mild volume overload to life-threatening cardiogenic shock and multi-organ failure unresponsive to pharmacologic therapy.2

Initial management of AHFS depends on definition of the patient’s hemodynamic profile. To guide initial therapy, classify patients into one of four hemodynamic profiles during a brief bedside assessment that relies on evaluation of filling pressures (wet or dry) and adequacy of perfusion (hot or cold) (see figure 1).3

Treating volume overload or elevated filling pressures generally begins with diuretics. Diuretics have been shown to provide symptomatic relief, though they have not yet been proven safe.4 Initial treatment can include a loop diuretic at a dose higher than the patient’s chronic dose, with intravenous dosing offering greater bio-absorption and rapidity in onset of action.5 If perfusion is inadequate, escalate therapy beyond diuretics to include vasoactive agents.

Review of the Data

The use of vasoactive medications is largely based on anecdotal experiences and physiologic assumptions rather than on adequately powered prospective randomized controlled trials.6 Vasoactive therapy includes vasodilator and inotropic support and is generally limited for use in patients with advanced disease not responding to standard medical treatment and diuresis. The physiologic premise rests in the expected improvement in ventricular filling pressures and cardiac output with reduction in afterload and/or preload. Vasodilators counteract vascular constriction, reducing both preload and afterload. Positive inotropic agents amplify cardiac output by increasing the strength of myocardial contraction.

Vasodilators

The Heart Failure Society of America (HFSA) 2006 Comprehensive Heart Failure Practice Guidelines state, “In the absence of symptomatic hypotension, intravenous vasodilators (nitroglycerin, nitroprusside, or nesiritide) may be considered as an addition to diuretic therapy for rapid improvement of congestive symptoms.”7 The clinical utility of nesiritide remains in question with clinical and hemodynamic improvement demonstrated in three randomized trials 8-10; but tempered against meta-analyses 11-12 of selected trials, demonstrating a non-significant trend toward increased kidney dysfunction and death within 30 days (35/485 [7.2%] vs. 15/377 [4.0%] patients; risk ratio from meta-analyses, 1.74; 95% confidence interval, 0.97-3.12; p=0.059). In a randomized trial of 489 in-patients with dyspnea at rest from AHFS, treatment with three hours of intravenous nesiritide resulted in a significant improvement in dyspnea compared with placebo (p=0.03). Similar improvement was observed with intravenous nitroglycerin and did not differ statistically from that observed with nesiritide.8 Nitroprusside, an attractive option among those with hypertension and cardiogenic pulmonary edema, is limited by the need for invasive hemodynamic monitoring and potential for either cyanide toxicity or worsening myocardial ischemia.

click for large version

Inotropes

Again, there is little evidence from adequately powered randomized controlled trials guiding the use of inotropes. Their use is generally limited to the following indications (see figure 2): (1) Short-term treatment for AHFS that is unresponsive to adequate doses of diuretics and especially when associated with systemic hypotension, (2) Bridge to recovery (as following myocarditis) or to definitive treatment (as with transplant), or (3) For palliation when symptomatic relief is the agreed upon goal.13 The HFSA 2006 guideline states: “Intravenous inotropes may be considered to relieve symptoms and improve end-organ function in patients with advanced HF characterized by left ventricle dilation, reduced left ventricular ejection fraction, and diminished peripheral perfusion or end-organ dysfunction, particularly if these patients have marginal systolic blood pressure, have symptomatic hypotension despite adequate filling pressures, or are unresponsive to, or intolerant of, intravenous vasodilators.”7

Dobutamine and milrinone are the most commonly used IV inotropes for the treatment of AHFS and increase contractility by increasing intracellular levels of cyclic adenylate monophosphate (cAMP). Dobutamine is a catechlamine agonist that increases cAMP production through stimulation of adenylate cyclase. Milrinone selectively inhibits phosphodiesterase III, which catalyzes the breakdown of cAMP.

Despite their frequent use when traditional treatments have failed, the data supporting the use of dobutamine and milrinone is limited. The largest registry of patients with AHFS to date associated excess mortality with intravenous inotrope use compared to nitroglycerin or nesiritide.14 In a study population of 255 patients randomized to receive either intravenous nesiritide or intravenous dobutamine, Burger et al.15 demonstrated that dobutamine significantly increased the mean number of ventricular tachycardia events per 24 hours (p=0.001), suggesting increased arrhythmogenicity associated with inotrope use. Nonetheless, in a randomized trial of 15 patients admitted with AHFS, functional class improved in six of eight dobutamine-treated patients, but in only two of seven patients treated with placebo, suggesting clinical improvement as a consequence of inotropic stimulation.16 Unverferth et al. demonstrated a similar sustained functional improvement up to 10 weeks following a 72-hour infusion of intravenous dobutamine. 17

The Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure trial (OPTIME-CHF), randomized 951 patients with AHFS to receive either intravenous milrinone or placebo within 48 hours of hospitalization.18 Compared to placebo, milrinone was associated with a significant increase in sustained hypotension requiring intervention (10.7% vs. 3.2%; p<.001) and new atrial arrhythmias (4.6% vs. 1.5%; p=0.004), along with a non-significant trend toward increased mortality (3.8% vs. 2.3%; p=0.19). However, as measured by a visual analog scale, milrinone-treated patients reported feeling better than those treated with placebo at 30 days post-randomization (p=0.02).

Although there are not randomized data comparing the efficacy of milrinone and dobutamine in AHFS, a retrospective analysis of 329 patients compared the hemodynamic and clinical effects of these two inotropes.19 Milrinone consistently was associated with a more favorable hemodynamic response, including lower systemic vascular resistance (p=0.01); lower pulmonary artery wedge pressure (p<0.001); larger percentage increase in cardiac index (p=0.03); and larger percentage decrease in pulmonary vascular resistance (p=0.0001). In-hospital mortality (dobutamine 7.8% vs. milrinone 10%) was not significantly different.

Conclusion

Clearly, vasoactive and inotropic agents are available when AHFS is refractory to traditional diuresis and may offer short-term symptomatic relief, palliation in the context of end-of-life care, or bridge to recovery or more definitive treatment. Unfortunately, sufficient and robust evidence that supports the safety and efficacy of such agents is lacking and their use is largely guided by historical practices, clinical experience, and anticipation of theoretic physiologic changes. While adequately powered prospective randomized data emerge, newer agents such as vasopressin receptor antagonists, cardiac myosin activators, calcium sensitizers, and adenosine-receptor antagonists will offer additional pharmacologic options.20 When continued pharmacologic support becomes ineffective, device therapy is available to aid in the treatment of AHFS and includes ultrafiltration to reduce filling pressures and intra-aortic balloon pump counterpulsation or left ventricular assist device placement for pharmacologically resistant cardiogenic shock.21

Back to the Case

Despite maximal medical therapy for her chronic heart failure and biventricular pacing, the patient continued to have markedly limited functional status and repeated hospitalizations for AHFS. Given her advanced age and poor nutritional status, she was not a candidate for cardiac transplantation or placement of a left ventricular assist device. To allow for palliative tailored therapy, right heart catheterization was performed. Right heart catheterization revealed elevated filling pressures, as follows: right atrium, 20 mmHg; pulmonary artery, 63/34 mmHg (mean 47 mmHg); and pulmonary capillary wedge, 29 mmHg. Her mixed venous oxygen saturation was only 41% with a calculated cardiac output of 2.9 liters per minute and cardiac index of 2 liters per minute per meter squared.

As she expressed symptomatic relief as her goal, she was started on intravenous milrinone at 0.2 micrograms per kilogram per minute. This was done with the understanding her symptoms would likely would improve, at the expense of worsening longevity and prognosis. With uptitration of her intravenous milrinone and a continuous infusion of furosemide, she demonstrated the following filling pressures within 24 hours: right atrium, 18 mmHg; pulmonary artery, 63/33 mmHg (mean 43 mmHg); and pulmonary capillary wedge, 24. Importantly, her mixed venous oxygen saturation improved to 68% with a calculated cardiac output of 3.4 liters per minute and cardiac index of 2.4 liters per minute per meter squared. These favorable hemodynamic changes were accompanied by modest improvement in symptoms. After continued intravenous diuresis, she was transitioned back to an oral diuretic regimen and was ultimately discharged to home with a continuous infusion of milrinone for palliation. TH

Drs. Vaishnava, McKean, Nohria, and Baughman are from Brigham and Women’s Hospital and Harvard Medical School in Boston, Mass.

REFERENCES:

1. Thom T, Haase N, Rosamond W, et al. Heart disease and stroke statistics – 2006 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2006;113:85-151.
2. Iong P, Vowinckel E, Liu PP, Gong Y, Tu JV. Prognosis and determinants of survival in patients newly hospitalized for heart failure: a population-based study. Arch Intern Med. 2002;162:1689-94.
3. Nohria A, Lewis EF, Stevenson LW. Medical management of advanced heart failure. JAMA. 2002;287;628-40.
4. Faris R, Flather MD, Purcell H, et al. Diuretics for heart failure. Cochrane Database Syst Rev. 2006;1;CD003838.
5. Wang DJ and Gottlieb SS. Diuretics: Still the mainstay of treatment. Crit Care Med. 2008;36(Suppl.):S89-S94.
6. Fares WH. Management of acute decompensated heart failure in an evidence-based era: What is the evidence behind the current standard of care? Heart & Lung. 2008;37(3):173-8.
7. Adams KF, Lindenfield J, Arnold J, et al. Executive summary: HFSA 2006 comprehensive heart failure practice guidelines. J Card Fail. 2006;12:10-38.
8. Publication Committee for the VMAC Investigators (Vasodilatation in the Management of Acute CHF). Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: a randomized controlled trial. JAMA. 2002;297:1531-40.
9. Peacock WF, Enerman CL, Silver MA, on behalf of the PROACTION Study Group. Am J Emerg Med. 2005;23:327-31.
10. Cotter G, Metzkor E, Kaluski E, et al. Randomized trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary edema. Lancet. 1998;351:389-93.
11. Sackner-Bernstein JD, Kowalski M, Fox M, Aaronson K. Short-term risk of death after treatment with nesiritide for decompensated heart failure: a pooled analysis of randomized controlled trials. JAMA. 2005;293:1900-5.
12. Sackner-Bernstein JD, Skopicki HA, Aaronson K. Risk of worsening renal function with nesiritide in patients with acutely decompensated heart failure. Circulation. 2005;111:1487-91.
13. Felker GM and O’Connor CM. Inotropic therapy for heart failure: An evidence-based approach. American Heart Journal. 2001; 142:393-401.
14. Abrahm WT, Adams KF, Fonarow GC, et al. In-hospital mortality in patients with acute decompensated heart failure requiring intravenous vasoactive medications: an analysis from the Acute Decompensated Heart Failure National Registry (ADHERE). J Am Coll Cardiol. 2005;46:57-64.
15. Burger AJ, Houton DP, LeJemtel T, et al. Effect of nesiritide and dobutamine on ventricular arrhythmias in the treatment of patients with acutely decompensated congestive heart failure: the PRECEDENT study. American Heart Journal. 2002;144:1102-8.
16. Liang CS, Sherman LG, Doherty JU, et al. Sustained improvement of cardiac function in patients with congestive heart failure after short-term infusion of dobutamine. Circulation. 1984;69:113-9.
17. Unverferth DV, Magorien RD, Lewis RP, et al. Long-term benefit of dobutamine in patients with congestive cardiomyopathy. American Heart Journal. 1980;100:622-30.
18. Cuffe MS, Califf RM, Adams KF Jr, et al. Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) Investigators. Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial. JAMA. 2002;287:1541-7.
19. Yamani MH, Haji SA, Starling RC, et al. Comparison of dobutamine-based and milrinone-based therapy for advanced decompensated congestive heart failure: Hemodynamic efficacy, clinical outcome, and economic impact. American Heart Journal. 2001;142:998-1002.
20. Shin, DD, Brandimarte F, De Luca L, et al. Review of current and investigational pharmacologic agents for acute heart failure syndromes. Am J Cardiol. 2007;99(suppl):4A-23A.
21. Kale P and Fang JC. Devices in acute heart failure. Crit Care Med. 2008;36(Suppl.):S121-128.

Hospitalists who work in teaching hospitals need to understand the teaching physician (TP) rules, to know what qualifies for payment and how to document to receive that payment. TP services are payable when they are furnished by a physician who is not a resident or a resident with a teaching physician physically present during the critical or key portions of the service.

This article will focus on the documentation guidelines for inpatient services provided by the hospitalist in a teaching setting.

Evaluation and Management Services

Teaching physicians participate in evaluation and management (E/M) services with residents in several different ways. Below, three scenarios discuss documentation requirements:

Scenario One: The Stand-Alone Service. In this scenario, the teaching physician independently performs the entire service (i.e., all required elements of the billed visit) though the resident also may have seen the patient that same day. The TP may choose to document as if the care took place in a non-teaching setting. This documentation stands alone and independently supports the reported visit level.

Alternatively, the teaching physician may use the resident’s note. He or she does this by first documenting involvement in patient management and performance of the critical or key portion(s) of the service, and then linking to the resident’s note. The teaching physician selects the visit level based on the combined documentation (i.e., that of the teaching physician and the resident).

When referencing resident documentation, the teaching physician should use Medicare-approved linkage statements. Common examples include the following:

• “I performed a history and physical examination of the patient and discussed his management with the resident. I reviewed the resident’s note and agree with the documented findings and plan of care.”
• “I saw and evaluated the patient. I agree with the findings and the plan of care as documented in the resident’s note.”
• “I saw and examined the patient. I agree with the resident’s note except the heart murmur is louder than documented, so I will obtain an echo to evaluate.”

Although all of these examples are acceptable, the last one best identifies the teaching physician’s involvement in patient management, which is a requirement of TP documentation.

Scenario Two: The Supervised Service. In this scenario, resident and teaching physician provide services simultaneously. The teaching physician either may supervise the resident’s performance of required service elements or personally perform some of them.

Documentation includes information about the teaching physician’s presence during the encounter, performance of the critical or key portions of the service and involvement in patient management, as well as a reference to the resident’s note. As in scenario one, the teaching physician selects the visit level based on the combined documentation.

Teaching physician statements associated with scenario two and accepted by Medicare reviewers include the following:

• “I was present with the resident during the history and exam. I discussed the case with the resident and agree with the findings and plan as documented in the resident’s note.”
• “I saw the patient with the resident and agree with the resident’s findings and plan.”

Scenario two examples contain generalized statements considered acceptable for billing under teaching physician rules. Documenting patient-specific elements of the assessment and plan, however, not only demonstrate teaching physician involvement in patient care, but also evidence better quality of care.

Scenario Three: The Shared Service. In this case, the resident performs a portion or all of the required service elements without the teaching physician present and then documents the services. The teaching physician independently performs only the critical, or key, portions of the service and, as appropriate, discusses the case with the resident. Similar to scenario two, the TP references the resident’s note and documents presence during the encounter, performance of the critical or key portions of the service and involvement in patient management.

Remember, the teaching physician can not link to a resident note that does not exist. In other words, if the resident’s note is not available when the teaching physician is documenting, the note cannot be considered for billing purposes. When documented appropriately, as in the scenarios above, the teaching physician selects the visit level based on the combined documentation.

Medicare-approved linkage statements for use by teaching physicians in this scenario include the following:

• “I saw and evaluated the patient. I reviewed the resident’s note and agree, except that the picture is more consistent with pericarditis than myocardial ischemia. Will begin NSAIDs.”
• “I saw and evaluated the patient. Discussed with resident and agree with resident’s findings and plan as documented in the resident’s note.”
• “See resident’s note for details. I saw and evaluated the patient and agree with the resident’s finding and plans as written.”
• “I saw and evaluated the patient. Agree with resident’s note but lower extremities are weaker, now 3/5; MRI of L/S spine today.”

Documentation of teaching physician presence and participation provided solely by the resident is not sufficient to support the teaching physician service. Some examples of unacceptable documentation include:

• “Agree with above,” followed by legible countersignature or identity;
• “Rounded, Reviewed, Agree,” followed by legible countersignature or identity;
• “Discussed with resident. Agree,” followed by legible countersignature or identity;
• “Seen and agree,” followed by legible countersignature or identity;
• “Patient seen and evaluated,” followed by legible countersignature or identity; and
• Legible countersignature or identity alone.

Time-Based Services

Time-based E/M services require the teaching physician be present for the entire period for which the claim is made. Medical record documentation should reflect the teaching physician’s total visit time (i.e., spent on the unit/floor for inpatient services), including face-to-face time with the patient.

Time spent by the resident without the presence of the teaching physician does not count toward the teaching physician’s time, nor does time the TP spends teaching activities unrelated to patient care. Examples of time-based services typically provided by hospitalists include:

• Critical-care services (CPT codes 99291-99292);
• Hospital discharge day management (CPT codes 99238-99239);
• E/M codes in which counseling and/or coordination of care dominates (more than 50% of) the encounter, and time is considered the key or controlling factor to qualify for a particular level of E/M service; and
• Prolonged services (CPT codes 99358-99359).

Surgical Services

Surgical services, which are defined as minor or major, also are subject to teaching physician rules. Teaching physician regulations identify minor procedures as those that take five minutes or less to complete and involve relatively little decision making once the need for the service is determined. Appropriate billing and payment hinges on the teaching physician’s presence for the entire procedure. Documentation should include a statement of presence, written and signed by the teaching physician.

Services that require more than five minutes are considered major surgical services, requiring teaching physician presence only during the (physician-determined) critical and key portions of the procedure. However, the teaching physician must be available to return to the procedure area during the surgery’s entirety, and not be involved in another procedure. Arrangements must be made to have another qualified physician available should the teaching physician get called away. TH

Carol Pohlig is a billing and coding expert with the University of Pennsylvania Medical Center, Philadelphia. She also is on the faculty of SHM’s inpatient coding course.

References:

1. Centers for Medicare & Medicaid Services. Medicare Claims Processing Manual: Chapter 12, Section 100, www.cms.hhs.gov/manuals/downloads/clm104c12.pdf.

2. Centers for Medicare & Medicaid Services. Medicare Benefit Policy Manual: Chapter 15, Section 30.2, www.cms.hhs.gov/manuals/Downloads/bp102c15.pdf.

3. Centers for Medicare & Medicaid Services. Guidelines for Teaching Physicians, Interns, Residents, www.cms.hhs.gov/MLNProducts/downloads/gdelinesteachgresfctsht.pdf.

4. Manaker, S. Teaching Physician Regulations. Coding for Chest Medicine 2008, American College of Chest Physicians, 2008; 279-285.

5. Pohlig, C. Evaluation & Management Services: An Overview. Coding for Chest Medicine 2008, American College of Chest Physicians, 2008;57-69.

6. American Medical Association. cpt® 2008, Current Procedural Terminology Professional Edition. American Medical Association, 2007; 9-16.

Hospitalists who work in teaching hospitals need to understand the teaching physician (TP) rules, to know what qualifies for payment and how to document to receive that payment. TP services are payable when they are furnished by a physician who is not a resident or a resident with a teaching physician physically present during the critical or key portions of the service.

This article will focus on the documentation guidelines for inpatient services provided by the hospitalist in a teaching setting.

Evaluation and Management Services

Teaching physicians participate in evaluation and management (E/M) services with residents in several different ways. Below, three scenarios discuss documentation requirements:

Scenario One: The Stand-Alone Service. In this scenario, the teaching physician independently performs the entire service (i.e., all required elements of the billed visit) though the resident also may have seen the patient that same day. The TP may choose to document as if the care took place in a non-teaching setting. This documentation stands alone and independently supports the reported visit level.

Alternatively, the teaching physician may use the resident’s note. He or she does this by first documenting involvement in patient management and performance of the critical or key portion(s) of the service, and then linking to the resident’s note. The teaching physician selects the visit level based on the combined documentation (i.e., that of the teaching physician and the resident).

When referencing resident documentation, the teaching physician should use Medicare-approved linkage statements. Common examples include the following:

• “I performed a history and physical examination of the patient and discussed his management with the resident. I reviewed the resident’s note and agree with the documented findings and plan of care.”
• “I saw and evaluated the patient. I agree with the findings and the plan of care as documented in the resident’s note.”
• “I saw and examined the patient. I agree with the resident’s note except the heart murmur is louder than documented, so I will obtain an echo to evaluate.”

Although all of these examples are acceptable, the last one best identifies the teaching physician’s involvement in patient management, which is a requirement of TP documentation.

Scenario Two: The Supervised Service. In this scenario, resident and teaching physician provide services simultaneously. The teaching physician either may supervise the resident’s performance of required service elements or personally perform some of them.

Documentation includes information about the teaching physician’s presence during the encounter, performance of the critical or key portions of the service and involvement in patient management, as well as a reference to the resident’s note. As in scenario one, the teaching physician selects the visit level based on the combined documentation.

Teaching physician statements associated with scenario two and accepted by Medicare reviewers include the following:

• “I was present with the resident during the history and exam. I discussed the case with the resident and agree with the findings and plan as documented in the resident’s note.”
• “I saw the patient with the resident and agree with the resident’s findings and plan.”

Scenario two examples contain generalized statements considered acceptable for billing under teaching physician rules. Documenting patient-specific elements of the assessment and plan, however, not only demonstrate teaching physician involvement in patient care, but also evidence better quality of care.

Scenario Three: The Shared Service. In this case, the resident performs a portion or all of the required service elements without the teaching physician present and then documents the services. The teaching physician independently performs only the critical, or key, portions of the service and, as appropriate, discusses the case with the resident. Similar to scenario two, the TP references the resident’s note and documents presence during the encounter, performance of the critical or key portions of the service and involvement in patient management.

Remember, the teaching physician can not link to a resident note that does not exist. In other words, if the resident’s note is not available when the teaching physician is documenting, the note cannot be considered for billing purposes. When documented appropriately, as in the scenarios above, the teaching physician selects the visit level based on the combined documentation.

Medicare-approved linkage statements for use by teaching physicians in this scenario include the following:

• “I saw and evaluated the patient. I reviewed the resident’s note and agree, except that the picture is more consistent with pericarditis than myocardial ischemia. Will begin NSAIDs.”
• “I saw and evaluated the patient. Discussed with resident and agree with resident’s findings and plan as documented in the resident’s note.”
• “See resident’s note for details. I saw and evaluated the patient and agree with the resident’s finding and plans as written.”
• “I saw and evaluated the patient. Agree with resident’s note but lower extremities are weaker, now 3/5; MRI of L/S spine today.”

Documentation of teaching physician presence and participation provided solely by the resident is not sufficient to support the teaching physician service. Some examples of unacceptable documentation include:

• “Agree with above,” followed by legible countersignature or identity;
• “Rounded, Reviewed, Agree,” followed by legible countersignature or identity;
• “Discussed with resident. Agree,” followed by legible countersignature or identity;
• “Seen and agree,” followed by legible countersignature or identity;
• “Patient seen and evaluated,” followed by legible countersignature or identity; and
• Legible countersignature or identity alone.

Time-Based Services

Time-based E/M services require the teaching physician be present for the entire period for which the claim is made. Medical record documentation should reflect the teaching physician’s total visit time (i.e., spent on the unit/floor for inpatient services), including face-to-face time with the patient.

Time spent by the resident without the presence of the teaching physician does not count toward the teaching physician’s time, nor does time the TP spends teaching activities unrelated to patient care. Examples of time-based services typically provided by hospitalists include:

• Critical-care services (CPT codes 99291-99292);
• Hospital discharge day management (CPT codes 99238-99239);
• E/M codes in which counseling and/or coordination of care dominates (more than 50% of) the encounter, and time is considered the key or controlling factor to qualify for a particular level of E/M service; and
• Prolonged services (CPT codes 99358-99359).

Surgical Services

Surgical services, which are defined as minor or major, also are subject to teaching physician rules. Teaching physician regulations identify minor procedures as those that take five minutes or less to complete and involve relatively little decision making once the need for the service is determined. Appropriate billing and payment hinges on the teaching physician’s presence for the entire procedure. Documentation should include a statement of presence, written and signed by the teaching physician.

Services that require more than five minutes are considered major surgical services, requiring teaching physician presence only during the (physician-determined) critical and key portions of the procedure. However, the teaching physician must be available to return to the procedure area during the surgery’s entirety, and not be involved in another procedure. Arrangements must be made to have another qualified physician available should the teaching physician get called away. TH

Carol Pohlig is a billing and coding expert with the University of Pennsylvania Medical Center, Philadelphia. She also is on the faculty of SHM’s inpatient coding course.

References:

1. Centers for Medicare & Medicaid Services. Medicare Claims Processing Manual: Chapter 12, Section 100, www.cms.hhs.gov/manuals/downloads/clm104c12.pdf.

2. Centers for Medicare & Medicaid Services. Medicare Benefit Policy Manual: Chapter 15, Section 30.2, www.cms.hhs.gov/manuals/Downloads/bp102c15.pdf.

3. Centers for Medicare & Medicaid Services. Guidelines for Teaching Physicians, Interns, Residents, www.cms.hhs.gov/MLNProducts/downloads/gdelinesteachgresfctsht.pdf.

4. Manaker, S. Teaching Physician Regulations. Coding for Chest Medicine 2008, American College of Chest Physicians, 2008; 279-285.

5. Pohlig, C. Evaluation & Management Services: An Overview. Coding for Chest Medicine 2008, American College of Chest Physicians, 2008;57-69.

6. American Medical Association. cpt® 2008, Current Procedural Terminology Professional Edition. American Medical Association, 2007; 9-16.

Hospitalists who work in teaching hospitals need to understand the teaching physician (TP) rules, to know what qualifies for payment and how to document to receive that payment. TP services are payable when they are furnished by a physician who is not a resident or a resident with a teaching physician physically present during the critical or key portions of the service.

This article will focus on the documentation guidelines for inpatient services provided by the hospitalist in a teaching setting.

Evaluation and Management Services

Teaching physicians participate in evaluation and management (E/M) services with residents in several different ways. Below, three scenarios discuss documentation requirements:

Scenario One: The Stand-Alone Service. In this scenario, the teaching physician independently performs the entire service (i.e., all required elements of the billed visit) though the resident also may have seen the patient that same day. The TP may choose to document as if the care took place in a non-teaching setting. This documentation stands alone and independently supports the reported visit level.

Alternatively, the teaching physician may use the resident’s note. He or she does this by first documenting involvement in patient management and performance of the critical or key portion(s) of the service, and then linking to the resident’s note. The teaching physician selects the visit level based on the combined documentation (i.e., that of the teaching physician and the resident).

When referencing resident documentation, the teaching physician should use Medicare-approved linkage statements. Common examples include the following:

• “I performed a history and physical examination of the patient and discussed his management with the resident. I reviewed the resident’s note and agree with the documented findings and plan of care.”
• “I saw and evaluated the patient. I agree with the findings and the plan of care as documented in the resident’s note.”
• “I saw and examined the patient. I agree with the resident’s note except the heart murmur is louder than documented, so I will obtain an echo to evaluate.”

Although all of these examples are acceptable, the last one best identifies the teaching physician’s involvement in patient management, which is a requirement of TP documentation.

Scenario Two: The Supervised Service. In this scenario, resident and teaching physician provide services simultaneously. The teaching physician either may supervise the resident’s performance of required service elements or personally perform some of them.

Documentation includes information about the teaching physician’s presence during the encounter, performance of the critical or key portions of the service and involvement in patient management, as well as a reference to the resident’s note. As in scenario one, the teaching physician selects the visit level based on the combined documentation.

Teaching physician statements associated with scenario two and accepted by Medicare reviewers include the following:

• “I was present with the resident during the history and exam. I discussed the case with the resident and agree with the findings and plan as documented in the resident’s note.”
• “I saw the patient with the resident and agree with the resident’s findings and plan.”

Scenario two examples contain generalized statements considered acceptable for billing under teaching physician rules. Documenting patient-specific elements of the assessment and plan, however, not only demonstrate teaching physician involvement in patient care, but also evidence better quality of care.

Scenario Three: The Shared Service. In this case, the resident performs a portion or all of the required service elements without the teaching physician present and then documents the services. The teaching physician independently performs only the critical, or key, portions of the service and, as appropriate, discusses the case with the resident. Similar to scenario two, the TP references the resident’s note and documents presence during the encounter, performance of the critical or key portions of the service and involvement in patient management.

Remember, the teaching physician can not link to a resident note that does not exist. In other words, if the resident’s note is not available when the teaching physician is documenting, the note cannot be considered for billing purposes. When documented appropriately, as in the scenarios above, the teaching physician selects the visit level based on the combined documentation.

Medicare-approved linkage statements for use by teaching physicians in this scenario include the following:

• “I saw and evaluated the patient. I reviewed the resident’s note and agree, except that the picture is more consistent with pericarditis than myocardial ischemia. Will begin NSAIDs.”
• “I saw and evaluated the patient. Discussed with resident and agree with resident’s findings and plan as documented in the resident’s note.”
• “See resident’s note for details. I saw and evaluated the patient and agree with the resident’s finding and plans as written.”
• “I saw and evaluated the patient. Agree with resident’s note but lower extremities are weaker, now 3/5; MRI of L/S spine today.”

Documentation of teaching physician presence and participation provided solely by the resident is not sufficient to support the teaching physician service. Some examples of unacceptable documentation include:

• “Agree with above,” followed by legible countersignature or identity;
• “Rounded, Reviewed, Agree,” followed by legible countersignature or identity;
• “Discussed with resident. Agree,” followed by legible countersignature or identity;
• “Seen and agree,” followed by legible countersignature or identity;
• “Patient seen and evaluated,” followed by legible countersignature or identity; and
• Legible countersignature or identity alone.

Time-Based Services

Time-based E/M services require the teaching physician be present for the entire period for which the claim is made. Medical record documentation should reflect the teaching physician’s total visit time (i.e., spent on the unit/floor for inpatient services), including face-to-face time with the patient.

Time spent by the resident without the presence of the teaching physician does not count toward the teaching physician’s time, nor does time the TP spends teaching activities unrelated to patient care. Examples of time-based services typically provided by hospitalists include:

• Critical-care services (CPT codes 99291-99292);
• Hospital discharge day management (CPT codes 99238-99239);
• E/M codes in which counseling and/or coordination of care dominates (more than 50% of) the encounter, and time is considered the key or controlling factor to qualify for a particular level of E/M service; and
• Prolonged services (CPT codes 99358-99359).

Surgical Services

Surgical services, which are defined as minor or major, also are subject to teaching physician rules. Teaching physician regulations identify minor procedures as those that take five minutes or less to complete and involve relatively little decision making once the need for the service is determined. Appropriate billing and payment hinges on the teaching physician’s presence for the entire procedure. Documentation should include a statement of presence, written and signed by the teaching physician.

Services that require more than five minutes are considered major surgical services, requiring teaching physician presence only during the (physician-determined) critical and key portions of the procedure. However, the teaching physician must be available to return to the procedure area during the surgery’s entirety, and not be involved in another procedure. Arrangements must be made to have another qualified physician available should the teaching physician get called away. TH

Carol Pohlig is a billing and coding expert with the University of Pennsylvania Medical Center, Philadelphia. She also is on the faculty of SHM’s inpatient coding course.

References:

1. Centers for Medicare & Medicaid Services. Medicare Claims Processing Manual: Chapter 12, Section 100, www.cms.hhs.gov/manuals/downloads/clm104c12.pdf.

2. Centers for Medicare & Medicaid Services. Medicare Benefit Policy Manual: Chapter 15, Section 30.2, www.cms.hhs.gov/manuals/Downloads/bp102c15.pdf.

3. Centers for Medicare & Medicaid Services. Guidelines for Teaching Physicians, Interns, Residents, www.cms.hhs.gov/MLNProducts/downloads/gdelinesteachgresfctsht.pdf.

4. Manaker, S. Teaching Physician Regulations. Coding for Chest Medicine 2008, American College of Chest Physicians, 2008; 279-285.

5. Pohlig, C. Evaluation & Management Services: An Overview. Coding for Chest Medicine 2008, American College of Chest Physicians, 2008;57-69.

6. American Medical Association. cpt® 2008, Current Procedural Terminology Professional Edition. American Medical Association, 2007; 9-16.

Congress made history in July when it passed legislation that makes Medicare’s voluntary pay-for-reporting program permanent.

The program, the Physician Quality Reporting Initiative, or PQRI, which began in 2007 as a six-month trial and was continued through 2008, rewards physicians who successfully report on specific applicable quality measures with a cash bonus. The new bill, the Medicare Improvement for Patients and Providers Act (MIPPA), extends the Centers for Medicare and Medicaid (CMS) program beyond 2010.

“PQRI is now a permanent program, even though the details have only been provided through 2010,” says Michael Rapp, MD, of the CMS Office of Clinical Standards and Quality.

Here, is a look at PQRI past, present, and future, from a hospitalist’s point of view.

Pay-for-Performance Pilot Proves Worthwhile

In August, CMS released statistics on that first pay-for-reporting period. During the trial, 101,138 physicians submitted a quality-data code. Of those, 70,207 reported on at least one measure, and 56,722 earned a bonus.

Asked about those numbers, Patrick J. Torcson, MD, MMM, FACP, director of hospital medicine at St. Tammany Parish Hospital in Covington, La., and chair of SHM’s Performance and Standards Committee, says: “I think the folks at Medicare were pleased with that level of participation. This data helped convince them that the program should be permanent.”

What to Expect in 2009

The PQRI for 2009 is subject to revisions until the 2009 Physician Fee Schedule Final Rule is published sometime around Nov. 1. (Find the latest information on CMS Web site at www.cms.hhs.gov/pqri.) A number of proposed enhancements make it attractive and important to physicians, Dr. Torcson says.

CMS proposed 175 quality measures for physicians to report on, and MIPPA boosts payment for successful reporting of data on those measures. For 2009 and 2010, physicians who participate in the PQRI can earn an incentive payment of 2% (up from 1.5%) of their total allowed charges for Physician Fee Schedule (PFS) covered professional services.

However, except for a bigger check from CMS, hospitalists who currently report may not see much difference next year. “Overall, for hospitalists, PQRI will look pretty similar to 2007 and 2008,” Dr. Torcson warns. “The bonus is going to increase and the measures will be the same. That means that all of the background and education that SHM has provided on PQRI reporting remains relevant.”

One addition for 2009 is the use of patient registries to avoid claims systems for certain outpatient measures. “I don’t see the registry-reporting option being available to hospitalists in the short term,” Dr. Torcson says, “but it’s worth watching for the future.”

Beginning in 2009 and continuing through the next four years, Medicare also will provide incentive payments to eligible professionals who are successful electronic prescribers. (See the “Public Policy” article on p. 15 of the September 2008 The Hospitalist.) The e-prescribing measure in the 2008 PQRI will be removed for next year and used wholesale for a separate pay-for-reporting initiative pending changes from the Department of Health & Human Services. Unfortunately, none of the 2008 coding specifications for e-prescribing are available for hospitalist reporting.

“A lot of [the PQRI] measures have been created from the perspective of the cottage-industry model of an office-based private practice,” Dr. Torcson explains. “This 2008 (e-prescribing) measure was geared for an office-based physician practice—and the unforeseen consequence of the measure is that it’s not inclusive of patients being discharged from the hospital.”

Where Hospital Medicine Fits

By now, hospitalists should be resigned to the idea that many measures in PQRI don’t apply to their patients. However, SHM continues to work toward more inclusion for hospital-based physicians, by commenting on proposed rules and participating in the National Quality Forum and the American Medical Association’s Physician Consortium for Performance Improvement.

“We have been advocating for including performance measures for care processes, including transitions of care,” Dr. Torcson says. “This will probably come into play more in 2010 than 2009.”

SHM also has submitted comments on the proposed e-prescribing measures. Dr. Torcson says the organization is lobbying to make e-prescribing applicable to all hospital-based physicians, including ER doctors, and for discharged patients. “We want the whole process to harmonize with a comprehensive and safe discharge process that includes medication reconciliation,” he says.

To Report or Not to Report?

Regardless of whether lobbying efforts succeed in making more reporting applicable to hospital medicine, should groups start reporting in 2009? “It’s going to be a tough decision,” Dr. Torcson admits. “There’s a pretty significant investment in time and infrastructure to set this up. For the groups I know, the return on investment was negative.” In other words, PQRI does not pay for itself in a hospital medicine setting.

He says any hospital medicine group that wants to report should have in place a computerized system, and be willing to start slowly. “I’m convinced that it’s going to take an electronic coding/documentation system, as well as designated support staff within the hospital medicine group to pull it off,” he says. “This almost requires a full-time person.”

Dr. Torcson recommends starting with the reporting of three or four measures. “If you’re using a manual process or a homegrown system,” he says, “then the fewer measures the better, in terms of doing PQRI right to reach the 80% threshold.”

If you’re interested in reporting under the 2009 PQRI, go to SHM’s Web site at www.hospitalmedicine.org/ and type “PQRI 2008” into the advanced search bar. The article, “Information on PQRI 2008,” from May 17, 2007, provides important details about the program, including which measures apply to hospitalists. TH

Jane Jerrard is a medical writer based in Chicago.

Congress made history in July when it passed legislation that makes Medicare’s voluntary pay-for-reporting program permanent.

The program, the Physician Quality Reporting Initiative, or PQRI, which began in 2007 as a six-month trial and was continued through 2008, rewards physicians who successfully report on specific applicable quality measures with a cash bonus. The new bill, the Medicare Improvement for Patients and Providers Act (MIPPA), extends the Centers for Medicare and Medicaid (CMS) program beyond 2010.

“PQRI is now a permanent program, even though the details have only been provided through 2010,” says Michael Rapp, MD, of the CMS Office of Clinical Standards and Quality.

Here, is a look at PQRI past, present, and future, from a hospitalist’s point of view.

Pay-for-Performance Pilot Proves Worthwhile

In August, CMS released statistics on that first pay-for-reporting period. During the trial, 101,138 physicians submitted a quality-data code. Of those, 70,207 reported on at least one measure, and 56,722 earned a bonus.

Asked about those numbers, Patrick J. Torcson, MD, MMM, FACP, director of hospital medicine at St. Tammany Parish Hospital in Covington, La., and chair of SHM’s Performance and Standards Committee, says: “I think the folks at Medicare were pleased with that level of participation. This data helped convince them that the program should be permanent.”

What to Expect in 2009

The PQRI for 2009 is subject to revisions until the 2009 Physician Fee Schedule Final Rule is published sometime around Nov. 1. (Find the latest information on CMS Web site at www.cms.hhs.gov/pqri.) A number of proposed enhancements make it attractive and important to physicians, Dr. Torcson says.

CMS proposed 175 quality measures for physicians to report on, and MIPPA boosts payment for successful reporting of data on those measures. For 2009 and 2010, physicians who participate in the PQRI can earn an incentive payment of 2% (up from 1.5%) of their total allowed charges for Physician Fee Schedule (PFS) covered professional services.

However, except for a bigger check from CMS, hospitalists who currently report may not see much difference next year. “Overall, for hospitalists, PQRI will look pretty similar to 2007 and 2008,” Dr. Torcson warns. “The bonus is going to increase and the measures will be the same. That means that all of the background and education that SHM has provided on PQRI reporting remains relevant.”

One addition for 2009 is the use of patient registries to avoid claims systems for certain outpatient measures. “I don’t see the registry-reporting option being available to hospitalists in the short term,” Dr. Torcson says, “but it’s worth watching for the future.”

Beginning in 2009 and continuing through the next four years, Medicare also will provide incentive payments to eligible professionals who are successful electronic prescribers. (See the “Public Policy” article on p. 15 of the September 2008 The Hospitalist.) The e-prescribing measure in the 2008 PQRI will be removed for next year and used wholesale for a separate pay-for-reporting initiative pending changes from the Department of Health & Human Services. Unfortunately, none of the 2008 coding specifications for e-prescribing are available for hospitalist reporting.

“A lot of [the PQRI] measures have been created from the perspective of the cottage-industry model of an office-based private practice,” Dr. Torcson explains. “This 2008 (e-prescribing) measure was geared for an office-based physician practice—and the unforeseen consequence of the measure is that it’s not inclusive of patients being discharged from the hospital.”

Where Hospital Medicine Fits

By now, hospitalists should be resigned to the idea that many measures in PQRI don’t apply to their patients. However, SHM continues to work toward more inclusion for hospital-based physicians, by commenting on proposed rules and participating in the National Quality Forum and the American Medical Association’s Physician Consortium for Performance Improvement.

“We have been advocating for including performance measures for care processes, including transitions of care,” Dr. Torcson says. “This will probably come into play more in 2010 than 2009.”

SHM also has submitted comments on the proposed e-prescribing measures. Dr. Torcson says the organization is lobbying to make e-prescribing applicable to all hospital-based physicians, including ER doctors, and for discharged patients. “We want the whole process to harmonize with a comprehensive and safe discharge process that includes medication reconciliation,” he says.

To Report or Not to Report?

Regardless of whether lobbying efforts succeed in making more reporting applicable to hospital medicine, should groups start reporting in 2009? “It’s going to be a tough decision,” Dr. Torcson admits. “There’s a pretty significant investment in time and infrastructure to set this up. For the groups I know, the return on investment was negative.” In other words, PQRI does not pay for itself in a hospital medicine setting.

He says any hospital medicine group that wants to report should have in place a computerized system, and be willing to start slowly. “I’m convinced that it’s going to take an electronic coding/documentation system, as well as designated support staff within the hospital medicine group to pull it off,” he says. “This almost requires a full-time person.”

Dr. Torcson recommends starting with the reporting of three or four measures. “If you’re using a manual process or a homegrown system,” he says, “then the fewer measures the better, in terms of doing PQRI right to reach the 80% threshold.”

If you’re interested in reporting under the 2009 PQRI, go to SHM’s Web site at www.hospitalmedicine.org/ and type “PQRI 2008” into the advanced search bar. The article, “Information on PQRI 2008,” from May 17, 2007, provides important details about the program, including which measures apply to hospitalists. TH

Jane Jerrard is a medical writer based in Chicago.

Congress made history in July when it passed legislation that makes Medicare’s voluntary pay-for-reporting program permanent.

The program, the Physician Quality Reporting Initiative, or PQRI, which began in 2007 as a six-month trial and was continued through 2008, rewards physicians who successfully report on specific applicable quality measures with a cash bonus. The new bill, the Medicare Improvement for Patients and Providers Act (MIPPA), extends the Centers for Medicare and Medicaid (CMS) program beyond 2010.

“PQRI is now a permanent program, even though the details have only been provided through 2010,” says Michael Rapp, MD, of the CMS Office of Clinical Standards and Quality.

Here, is a look at PQRI past, present, and future, from a hospitalist’s point of view.

Pay-for-Performance Pilot Proves Worthwhile

In August, CMS released statistics on that first pay-for-reporting period. During the trial, 101,138 physicians submitted a quality-data code. Of those, 70,207 reported on at least one measure, and 56,722 earned a bonus.

Asked about those numbers, Patrick J. Torcson, MD, MMM, FACP, director of hospital medicine at St. Tammany Parish Hospital in Covington, La., and chair of SHM’s Performance and Standards Committee, says: “I think the folks at Medicare were pleased with that level of participation. This data helped convince them that the program should be permanent.”

What to Expect in 2009

The PQRI for 2009 is subject to revisions until the 2009 Physician Fee Schedule Final Rule is published sometime around Nov. 1. (Find the latest information on CMS Web site at www.cms.hhs.gov/pqri.) A number of proposed enhancements make it attractive and important to physicians, Dr. Torcson says.

CMS proposed 175 quality measures for physicians to report on, and MIPPA boosts payment for successful reporting of data on those measures. For 2009 and 2010, physicians who participate in the PQRI can earn an incentive payment of 2% (up from 1.5%) of their total allowed charges for Physician Fee Schedule (PFS) covered professional services.

However, except for a bigger check from CMS, hospitalists who currently report may not see much difference next year. “Overall, for hospitalists, PQRI will look pretty similar to 2007 and 2008,” Dr. Torcson warns. “The bonus is going to increase and the measures will be the same. That means that all of the background and education that SHM has provided on PQRI reporting remains relevant.”

One addition for 2009 is the use of patient registries to avoid claims systems for certain outpatient measures. “I don’t see the registry-reporting option being available to hospitalists in the short term,” Dr. Torcson says, “but it’s worth watching for the future.”

Beginning in 2009 and continuing through the next four years, Medicare also will provide incentive payments to eligible professionals who are successful electronic prescribers. (See the “Public Policy” article on p. 15 of the September 2008 The Hospitalist.) The e-prescribing measure in the 2008 PQRI will be removed for next year and used wholesale for a separate pay-for-reporting initiative pending changes from the Department of Health & Human Services. Unfortunately, none of the 2008 coding specifications for e-prescribing are available for hospitalist reporting.

“A lot of [the PQRI] measures have been created from the perspective of the cottage-industry model of an office-based private practice,” Dr. Torcson explains. “This 2008 (e-prescribing) measure was geared for an office-based physician practice—and the unforeseen consequence of the measure is that it’s not inclusive of patients being discharged from the hospital.”

Where Hospital Medicine Fits

By now, hospitalists should be resigned to the idea that many measures in PQRI don’t apply to their patients. However, SHM continues to work toward more inclusion for hospital-based physicians, by commenting on proposed rules and participating in the National Quality Forum and the American Medical Association’s Physician Consortium for Performance Improvement.

“We have been advocating for including performance measures for care processes, including transitions of care,” Dr. Torcson says. “This will probably come into play more in 2010 than 2009.”

SHM also has submitted comments on the proposed e-prescribing measures. Dr. Torcson says the organization is lobbying to make e-prescribing applicable to all hospital-based physicians, including ER doctors, and for discharged patients. “We want the whole process to harmonize with a comprehensive and safe discharge process that includes medication reconciliation,” he says.

To Report or Not to Report?

Regardless of whether lobbying efforts succeed in making more reporting applicable to hospital medicine, should groups start reporting in 2009? “It’s going to be a tough decision,” Dr. Torcson admits. “There’s a pretty significant investment in time and infrastructure to set this up. For the groups I know, the return on investment was negative.” In other words, PQRI does not pay for itself in a hospital medicine setting.

He says any hospital medicine group that wants to report should have in place a computerized system, and be willing to start slowly. “I’m convinced that it’s going to take an electronic coding/documentation system, as well as designated support staff within the hospital medicine group to pull it off,” he says. “This almost requires a full-time person.”

Dr. Torcson recommends starting with the reporting of three or four measures. “If you’re using a manual process or a homegrown system,” he says, “then the fewer measures the better, in terms of doing PQRI right to reach the 80% threshold.”

If you’re interested in reporting under the 2009 PQRI, go to SHM’s Web site at www.hospitalmedicine.org/ and type “PQRI 2008” into the advanced search bar. The article, “Information on PQRI 2008,” from May 17, 2007, provides important details about the program, including which measures apply to hospitalists. TH

Jane Jerrard is a medical writer based in Chicago.

You’re unhappy with your workload or schedule.

Your spouse has been transferred to a different state.

You simply want a change of scenery.

Regardless of the reason, you’re looking for a new job. In hospital medicine, how and when is it appropriate to give notice? To maintain good relations with your current employer now and in the future, make sure you consider your departure from both sides of the desk.

Timing is Everything

Before you start skimming classified ads and phoning friends in the field to ask about job openings, consider how much time your employer needs to fill your position.

“When you’re thinking about leaving a group, you have to realize that the timing for getting your replacement is longer than you might think,” says Heather A. Harris, MD, a hospitalist who splits her time between the University of California, San Francisco and the Palo Alto Medical Foundation. “The traditional two-week notice in other jobs is tough for most [hospital medicine] groups to handle—unless it’s a really big group or already overstaffed, which is never the case.”

Dr. Harris, who hired many hospitalists when she was director of Eden Inpatient Services, Eden Medical Center, Castro Valley, Calif., recommends giving a minimum of two months notice. “That gives your group time to figure out what to do,” she says. “Otherwise, you’re putting the entire group in a bind.”

Other physicians suggest an even longer timeframe. “My preference would be that a hospitalist give me no less than six months notification,” says Fred A. McCurdy, MD, PhD, MBA, associate dean for faculty development, Texas Tech University Health Sciences Center at Amarillo. “That’s a best-case scenario for finding a replacement. It could take longer than that.”

The issue is workload for the doctors left behind: “The other hospitalists are going to have to cover the slack in the meantime,” Dr. Harris points out. “Keep that in mind when you’re giving notice; you’re putting everyone else in a position where they have to cover the work.”

A lengthy timeframe actually could dovetail with your own transition. “You’ll have to get credentialed at that new hospital,” Dr. Harris says. “It’s important to realize when you get that job offer that group might want you to start the next day, but you have to wait until the credentialing process is complete.” Depending on the hospital, that could take as long as three months.

It’s important to know the specifics of your new hospital’s credential process. “You don’t want to leave a job before you have the means to enter a new job,” Dr. McCurdy warns. “Make sure you understand when you can actually start the work.”

Meanwhile, your current employer will need time to move your replacement through the same process. “Some hospitals are slower than others,” Dr. Harris says, “but even if I have a hospitalist in mind who’s available to start right away, they won’t be able to step in until the hospital’s credentialing is complete.”

Speak Up

When you decide to leave a job, tell your immediate supervisor directly and be open about your job search. “Ideally, the person who is leaving would sit down with me and tell me their intention to leave, where they intend to go, and the circumstances of their leaving,” Dr. McCurdy says. “I don’t want to hear about it third hand or through the grapevine, and I don’t want to find out that it’s some sort of negotiating tactic.”

If you want a new job because you’re unhappy with the one you have, consider whether the issues causing your discontent can be rectified. Dr. McCurdy says he would make every effort to keep a hospitalist in his group. “Obviously, there are some things I can’t help with,” he says. “I can’t change the weather, I can’t change the school systems, but I might be able to help with work issues.”

Build Bridges, Don’t Burn Them

It should go without saying that once you officially give notice, you should make every effort to maintain good relations with your employer and colleagues, by continuing to do your job well and remaining an active, positive member of your group, Dr. Harris says. This is particularly important if you stay in the same geographic area.

“There is a lot of fluidity in hospital medicine; people move from place to place,” she says. “It’s a small community and people know each other.”

If you feel comfortable doing so, offer to help your old employer find your replacement. Dr. McCurdy asks departing physicians for this favor. “I’d ask if they know someone who would be a good fit here,” he says. “The hospitalist community is small and pretty cohesive, so they may know someone.” Helping fill your position is a great way to stay connected and to show your good will toward the group.

If your employer asks you to stay a few weeks longer than you planned, consider whether you can jockey your upcoming start date to accommodate the request—but not at the price of being unhappy or risking your new job. “I might try to get someone to stay on a bit longer, but I’m not going to twist their arm if they aren’t interested,” Dr. McCurdy says. “It’s better to be without a physician than to have a disgruntled one.”

When you decide to move on to a new job, remember that you have a long career ahead of you. Be thoughtful and professional about how and when you leave. This small consideration can help maintain your reputation and connections for years to come. TH

Jane Jerrard also writes “Public Policy” for The Hospitalist.

You’re unhappy with your workload or schedule.

Your spouse has been transferred to a different state.

You simply want a change of scenery.

Regardless of the reason, you’re looking for a new job. In hospital medicine, how and when is it appropriate to give notice? To maintain good relations with your current employer now and in the future, make sure you consider your departure from both sides of the desk.

Timing is Everything

Before you start skimming classified ads and phoning friends in the field to ask about job openings, consider how much time your employer needs to fill your position.

“When you’re thinking about leaving a group, you have to realize that the timing for getting your replacement is longer than you might think,” says Heather A. Harris, MD, a hospitalist who splits her time between the University of California, San Francisco and the Palo Alto Medical Foundation. “The traditional two-week notice in other jobs is tough for most [hospital medicine] groups to handle—unless it’s a really big group or already overstaffed, which is never the case.”

Dr. Harris, who hired many hospitalists when she was director of Eden Inpatient Services, Eden Medical Center, Castro Valley, Calif., recommends giving a minimum of two months notice. “That gives your group time to figure out what to do,” she says. “Otherwise, you’re putting the entire group in a bind.”

Other physicians suggest an even longer timeframe. “My preference would be that a hospitalist give me no less than six months notification,” says Fred A. McCurdy, MD, PhD, MBA, associate dean for faculty development, Texas Tech University Health Sciences Center at Amarillo. “That’s a best-case scenario for finding a replacement. It could take longer than that.”

The issue is workload for the doctors left behind: “The other hospitalists are going to have to cover the slack in the meantime,” Dr. Harris points out. “Keep that in mind when you’re giving notice; you’re putting everyone else in a position where they have to cover the work.”

A lengthy timeframe actually could dovetail with your own transition. “You’ll have to get credentialed at that new hospital,” Dr. Harris says. “It’s important to realize when you get that job offer that group might want you to start the next day, but you have to wait until the credentialing process is complete.” Depending on the hospital, that could take as long as three months.

It’s important to know the specifics of your new hospital’s credential process. “You don’t want to leave a job before you have the means to enter a new job,” Dr. McCurdy warns. “Make sure you understand when you can actually start the work.”

Meanwhile, your current employer will need time to move your replacement through the same process. “Some hospitals are slower than others,” Dr. Harris says, “but even if I have a hospitalist in mind who’s available to start right away, they won’t be able to step in until the hospital’s credentialing is complete.”

Speak Up

When you decide to leave a job, tell your immediate supervisor directly and be open about your job search. “Ideally, the person who is leaving would sit down with me and tell me their intention to leave, where they intend to go, and the circumstances of their leaving,” Dr. McCurdy says. “I don’t want to hear about it third hand or through the grapevine, and I don’t want to find out that it’s some sort of negotiating tactic.”

If you want a new job because you’re unhappy with the one you have, consider whether the issues causing your discontent can be rectified. Dr. McCurdy says he would make every effort to keep a hospitalist in his group. “Obviously, there are some things I can’t help with,” he says. “I can’t change the weather, I can’t change the school systems, but I might be able to help with work issues.”

Build Bridges, Don’t Burn Them

It should go without saying that once you officially give notice, you should make every effort to maintain good relations with your employer and colleagues, by continuing to do your job well and remaining an active, positive member of your group, Dr. Harris says. This is particularly important if you stay in the same geographic area.

“There is a lot of fluidity in hospital medicine; people move from place to place,” she says. “It’s a small community and people know each other.”

If you feel comfortable doing so, offer to help your old employer find your replacement. Dr. McCurdy asks departing physicians for this favor. “I’d ask if they know someone who would be a good fit here,” he says. “The hospitalist community is small and pretty cohesive, so they may know someone.” Helping fill your position is a great way to stay connected and to show your good will toward the group.

If your employer asks you to stay a few weeks longer than you planned, consider whether you can jockey your upcoming start date to accommodate the request—but not at the price of being unhappy or risking your new job. “I might try to get someone to stay on a bit longer, but I’m not going to twist their arm if they aren’t interested,” Dr. McCurdy says. “It’s better to be without a physician than to have a disgruntled one.”

When you decide to move on to a new job, remember that you have a long career ahead of you. Be thoughtful and professional about how and when you leave. This small consideration can help maintain your reputation and connections for years to come. TH

Jane Jerrard also writes “Public Policy” for The Hospitalist.

You’re unhappy with your workload or schedule.

Your spouse has been transferred to a different state.

You simply want a change of scenery.

Regardless of the reason, you’re looking for a new job. In hospital medicine, how and when is it appropriate to give notice? To maintain good relations with your current employer now and in the future, make sure you consider your departure from both sides of the desk.

Timing is Everything

Before you start skimming classified ads and phoning friends in the field to ask about job openings, consider how much time your employer needs to fill your position.

“When you’re thinking about leaving a group, you have to realize that the timing for getting your replacement is longer than you might think,” says Heather A. Harris, MD, a hospitalist who splits her time between the University of California, San Francisco and the Palo Alto Medical Foundation. “The traditional two-week notice in other jobs is tough for most [hospital medicine] groups to handle—unless it’s a really big group or already overstaffed, which is never the case.”

Dr. Harris, who hired many hospitalists when she was director of Eden Inpatient Services, Eden Medical Center, Castro Valley, Calif., recommends giving a minimum of two months notice. “That gives your group time to figure out what to do,” she says. “Otherwise, you’re putting the entire group in a bind.”

Other physicians suggest an even longer timeframe. “My preference would be that a hospitalist give me no less than six months notification,” says Fred A. McCurdy, MD, PhD, MBA, associate dean for faculty development, Texas Tech University Health Sciences Center at Amarillo. “That’s a best-case scenario for finding a replacement. It could take longer than that.”

The issue is workload for the doctors left behind: “The other hospitalists are going to have to cover the slack in the meantime,” Dr. Harris points out. “Keep that in mind when you’re giving notice; you’re putting everyone else in a position where they have to cover the work.”

A lengthy timeframe actually could dovetail with your own transition. “You’ll have to get credentialed at that new hospital,” Dr. Harris says. “It’s important to realize when you get that job offer that group might want you to start the next day, but you have to wait until the credentialing process is complete.” Depending on the hospital, that could take as long as three months.

It’s important to know the specifics of your new hospital’s credential process. “You don’t want to leave a job before you have the means to enter a new job,” Dr. McCurdy warns. “Make sure you understand when you can actually start the work.”

Meanwhile, your current employer will need time to move your replacement through the same process. “Some hospitals are slower than others,” Dr. Harris says, “but even if I have a hospitalist in mind who’s available to start right away, they won’t be able to step in until the hospital’s credentialing is complete.”

Speak Up

When you decide to leave a job, tell your immediate supervisor directly and be open about your job search. “Ideally, the person who is leaving would sit down with me and tell me their intention to leave, where they intend to go, and the circumstances of their leaving,” Dr. McCurdy says. “I don’t want to hear about it third hand or through the grapevine, and I don’t want to find out that it’s some sort of negotiating tactic.”

If you want a new job because you’re unhappy with the one you have, consider whether the issues causing your discontent can be rectified. Dr. McCurdy says he would make every effort to keep a hospitalist in his group. “Obviously, there are some things I can’t help with,” he says. “I can’t change the weather, I can’t change the school systems, but I might be able to help with work issues.”

Build Bridges, Don’t Burn Them

It should go without saying that once you officially give notice, you should make every effort to maintain good relations with your employer and colleagues, by continuing to do your job well and remaining an active, positive member of your group, Dr. Harris says. This is particularly important if you stay in the same geographic area.

“There is a lot of fluidity in hospital medicine; people move from place to place,” she says. “It’s a small community and people know each other.”

If you feel comfortable doing so, offer to help your old employer find your replacement. Dr. McCurdy asks departing physicians for this favor. “I’d ask if they know someone who would be a good fit here,” he says. “The hospitalist community is small and pretty cohesive, so they may know someone.” Helping fill your position is a great way to stay connected and to show your good will toward the group.

If your employer asks you to stay a few weeks longer than you planned, consider whether you can jockey your upcoming start date to accommodate the request—but not at the price of being unhappy or risking your new job. “I might try to get someone to stay on a bit longer, but I’m not going to twist their arm if they aren’t interested,” Dr. McCurdy says. “It’s better to be without a physician than to have a disgruntled one.”

When you decide to move on to a new job, remember that you have a long career ahead of you. Be thoughtful and professional about how and when you leave. This small consideration can help maintain your reputation and connections for years to come. TH

Jane Jerrard also writes “Public Policy” for The Hospitalist.

Most of us learned in our professional training that neuroleptic agents cause movement disorders, or extrapyramidal symptoms (EPS).1 Neuroleptics, the older class of antipsychotic agents, which includes dopamine receptor blocking agents (DRBA), can cause tardive dyskinesia (TD), dystonia, akathisia, and Parkinsonism.

We also learned that newer antipsychotic agents, the so-called second-generation antipsychotics, do not cause EPS. However, dose-related EPS has been associated with olanzapine and risperidone use (> 6 mg/day doses), and there have been two reported cases of aripiprazole-induced EPS.2,3

So which symptoms indicate a drug-induced movement disorder (DIMD)? Patients with DIMDs have difficulty with social functioning, motor-task performance, interpersonal communication, and activities of daily living. They also are less likely to adhere to a medication regimen, making disease relapse and rehospitalization more likely.

Some DIMDs are worse than others. Neuroleptic-induced TD, for example, is in some cases irreversible and can lead to functional impairment so severe a patient cannot feed himself, speak clearly, or breathe easily. In addition, removal of the offending agent does not always resolve TD.4

Milder forms of neuroleptic-induced TD occur in about 20% of patients. In higher risk groups, such as older patients, milder forms of neuroleptic-induced TD may exceed 50%.

DIMDs often elude diagnosis by clinicians, partially because they look like other medical conditions such as restless legs syndrome, agitation, or drug withdrawal. Clinicians who understand the most likely DIMD culprits and the effect of each can better manage their patients. It’s also crucial for clinicians to pay attention to

• Patient stress and anxiety levels, as both of these can exacerbate DIMD symptoms;
• Patient drug history; and
• Demographic information. Older women are most likely to develop tardive dyskinesia. Young men more commonly experience dystonic reactions. The elderly are at higher risk for Parkinsonism and akathisia.

Clinicians must watch for DIMD in any patient who has taken antipsychotics. Symptoms can occur within hours to days (acute), weeks (subacute) or even months to years (tardive) following exposure.

The Agents

Causative DRBAs include:

• Haloperidol;
• Thioridazine;
• Perphenazine;
• Droperidol;
• Metoclopramide;
• Prochlorperazine; and
• Promethazine.

DIMDs can also occur from:

• Lithium, which can cause tremors or chorea;
• Stimulants (e.g., amphetamines), which can cause tremor, tics, dystonia, and dyskinesia;
• Selective-serotonin reuptake inhibitors (SSRIs), which can cause tremors, akathisia, and possible dyskinesia, dystonia, and Parkinsonism;
• Tricyclic antidepressants (TCAs) (e.g., amitriptyline, nortriptyline, etc), which can cause myoclonus and tremors;
• Valproic acid, which causes tremors; and
• Cyclosporine A, which was implicated in one study as causing tremors and Parkinsonism.6

Management

For neuroleptics, withdrawal of the offending agent may lead to partial improvement in about half of patients. The outcome, of course, depends on the DIMD.

Early detection of TD is important to improve remission rates, which are inversely related to the disorder’s duration and severity. To treat, gradually taper the patient off the medication. It may take as long as two years after discontinuation for the condition to resolve itself. Continually re-evaluate how much a patient needs this agent. There may be another that’s just as effective but with a lower TD incidence. 7

Treat acute dystonic reactions with a short course of a potent antimuscarinic agent such as oral, intravenous (IV), or intramuscular benztropine, or diphenhydramine. If the patient’s reaction is life-threatening, use IV administration of an antimuscarinic agent and supportive measures. In some cases, you can use benzodiazepines in place of antimuscarinic agents. For tardive dystonia, prevention is the most important treatment since few pharmacologic treatments have proven efficacy.

Prevention also is the key to managing akathisia. To prevent this manifestation, prescribe atypical antipsychotics or use a standardized dose titration to avoid excessive dose escalation. In high-risk patients, consider prophylactic treatment with diphenhydramine or benztropine. Other potentially useful agents include benzodiazepines, propranolol, or cyproheptadine. For acute reactions, remove the causative agent.

Treat drug-induced Parkinsonism by withdrawing the causative agent or reducing the dose, switching to an atypical antipsychotic (if neuroleptic-induced), and possibly prescribing a trial of amantadine, an antimuscarinic agent, a dopamine agonist, or levodopa.

Though antiemetics and conventional antipsychotics are most commonly implicated, other agents also cause DIMDs. To prevent and treat these disorders, clinicians need to be particularly aware of the causative agents and symptoms. TH

Michele B. Kaufman, PharmD, BSc, RPh, is a registered pharmacist based in New York City.

References

1. Chen JJ. Drug-induced Movement Disorders. Journal of Pharmacy Practice. 2007; 20(6):415-429.
2. Zacher JL, Hatchett AD. Aripiprazole-induced movement disorder. Am J Psychiatry. 2006;163:160-161[letter].
3. Sajbel TA, Cheney EM, DeQuardo JR. Aripiprazole-associated dyskinesia. Ann Pharmacother. 2005;39:200-201[letter].
4. Lee PE, Synkora K, Gill SS., et al. Antipsychotic medications and drug-induced movement disorders other than Parkinsonism: A population-based cohort study in older adults. J Am Geriatr Soc. 2005;53:1374-1379.
5. Munhoz RP, Teive HAG, Germiniani FMB et al. Movement disorders secondary to long-term treatment with cyclosporine A. Arq Neuropsiquiatr. 2005;63(3-A)L592-596.
6. Vernon, Gwen M. Drug-Induced & Tardive Movement Disorders. National Alliance for the Mentally Ill, July 2001.www.namiscc.org/newsletters/July01/tardive.htm

Most of us learned in our professional training that neuroleptic agents cause movement disorders, or extrapyramidal symptoms (EPS).1 Neuroleptics, the older class of antipsychotic agents, which includes dopamine receptor blocking agents (DRBA), can cause tardive dyskinesia (TD), dystonia, akathisia, and Parkinsonism.

We also learned that newer antipsychotic agents, the so-called second-generation antipsychotics, do not cause EPS. However, dose-related EPS has been associated with olanzapine and risperidone use (> 6 mg/day doses), and there have been two reported cases of aripiprazole-induced EPS.2,3

So which symptoms indicate a drug-induced movement disorder (DIMD)? Patients with DIMDs have difficulty with social functioning, motor-task performance, interpersonal communication, and activities of daily living. They also are less likely to adhere to a medication regimen, making disease relapse and rehospitalization more likely.

Some DIMDs are worse than others. Neuroleptic-induced TD, for example, is in some cases irreversible and can lead to functional impairment so severe a patient cannot feed himself, speak clearly, or breathe easily. In addition, removal of the offending agent does not always resolve TD.4

Milder forms of neuroleptic-induced TD occur in about 20% of patients. In higher risk groups, such as older patients, milder forms of neuroleptic-induced TD may exceed 50%.

DIMDs often elude diagnosis by clinicians, partially because they look like other medical conditions such as restless legs syndrome, agitation, or drug withdrawal. Clinicians who understand the most likely DIMD culprits and the effect of each can better manage their patients. It’s also crucial for clinicians to pay attention to

• Patient stress and anxiety levels, as both of these can exacerbate DIMD symptoms;
• Patient drug history; and
• Demographic information. Older women are most likely to develop tardive dyskinesia. Young men more commonly experience dystonic reactions. The elderly are at higher risk for Parkinsonism and akathisia.

Clinicians must watch for DIMD in any patient who has taken antipsychotics. Symptoms can occur within hours to days (acute), weeks (subacute) or even months to years (tardive) following exposure.

The Agents

Causative DRBAs include:

• Haloperidol;
• Thioridazine;
• Perphenazine;
• Droperidol;
• Metoclopramide;
• Prochlorperazine; and
• Promethazine.

DIMDs can also occur from:

• Lithium, which can cause tremors or chorea;
• Stimulants (e.g., amphetamines), which can cause tremor, tics, dystonia, and dyskinesia;
• Selective-serotonin reuptake inhibitors (SSRIs), which can cause tremors, akathisia, and possible dyskinesia, dystonia, and Parkinsonism;
• Tricyclic antidepressants (TCAs) (e.g., amitriptyline, nortriptyline, etc), which can cause myoclonus and tremors;
• Valproic acid, which causes tremors; and
• Cyclosporine A, which was implicated in one study as causing tremors and Parkinsonism.6

Management

For neuroleptics, withdrawal of the offending agent may lead to partial improvement in about half of patients. The outcome, of course, depends on the DIMD.

Early detection of TD is important to improve remission rates, which are inversely related to the disorder’s duration and severity. To treat, gradually taper the patient off the medication. It may take as long as two years after discontinuation for the condition to resolve itself. Continually re-evaluate how much a patient needs this agent. There may be another that’s just as effective but with a lower TD incidence. 7

Treat acute dystonic reactions with a short course of a potent antimuscarinic agent such as oral, intravenous (IV), or intramuscular benztropine, or diphenhydramine. If the patient’s reaction is life-threatening, use IV administration of an antimuscarinic agent and supportive measures. In some cases, you can use benzodiazepines in place of antimuscarinic agents. For tardive dystonia, prevention is the most important treatment since few pharmacologic treatments have proven efficacy.

Prevention also is the key to managing akathisia. To prevent this manifestation, prescribe atypical antipsychotics or use a standardized dose titration to avoid excessive dose escalation. In high-risk patients, consider prophylactic treatment with diphenhydramine or benztropine. Other potentially useful agents include benzodiazepines, propranolol, or cyproheptadine. For acute reactions, remove the causative agent.

Treat drug-induced Parkinsonism by withdrawing the causative agent or reducing the dose, switching to an atypical antipsychotic (if neuroleptic-induced), and possibly prescribing a trial of amantadine, an antimuscarinic agent, a dopamine agonist, or levodopa.

Though antiemetics and conventional antipsychotics are most commonly implicated, other agents also cause DIMDs. To prevent and treat these disorders, clinicians need to be particularly aware of the causative agents and symptoms. TH

Michele B. Kaufman, PharmD, BSc, RPh, is a registered pharmacist based in New York City.

References

1. Chen JJ. Drug-induced Movement Disorders. Journal of Pharmacy Practice. 2007; 20(6):415-429.
2. Zacher JL, Hatchett AD. Aripiprazole-induced movement disorder. Am J Psychiatry. 2006;163:160-161[letter].
3. Sajbel TA, Cheney EM, DeQuardo JR. Aripiprazole-associated dyskinesia. Ann Pharmacother. 2005;39:200-201[letter].
4. Lee PE, Synkora K, Gill SS., et al. Antipsychotic medications and drug-induced movement disorders other than Parkinsonism: A population-based cohort study in older adults. J Am Geriatr Soc. 2005;53:1374-1379.
5. Munhoz RP, Teive HAG, Germiniani FMB et al. Movement disorders secondary to long-term treatment with cyclosporine A. Arq Neuropsiquiatr. 2005;63(3-A)L592-596.
6. Vernon, Gwen M. Drug-Induced & Tardive Movement Disorders. National Alliance for the Mentally Ill, July 2001.www.namiscc.org/newsletters/July01/tardive.htm

Most of us learned in our professional training that neuroleptic agents cause movement disorders, or extrapyramidal symptoms (EPS).1 Neuroleptics, the older class of antipsychotic agents, which includes dopamine receptor blocking agents (DRBA), can cause tardive dyskinesia (TD), dystonia, akathisia, and Parkinsonism.

We also learned that newer antipsychotic agents, the so-called second-generation antipsychotics, do not cause EPS. However, dose-related EPS has been associated with olanzapine and risperidone use (> 6 mg/day doses), and there have been two reported cases of aripiprazole-induced EPS.2,3

So which symptoms indicate a drug-induced movement disorder (DIMD)? Patients with DIMDs have difficulty with social functioning, motor-task performance, interpersonal communication, and activities of daily living. They also are less likely to adhere to a medication regimen, making disease relapse and rehospitalization more likely.

Some DIMDs are worse than others. Neuroleptic-induced TD, for example, is in some cases irreversible and can lead to functional impairment so severe a patient cannot feed himself, speak clearly, or breathe easily. In addition, removal of the offending agent does not always resolve TD.4

Milder forms of neuroleptic-induced TD occur in about 20% of patients. In higher risk groups, such as older patients, milder forms of neuroleptic-induced TD may exceed 50%.

DIMDs often elude diagnosis by clinicians, partially because they look like other medical conditions such as restless legs syndrome, agitation, or drug withdrawal. Clinicians who understand the most likely DIMD culprits and the effect of each can better manage their patients. It’s also crucial for clinicians to pay attention to

• Patient stress and anxiety levels, as both of these can exacerbate DIMD symptoms;
• Patient drug history; and
• Demographic information. Older women are most likely to develop tardive dyskinesia. Young men more commonly experience dystonic reactions. The elderly are at higher risk for Parkinsonism and akathisia.

Clinicians must watch for DIMD in any patient who has taken antipsychotics. Symptoms can occur within hours to days (acute), weeks (subacute) or even months to years (tardive) following exposure.

The Agents

Causative DRBAs include:

• Haloperidol;
• Thioridazine;
• Perphenazine;
• Droperidol;
• Metoclopramide;
• Prochlorperazine; and
• Promethazine.

DIMDs can also occur from:

• Lithium, which can cause tremors or chorea;
• Stimulants (e.g., amphetamines), which can cause tremor, tics, dystonia, and dyskinesia;
• Selective-serotonin reuptake inhibitors (SSRIs), which can cause tremors, akathisia, and possible dyskinesia, dystonia, and Parkinsonism;
• Tricyclic antidepressants (TCAs) (e.g., amitriptyline, nortriptyline, etc), which can cause myoclonus and tremors;
• Valproic acid, which causes tremors; and
• Cyclosporine A, which was implicated in one study as causing tremors and Parkinsonism.6

Management

For neuroleptics, withdrawal of the offending agent may lead to partial improvement in about half of patients. The outcome, of course, depends on the DIMD.

Early detection of TD is important to improve remission rates, which are inversely related to the disorder’s duration and severity. To treat, gradually taper the patient off the medication. It may take as long as two years after discontinuation for the condition to resolve itself. Continually re-evaluate how much a patient needs this agent. There may be another that’s just as effective but with a lower TD incidence. 7

Treat acute dystonic reactions with a short course of a potent antimuscarinic agent such as oral, intravenous (IV), or intramuscular benztropine, or diphenhydramine. If the patient’s reaction is life-threatening, use IV administration of an antimuscarinic agent and supportive measures. In some cases, you can use benzodiazepines in place of antimuscarinic agents. For tardive dystonia, prevention is the most important treatment since few pharmacologic treatments have proven efficacy.

Prevention also is the key to managing akathisia. To prevent this manifestation, prescribe atypical antipsychotics or use a standardized dose titration to avoid excessive dose escalation. In high-risk patients, consider prophylactic treatment with diphenhydramine or benztropine. Other potentially useful agents include benzodiazepines, propranolol, or cyproheptadine. For acute reactions, remove the causative agent.

Treat drug-induced Parkinsonism by withdrawing the causative agent or reducing the dose, switching to an atypical antipsychotic (if neuroleptic-induced), and possibly prescribing a trial of amantadine, an antimuscarinic agent, a dopamine agonist, or levodopa.

Though antiemetics and conventional antipsychotics are most commonly implicated, other agents also cause DIMDs. To prevent and treat these disorders, clinicians need to be particularly aware of the causative agents and symptoms. TH

Michele B. Kaufman, PharmD, BSc, RPh, is a registered pharmacist based in New York City.

References

1. Chen JJ. Drug-induced Movement Disorders. Journal of Pharmacy Practice. 2007; 20(6):415-429.
2. Zacher JL, Hatchett AD. Aripiprazole-induced movement disorder. Am J Psychiatry. 2006;163:160-161[letter].
3. Sajbel TA, Cheney EM, DeQuardo JR. Aripiprazole-associated dyskinesia. Ann Pharmacother. 2005;39:200-201[letter].
4. Lee PE, Synkora K, Gill SS., et al. Antipsychotic medications and drug-induced movement disorders other than Parkinsonism: A population-based cohort study in older adults. J Am Geriatr Soc. 2005;53:1374-1379.
5. Munhoz RP, Teive HAG, Germiniani FMB et al. Movement disorders secondary to long-term treatment with cyclosporine A. Arq Neuropsiquiatr. 2005;63(3-A)L592-596.
6. Vernon, Gwen M. Drug-Induced & Tardive Movement Disorders. National Alliance for the Mentally Ill, July 2001.www.namiscc.org/newsletters/July01/tardive.htm

It may be time for hospitalists to rethink their co-management relationships, says Eric Siegal, MD, chair of the Society of Hospital Medicine’s Public Policy Committee. Co-management is a mainstay of hospital medicine, but “recent, albeit limited evidence suggests hospitalist consultation and co-management may not be as effective as originally anticipated,” Dr. Siegal writes in this month’s Journal of Hospital Medicine.

He demonstrates his point with several studies, including the Hospitalist Orthopedic Team trial, which involved 526 patients who underwent elective hip or knee surgery at the Mayo Clinic. Hospitalist intervention reduced incidence of minor complications, such as urinary tract infections, but had no effect on more serious complications; it reduced adjusted length of stay (LOS) by a modest 0.5 days but did not affect actual LOS or cost per case. On the other hand, patients admitted to the Mayo Clinic for hip fractures derived a clear benefit from hospitalist co-management: Compared to the standard orthopedic service, the hospitalist team decreased time-to-surgery and lowered LOS by 2.2 days without compromising outcomes.

These and similar findings “support the common sense notion that hospitalists most benefit patients who are sick, frail, and medically or socially complex,” Dr. Siegal writes. “As a corollary, hospitalists probably offer relatively little benefit to surgical and specialty patients who are young or have compensated medical co-morbidities and/or straightforward disposition plans.”

Dr. Siegal says he wrote the article because he realized even though hospitalists share accountability and authority for patient care with other specialists, there’s rarely a clear line defining where one physician’s responsibilities end and the other’s begin. “My intention was to make people stop and think about what they were doing, rather than just doing it,” he tells The Hospitalist.

Co-management is a good example of the phenomenon known in the military as mission creep, Dr. Siegal explains. Mission creep occurs when a project originates with well-defined and perhaps limited goals, but then expands into areas for which it was never intended.

Co-management arose during California’s managed care heyday: Hospital administrators realized surgeons were having difficulty controlling patient length of stay and managing medical co-morbidities during surgery. Enter the hospitalist, charged with coordinating the care of the acutely ill in the most effective and efficient way possible. Surgeons and other specialists liked the idea of sharing responsibility with another physician, and administrators liked the effect on the bottom line.

So, little by little, co-management evolved from a strategy for managing only the most complicated cases to a routine practice at many institutions—even when hospitalists actually added little to a patient’s care. For example, a “patient with a stable GI bleed who needs little more than an endoscopy I would argue does not need co-management,” Dr. Siegal says. In fact, he points out in his paper, inserting the hospitalist into the situation above might work against the patient if it delays the gastroenterologist’s involvement and the endoscopy. A gastroenterologist who assumes a hospitalist is running the show may pay insufficient attention to the patient, Dr. Siegal writes.

Worse than that, having more than one physician involved may actually increase the risk of medical errors if the doctors give conflicting or inconsistent orders that confuse hospital staff, patients, or their families. In many cases, the specialist is simply better qualified to do the admitting, Dr. Siegal says. When a patient comes in with a cranial bleed, “if it was my mother, I wouldn’t want me admitting her,” he says.

Unnecessary co-management also can negatively affect hospitalists themselves to the extent that the process engenders burnout or unhappiness on the job, Dr. Siegal adds. Without set parameters, specialists may assume that hospitalists will conduct all patient admits. This “devalues the hospitalist,” he writes. “People start seeing us as glorified residents,” leading to “huge job dissatisfaction.”

Co-management does offer some benefits, though they vary based on situation, he says. At institutions with a limited pool of surgeons, neurologists, or other specialists, sharing duties with hospitalists can free up specialists for cases that need their specific expertise. When specialist availability isn’t a problem, however, the real—if unspoken—purpose of co-management may be to lighten the burden for superstar specialists who attract patients, prestige, and money. The result can be overworked, stressed out hospitalists who may inadvertently neglect patients requiring care.

The solution is to give hospitalists more of a say in the types of cases they co-manage, and a clearer delineation of the responsibilities of each party involved, according to Dr. Siegal. “Sit down with the specialists and revisit where you are,” he says. He also suggests calling on hospital administrators, if necessary, to mollify specialists who might dislike the idea of a change.

After all, Dr. Siegal warns, “just showing up to co-manage doesn’t mean you’re doing anything to help the patient. You should have definable outcomes that can help you say, “‘This is better.’” TH

Norra MacReady is a medical writer based in California.

It may be time for hospitalists to rethink their co-management relationships, says Eric Siegal, MD, chair of the Society of Hospital Medicine’s Public Policy Committee. Co-management is a mainstay of hospital medicine, but “recent, albeit limited evidence suggests hospitalist consultation and co-management may not be as effective as originally anticipated,” Dr. Siegal writes in this month’s Journal of Hospital Medicine.

He demonstrates his point with several studies, including the Hospitalist Orthopedic Team trial, which involved 526 patients who underwent elective hip or knee surgery at the Mayo Clinic. Hospitalist intervention reduced incidence of minor complications, such as urinary tract infections, but had no effect on more serious complications; it reduced adjusted length of stay (LOS) by a modest 0.5 days but did not affect actual LOS or cost per case. On the other hand, patients admitted to the Mayo Clinic for hip fractures derived a clear benefit from hospitalist co-management: Compared to the standard orthopedic service, the hospitalist team decreased time-to-surgery and lowered LOS by 2.2 days without compromising outcomes.

These and similar findings “support the common sense notion that hospitalists most benefit patients who are sick, frail, and medically or socially complex,” Dr. Siegal writes. “As a corollary, hospitalists probably offer relatively little benefit to surgical and specialty patients who are young or have compensated medical co-morbidities and/or straightforward disposition plans.”

Dr. Siegal says he wrote the article because he realized even though hospitalists share accountability and authority for patient care with other specialists, there’s rarely a clear line defining where one physician’s responsibilities end and the other’s begin. “My intention was to make people stop and think about what they were doing, rather than just doing it,” he tells The Hospitalist.

Co-management is a good example of the phenomenon known in the military as mission creep, Dr. Siegal explains. Mission creep occurs when a project originates with well-defined and perhaps limited goals, but then expands into areas for which it was never intended.

Co-management arose during California’s managed care heyday: Hospital administrators realized surgeons were having difficulty controlling patient length of stay and managing medical co-morbidities during surgery. Enter the hospitalist, charged with coordinating the care of the acutely ill in the most effective and efficient way possible. Surgeons and other specialists liked the idea of sharing responsibility with another physician, and administrators liked the effect on the bottom line.

So, little by little, co-management evolved from a strategy for managing only the most complicated cases to a routine practice at many institutions—even when hospitalists actually added little to a patient’s care. For example, a “patient with a stable GI bleed who needs little more than an endoscopy I would argue does not need co-management,” Dr. Siegal says. In fact, he points out in his paper, inserting the hospitalist into the situation above might work against the patient if it delays the gastroenterologist’s involvement and the endoscopy. A gastroenterologist who assumes a hospitalist is running the show may pay insufficient attention to the patient, Dr. Siegal writes.

Worse than that, having more than one physician involved may actually increase the risk of medical errors if the doctors give conflicting or inconsistent orders that confuse hospital staff, patients, or their families. In many cases, the specialist is simply better qualified to do the admitting, Dr. Siegal says. When a patient comes in with a cranial bleed, “if it was my mother, I wouldn’t want me admitting her,” he says.

Unnecessary co-management also can negatively affect hospitalists themselves to the extent that the process engenders burnout or unhappiness on the job, Dr. Siegal adds. Without set parameters, specialists may assume that hospitalists will conduct all patient admits. This “devalues the hospitalist,” he writes. “People start seeing us as glorified residents,” leading to “huge job dissatisfaction.”

Co-management does offer some benefits, though they vary based on situation, he says. At institutions with a limited pool of surgeons, neurologists, or other specialists, sharing duties with hospitalists can free up specialists for cases that need their specific expertise. When specialist availability isn’t a problem, however, the real—if unspoken—purpose of co-management may be to lighten the burden for superstar specialists who attract patients, prestige, and money. The result can be overworked, stressed out hospitalists who may inadvertently neglect patients requiring care.

The solution is to give hospitalists more of a say in the types of cases they co-manage, and a clearer delineation of the responsibilities of each party involved, according to Dr. Siegal. “Sit down with the specialists and revisit where you are,” he says. He also suggests calling on hospital administrators, if necessary, to mollify specialists who might dislike the idea of a change.

After all, Dr. Siegal warns, “just showing up to co-manage doesn’t mean you’re doing anything to help the patient. You should have definable outcomes that can help you say, “‘This is better.’” TH

Norra MacReady is a medical writer based in California.

It may be time for hospitalists to rethink their co-management relationships, says Eric Siegal, MD, chair of the Society of Hospital Medicine’s Public Policy Committee. Co-management is a mainstay of hospital medicine, but “recent, albeit limited evidence suggests hospitalist consultation and co-management may not be as effective as originally anticipated,” Dr. Siegal writes in this month’s Journal of Hospital Medicine.

He demonstrates his point with several studies, including the Hospitalist Orthopedic Team trial, which involved 526 patients who underwent elective hip or knee surgery at the Mayo Clinic. Hospitalist intervention reduced incidence of minor complications, such as urinary tract infections, but had no effect on more serious complications; it reduced adjusted length of stay (LOS) by a modest 0.5 days but did not affect actual LOS or cost per case. On the other hand, patients admitted to the Mayo Clinic for hip fractures derived a clear benefit from hospitalist co-management: Compared to the standard orthopedic service, the hospitalist team decreased time-to-surgery and lowered LOS by 2.2 days without compromising outcomes.

These and similar findings “support the common sense notion that hospitalists most benefit patients who are sick, frail, and medically or socially complex,” Dr. Siegal writes. “As a corollary, hospitalists probably offer relatively little benefit to surgical and specialty patients who are young or have compensated medical co-morbidities and/or straightforward disposition plans.”

Dr. Siegal says he wrote the article because he realized even though hospitalists share accountability and authority for patient care with other specialists, there’s rarely a clear line defining where one physician’s responsibilities end and the other’s begin. “My intention was to make people stop and think about what they were doing, rather than just doing it,” he tells The Hospitalist.

Co-management is a good example of the phenomenon known in the military as mission creep, Dr. Siegal explains. Mission creep occurs when a project originates with well-defined and perhaps limited goals, but then expands into areas for which it was never intended.

Co-management arose during California’s managed care heyday: Hospital administrators realized surgeons were having difficulty controlling patient length of stay and managing medical co-morbidities during surgery. Enter the hospitalist, charged with coordinating the care of the acutely ill in the most effective and efficient way possible. Surgeons and other specialists liked the idea of sharing responsibility with another physician, and administrators liked the effect on the bottom line.

So, little by little, co-management evolved from a strategy for managing only the most complicated cases to a routine practice at many institutions—even when hospitalists actually added little to a patient’s care. For example, a “patient with a stable GI bleed who needs little more than an endoscopy I would argue does not need co-management,” Dr. Siegal says. In fact, he points out in his paper, inserting the hospitalist into the situation above might work against the patient if it delays the gastroenterologist’s involvement and the endoscopy. A gastroenterologist who assumes a hospitalist is running the show may pay insufficient attention to the patient, Dr. Siegal writes.

Worse than that, having more than one physician involved may actually increase the risk of medical errors if the doctors give conflicting or inconsistent orders that confuse hospital staff, patients, or their families. In many cases, the specialist is simply better qualified to do the admitting, Dr. Siegal says. When a patient comes in with a cranial bleed, “if it was my mother, I wouldn’t want me admitting her,” he says.

Unnecessary co-management also can negatively affect hospitalists themselves to the extent that the process engenders burnout or unhappiness on the job, Dr. Siegal adds. Without set parameters, specialists may assume that hospitalists will conduct all patient admits. This “devalues the hospitalist,” he writes. “People start seeing us as glorified residents,” leading to “huge job dissatisfaction.”

Co-management does offer some benefits, though they vary based on situation, he says. At institutions with a limited pool of surgeons, neurologists, or other specialists, sharing duties with hospitalists can free up specialists for cases that need their specific expertise. When specialist availability isn’t a problem, however, the real—if unspoken—purpose of co-management may be to lighten the burden for superstar specialists who attract patients, prestige, and money. The result can be overworked, stressed out hospitalists who may inadvertently neglect patients requiring care.

The solution is to give hospitalists more of a say in the types of cases they co-manage, and a clearer delineation of the responsibilities of each party involved, according to Dr. Siegal. “Sit down with the specialists and revisit where you are,” he says. He also suggests calling on hospital administrators, if necessary, to mollify specialists who might dislike the idea of a change.

After all, Dr. Siegal warns, “just showing up to co-manage doesn’t mean you’re doing anything to help the patient. You should have definable outcomes that can help you say, “‘This is better.’” TH

Norra MacReady is a medical writer based in California.