LAHAINA, HAWAII – Hyperhidrosis affects nearly 5% of the U.S. population, and in a survey of U.S. teenagers, about 17% reported excessive sweating, Jashin Wu, MD, said at the Hawaii Dermatology Seminar provided by the Global Academy for Medical Education/Skin Disease Education Foundation.

In an interview with MDedge reporter Bruce Jancin, Dr. Wu, founder of the Dermatology Research and Education Foundation, Irvine, Calif., discussed the off-label use of oral agents to treat hyperhidrosis. Dr. Wu said he is a fan of oral glycopyrrolate in particular, which he tends to use even earlier than suggested in the International Hyperhidrosis Society guidelines.

Glycopyrrolate is available in 1 mg and 2 mg tablets; Dr. Wu starts patients at a dose of 1 mg twice a day, escalating by 1 mg per week until the “desired effects occur” or the patient has problems tolerating treatment because of side effects.

Other oral options include oxybutynin and propranolol. Sofpironium bromide, an analog of glycopyrrolate, is in the pipeline, he said.

During the interview, Dr. Wu discussed mydriasis, an adverse effect associated with both topical and systemic anticholinergic treatment. In the two pivotal phase 3 randomized trials of prescription glycopyrronium cloth (Qbrexza) for axillary hyperhidrosis, the incidence of mydriasis was 6.8% in 463 patients on active treatment for 4 weeks. Three-quarters of cases were unilateral. The mydriasis resolved without permanent treatment discontinuation in 27 of the 31 patients (J Am Acad Dermatol. 2019 Jan;80[1]:128-138.e2).

“The most important point is that patients need to be educated that they need to wash their hands very well after they apply it to the affected areas” to prevent accidental medication contact with the eyes, he advised.

Alarm bells can go off when a patient with anticholinergic therapy–induced mydriasis presents to an ED without mentioning their treatment status, Dr. Wu observed.

Dr. Wu had no relevant disclosures. SDEF/Global Academy for Medical Education and this news organization are owned by the same parent company.

To listen to the interview, click the play button below.

LAHAINA, HAWAII – Hyperhidrosis affects nearly 5% of the U.S. population, and in a survey of U.S. teenagers, about 17% reported excessive sweating, Jashin Wu, MD, said at the Hawaii Dermatology Seminar provided by the Global Academy for Medical Education/Skin Disease Education Foundation.

In an interview with MDedge reporter Bruce Jancin, Dr. Wu, founder of the Dermatology Research and Education Foundation, Irvine, Calif., discussed the off-label use of oral agents to treat hyperhidrosis. Dr. Wu said he is a fan of oral glycopyrrolate in particular, which he tends to use even earlier than suggested in the International Hyperhidrosis Society guidelines.

Glycopyrrolate is available in 1 mg and 2 mg tablets; Dr. Wu starts patients at a dose of 1 mg twice a day, escalating by 1 mg per week until the “desired effects occur” or the patient has problems tolerating treatment because of side effects.

Other oral options include oxybutynin and propranolol. Sofpironium bromide, an analog of glycopyrrolate, is in the pipeline, he said.

During the interview, Dr. Wu discussed mydriasis, an adverse effect associated with both topical and systemic anticholinergic treatment. In the two pivotal phase 3 randomized trials of prescription glycopyrronium cloth (Qbrexza) for axillary hyperhidrosis, the incidence of mydriasis was 6.8% in 463 patients on active treatment for 4 weeks. Three-quarters of cases were unilateral. The mydriasis resolved without permanent treatment discontinuation in 27 of the 31 patients (J Am Acad Dermatol. 2019 Jan;80[1]:128-138.e2).

“The most important point is that patients need to be educated that they need to wash their hands very well after they apply it to the affected areas” to prevent accidental medication contact with the eyes, he advised.

Alarm bells can go off when a patient with anticholinergic therapy–induced mydriasis presents to an ED without mentioning their treatment status, Dr. Wu observed.

Dr. Wu had no relevant disclosures. SDEF/Global Academy for Medical Education and this news organization are owned by the same parent company.

To listen to the interview, click the play button below.

LAHAINA, HAWAII – Hyperhidrosis affects nearly 5% of the U.S. population, and in a survey of U.S. teenagers, about 17% reported excessive sweating, Jashin Wu, MD, said at the Hawaii Dermatology Seminar provided by the Global Academy for Medical Education/Skin Disease Education Foundation.

In an interview with MDedge reporter Bruce Jancin, Dr. Wu, founder of the Dermatology Research and Education Foundation, Irvine, Calif., discussed the off-label use of oral agents to treat hyperhidrosis. Dr. Wu said he is a fan of oral glycopyrrolate in particular, which he tends to use even earlier than suggested in the International Hyperhidrosis Society guidelines.

Glycopyrrolate is available in 1 mg and 2 mg tablets; Dr. Wu starts patients at a dose of 1 mg twice a day, escalating by 1 mg per week until the “desired effects occur” or the patient has problems tolerating treatment because of side effects.

Other oral options include oxybutynin and propranolol. Sofpironium bromide, an analog of glycopyrrolate, is in the pipeline, he said.

During the interview, Dr. Wu discussed mydriasis, an adverse effect associated with both topical and systemic anticholinergic treatment. In the two pivotal phase 3 randomized trials of prescription glycopyrronium cloth (Qbrexza) for axillary hyperhidrosis, the incidence of mydriasis was 6.8% in 463 patients on active treatment for 4 weeks. Three-quarters of cases were unilateral. The mydriasis resolved without permanent treatment discontinuation in 27 of the 31 patients (J Am Acad Dermatol. 2019 Jan;80[1]:128-138.e2).

“The most important point is that patients need to be educated that they need to wash their hands very well after they apply it to the affected areas” to prevent accidental medication contact with the eyes, he advised.

Alarm bells can go off when a patient with anticholinergic therapy–induced mydriasis presents to an ED without mentioning their treatment status, Dr. Wu observed.

Dr. Wu had no relevant disclosures. SDEF/Global Academy for Medical Education and this news organization are owned by the same parent company.

To listen to the interview, click the play button below.

Key clinical point: Transcutaneous electrical nerve stimulation (TENS) is an effective option for treating migraine attacks in the emergency department.

Major finding: The verum group showed significant improvements on the visual analog scale change from 0 to 120 minutes (P less than .001) and a Likert-type verbal pain scale (P less than .001) compared with the sham group. The need for additional analgesics after 120 minutes was lower in the verum group vs. sham group (2.6% vs. 76.9%).

Study details: A randomized-controlled study evaluated the effectiveness of TENS for emergency treatment of migraine in the verum (n=39) and sham (n=39) groups.

Disclosures: The authors declared no conflicts of interest.

Citation: Hokenek NM et al. Am J Emerg Med. 2020 Jan 15. doi: 10.1016/j.ajem.2020.01.024.

Key clinical point: Transcutaneous electrical nerve stimulation (TENS) is an effective option for treating migraine attacks in the emergency department.

Major finding: The verum group showed significant improvements on the visual analog scale change from 0 to 120 minutes (P less than .001) and a Likert-type verbal pain scale (P less than .001) compared with the sham group. The need for additional analgesics after 120 minutes was lower in the verum group vs. sham group (2.6% vs. 76.9%).

Study details: A randomized-controlled study evaluated the effectiveness of TENS for emergency treatment of migraine in the verum (n=39) and sham (n=39) groups.

Disclosures: The authors declared no conflicts of interest.

Citation: Hokenek NM et al. Am J Emerg Med. 2020 Jan 15. doi: 10.1016/j.ajem.2020.01.024.

Key clinical point: Transcutaneous electrical nerve stimulation (TENS) is an effective option for treating migraine attacks in the emergency department.

Major finding: The verum group showed significant improvements on the visual analog scale change from 0 to 120 minutes (P less than .001) and a Likert-type verbal pain scale (P less than .001) compared with the sham group. The need for additional analgesics after 120 minutes was lower in the verum group vs. sham group (2.6% vs. 76.9%).

Study details: A randomized-controlled study evaluated the effectiveness of TENS for emergency treatment of migraine in the verum (n=39) and sham (n=39) groups.

Disclosures: The authors declared no conflicts of interest.

Citation: Hokenek NM et al. Am J Emerg Med. 2020 Jan 15. doi: 10.1016/j.ajem.2020.01.024.

Key clinical point: Migraine and asthma have a reciprocal association with each other.

Major finding: Patients with asthma had a 47% higher risk for migraine (P less than .001) than control participants, and patients with migraine had a 37% higher risk for asthma (P less than .001).

Study details: The data were obtained from 2 Korean longitudinal follow-up studies (Study 1: 113,059 patients with asthma and 113,059 control participants; Study 2: 36,044 patients with migraine and 114,176 control participants).

Disclosures: This study was partly supported by a grant from the National Research Foundation of Korea. The authors declared no conflicts of interest.

Citation: Kim SY et al. Sci Rep. 2019 Dec 4. doi: 10.1038/s41598-019-54972-8.

Key clinical point: Migraine and asthma have a reciprocal association with each other.

Major finding: Patients with asthma had a 47% higher risk for migraine (P less than .001) than control participants, and patients with migraine had a 37% higher risk for asthma (P less than .001).

Study details: The data were obtained from 2 Korean longitudinal follow-up studies (Study 1: 113,059 patients with asthma and 113,059 control participants; Study 2: 36,044 patients with migraine and 114,176 control participants).

Disclosures: This study was partly supported by a grant from the National Research Foundation of Korea. The authors declared no conflicts of interest.

Citation: Kim SY et al. Sci Rep. 2019 Dec 4. doi: 10.1038/s41598-019-54972-8.

Key clinical point: Migraine and asthma have a reciprocal association with each other.

Major finding: Patients with asthma had a 47% higher risk for migraine (P less than .001) than control participants, and patients with migraine had a 37% higher risk for asthma (P less than .001).

Study details: The data were obtained from 2 Korean longitudinal follow-up studies (Study 1: 113,059 patients with asthma and 113,059 control participants; Study 2: 36,044 patients with migraine and 114,176 control participants).

Disclosures: This study was partly supported by a grant from the National Research Foundation of Korea. The authors declared no conflicts of interest.

Citation: Kim SY et al. Sci Rep. 2019 Dec 4. doi: 10.1038/s41598-019-54972-8.

Key clinical point: Women of reproductive age experiencing migraines should be screened for endometriosis.

Major finding: Migraine headache was more frequent in women with endometriosis than in those without endometriosis (35.2% vs. 17.4%; P = .003).

Study details: The data were obtained from a French case-control study of 314 nonpregnant women younger than 42 years.

Disclosures: The authors declared no conflicts of interest.

Citation: Maitrot-Mantelet L et al. Cephalalgia. 2019 Dec 6. doi: 10.1177/0333102419893965.

Key clinical point: Women of reproductive age experiencing migraines should be screened for endometriosis.

Major finding: Migraine headache was more frequent in women with endometriosis than in those without endometriosis (35.2% vs. 17.4%; P = .003).

Study details: The data were obtained from a French case-control study of 314 nonpregnant women younger than 42 years.

Disclosures: The authors declared no conflicts of interest.

Citation: Maitrot-Mantelet L et al. Cephalalgia. 2019 Dec 6. doi: 10.1177/0333102419893965.

Key clinical point: Women of reproductive age experiencing migraines should be screened for endometriosis.

Major finding: Migraine headache was more frequent in women with endometriosis than in those without endometriosis (35.2% vs. 17.4%; P = .003).

Study details: The data were obtained from a French case-control study of 314 nonpregnant women younger than 42 years.

Disclosures: The authors declared no conflicts of interest.

Citation: Maitrot-Mantelet L et al. Cephalalgia. 2019 Dec 6. doi: 10.1177/0333102419893965.

Key clinical point: Shift workers are more likely to develop migraines and headaches than day workers.

Major finding: Shift workers had a 72% and 25% higher risk of developing migraine and unspecified headache, respectively, compared with day workers.

Study details: A longitudinal study included 2,952 individuals for the analyses of shift work and headache and 2,272 individuals for the analyses of shift work and migraine from the Danish PRISME cohort.

Disclosures: The study was funded by NordForsk, Nordic Program on Health and Welfare. The original PRISME study was supported by the Danish Working Environment Research Fund. The authors declared no conflicts of interest.

Citation: Appel AM et al. Int Arch Occup Environ Health. 2020 Jan 11. doi: 10.1007/s00420-019-01512-6.

Key clinical point: Shift workers are more likely to develop migraines and headaches than day workers.

Major finding: Shift workers had a 72% and 25% higher risk of developing migraine and unspecified headache, respectively, compared with day workers.

Study details: A longitudinal study included 2,952 individuals for the analyses of shift work and headache and 2,272 individuals for the analyses of shift work and migraine from the Danish PRISME cohort.

Disclosures: The study was funded by NordForsk, Nordic Program on Health and Welfare. The original PRISME study was supported by the Danish Working Environment Research Fund. The authors declared no conflicts of interest.

Citation: Appel AM et al. Int Arch Occup Environ Health. 2020 Jan 11. doi: 10.1007/s00420-019-01512-6.

Key clinical point: Shift workers are more likely to develop migraines and headaches than day workers.

Major finding: Shift workers had a 72% and 25% higher risk of developing migraine and unspecified headache, respectively, compared with day workers.

Study details: A longitudinal study included 2,952 individuals for the analyses of shift work and headache and 2,272 individuals for the analyses of shift work and migraine from the Danish PRISME cohort.

Disclosures: The study was funded by NordForsk, Nordic Program on Health and Welfare. The original PRISME study was supported by the Danish Working Environment Research Fund. The authors declared no conflicts of interest.

Citation: Appel AM et al. Int Arch Occup Environ Health. 2020 Jan 11. doi: 10.1007/s00420-019-01512-6.

LAS VEGAS – For Karen J. Hartwell, MD, few things in her clinical work bring more reward than providing medication-assisted treatment (MAT) to patients with opioid use disorder.

Doug Brunk/MDedge News

“Seeing people get into recovery on buprenorphine is as exciting as seeing your first person respond to clozapine, or to see a depression remit on your selection of an antidepressant,” she said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “We know that medication-assisted treatment is underused and, sadly, relapse rates remain high.”

According to the Centers for Disease Control and Prevention, there were 70,237 drug-related overdose deaths in 2017 – 47,600 from prescription and illicit opioids. “This is being driven predominately by fentanyl and other high-potency synthetic opioids, followed by prescription opioids and heroin,” said Dr. Hartwell, an associate professor in the addiction sciences division in the department of psychiatry and behavioral sciences at the Medical University of South Carolina, Charleston.

There were an estimated 2 million Americans with an opioid use disorder (OUD) in 2018, she said, and more than 10 million misused prescription opioids. At the same time, prescriptions for opioids have dropped to lowest level in 10 years from a peak in 2012 of 81.3 prescriptions per 100 persons to 58.7 prescriptions per 100 persons in 2017 – total of more than 191 million scripts. “There is a decline in the number of opioid prescriptions, but there is still a lot of diversion, and there are some prescription ‘hot spots’ in the Southeast,” Dr. Hartwell said. “Heroin is a very low cost, and we’re wrestling with the issue of fentanyl.”

To complicate matters, most Americans with opioid use disorder are not in treatment. “In many people, the disorder is never diagnosed, and even fewer engage in care,” she said. “There are challenges with treatment retention, and even fewer achieve remission. There’s a lot of work to be done. One of which is the availability of medication-assisted treatment.”

Dr. Hartwell said that she knows of physician colleagues who have obtained a waiver to prescribe buprenorphine but have yet to prescribe it. “Some people may prefer to avoid the dance [of buprenorphine prescribing],” she said. “I’m here to advise you to dance.” Clinicians can learn about MAT waiver training opportunities by visiting the website of the Providers Clinical Support System, a program funded by the Substance Abuse and Mental Health Services Administration (SAMHSA).

Another option is to join a telementoring session on the topic facilitated by Project ECHO, or Extension for Community Healthcare Outcomes, which is being used by the University of New Mexico, Albuquerque. The goal of this model is to break down the walls between specialty and primary care by linking experts at an academic “hub” with primary care doctors and nurses in nearby communities.

“Our Project ECHO at the Medical University of South Carolina is twice a month on Fridays,” Dr. Hartwell said. “The first half is a case. The second half is a didactic [session], and you get a free hour of CME.”

The most common drugs used for medication-assisted treatment of opioid disorder are buprenorphine (a partial agonist), naltrexone (an antagonist), and methadone (a full agonist). Methadone retention generally is better than buprenorphine or naltrexone. The recommended treatment duration is 6-12 months, yet many studies demonstrate that many only stay on treatment for 30-60 days.

“You want to keep patients on treatment as long as they benefit from the medication,” Dr. Hartwell said. One large study of Medicaid claims data found that the risk of acute care service use and overdose were high following buprenorphine discontinuation, regardless of treatment duration. Superior outcomes became significant with treatment duration beyond 15 months, although rates of the primary adverse outcomes remained high (Am J Psychiatry. 2020 Feb 1;177[2]:117-24). About 5% of patients across all cohorts experienced one or more medically treated overdoses.

“One thing I don’t want is for people to drop out of treatment and not come back to see me,” Dr. Hartwell said. “This is a time for us to use our shared decision-making skills. I like to use the Tapering Readiness Inventory, a list of 16 questions. It asks such things as ‘Are you able to cope with difficult situations without using?’ and ‘Do you have all of the [drug] paraphernalia out of the house?’ We then have a discussion. If the patient decides to go ahead and do a taper, I always leave the door open. So, as that taper persists and someone says, ‘I’m starting to think about using, Doctor,’ I’ll put them back on [buprenorphine]. Or, if they come off the drug and they find themselves at risk of relapsing, they come back in and see me.”

There’s also some evidence that contingency management might be helpful, both in terms of opioid negative urines, and retention and treatment. Meanwhile, extended-release forms of buprenorphine are emerging.

In 2017, the Food and Drug Administration approved Sublocade, the first once-monthly injectable buprenorphine product for the treatment of moderate-to-severe OUD in adult patients who have initiated treatment with a transmucosal buprenorphine-containing product. “The recommendations are that you have about a 7-day lead-in of sublingual buprenorphine, and then 2 months of a 300-mg IV injection,” Dr. Hartwell said. “This is followed by either 100-mg injections monthly or 300-mg maintenance in select cases. There is some pain at the injection site. Some clinicians are getting around this by using a little bit of lidocaine prior to giving the injection.”

Another product, Brixadi, is an extended-release weekly (8 mg, 16 mg, 24 mg, 32 mg) and monthly (64 mg, 96 mg, 128 mg) buprenorphine injection used for the treatment of moderate to severe OUD. It is expected to be available in December 2020.

In 2016, the FDA approved Probuphine, the first buprenorphine implant for the maintenance treatment of opioid dependence. Probuphine is designed to provide a constant, low-level dose of buprenorphine for 6 months in patients who are already stable on low to moderate doses of other forms of buprenorphine, as part of a complete treatment program. “The 6-month duration kind of takes the issue of adherence off the table,” Dr. Hartwell said. “The caveat with this is that you have to be stable on 8 mg of buprenorphine per day or less. The majority of my patients require much higher doses.”

Dr. Hartwell reported having no relevant disclosures.

[email protected]

LAS VEGAS – For Karen J. Hartwell, MD, few things in her clinical work bring more reward than providing medication-assisted treatment (MAT) to patients with opioid use disorder.

Doug Brunk/MDedge News

“Seeing people get into recovery on buprenorphine is as exciting as seeing your first person respond to clozapine, or to see a depression remit on your selection of an antidepressant,” she said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “We know that medication-assisted treatment is underused and, sadly, relapse rates remain high.”

According to the Centers for Disease Control and Prevention, there were 70,237 drug-related overdose deaths in 2017 – 47,600 from prescription and illicit opioids. “This is being driven predominately by fentanyl and other high-potency synthetic opioids, followed by prescription opioids and heroin,” said Dr. Hartwell, an associate professor in the addiction sciences division in the department of psychiatry and behavioral sciences at the Medical University of South Carolina, Charleston.

There were an estimated 2 million Americans with an opioid use disorder (OUD) in 2018, she said, and more than 10 million misused prescription opioids. At the same time, prescriptions for opioids have dropped to lowest level in 10 years from a peak in 2012 of 81.3 prescriptions per 100 persons to 58.7 prescriptions per 100 persons in 2017 – total of more than 191 million scripts. “There is a decline in the number of opioid prescriptions, but there is still a lot of diversion, and there are some prescription ‘hot spots’ in the Southeast,” Dr. Hartwell said. “Heroin is a very low cost, and we’re wrestling with the issue of fentanyl.”

To complicate matters, most Americans with opioid use disorder are not in treatment. “In many people, the disorder is never diagnosed, and even fewer engage in care,” she said. “There are challenges with treatment retention, and even fewer achieve remission. There’s a lot of work to be done. One of which is the availability of medication-assisted treatment.”

Dr. Hartwell said that she knows of physician colleagues who have obtained a waiver to prescribe buprenorphine but have yet to prescribe it. “Some people may prefer to avoid the dance [of buprenorphine prescribing],” she said. “I’m here to advise you to dance.” Clinicians can learn about MAT waiver training opportunities by visiting the website of the Providers Clinical Support System, a program funded by the Substance Abuse and Mental Health Services Administration (SAMHSA).

Another option is to join a telementoring session on the topic facilitated by Project ECHO, or Extension for Community Healthcare Outcomes, which is being used by the University of New Mexico, Albuquerque. The goal of this model is to break down the walls between specialty and primary care by linking experts at an academic “hub” with primary care doctors and nurses in nearby communities.

“Our Project ECHO at the Medical University of South Carolina is twice a month on Fridays,” Dr. Hartwell said. “The first half is a case. The second half is a didactic [session], and you get a free hour of CME.”

The most common drugs used for medication-assisted treatment of opioid disorder are buprenorphine (a partial agonist), naltrexone (an antagonist), and methadone (a full agonist). Methadone retention generally is better than buprenorphine or naltrexone. The recommended treatment duration is 6-12 months, yet many studies demonstrate that many only stay on treatment for 30-60 days.

“You want to keep patients on treatment as long as they benefit from the medication,” Dr. Hartwell said. One large study of Medicaid claims data found that the risk of acute care service use and overdose were high following buprenorphine discontinuation, regardless of treatment duration. Superior outcomes became significant with treatment duration beyond 15 months, although rates of the primary adverse outcomes remained high (Am J Psychiatry. 2020 Feb 1;177[2]:117-24). About 5% of patients across all cohorts experienced one or more medically treated overdoses.

“One thing I don’t want is for people to drop out of treatment and not come back to see me,” Dr. Hartwell said. “This is a time for us to use our shared decision-making skills. I like to use the Tapering Readiness Inventory, a list of 16 questions. It asks such things as ‘Are you able to cope with difficult situations without using?’ and ‘Do you have all of the [drug] paraphernalia out of the house?’ We then have a discussion. If the patient decides to go ahead and do a taper, I always leave the door open. So, as that taper persists and someone says, ‘I’m starting to think about using, Doctor,’ I’ll put them back on [buprenorphine]. Or, if they come off the drug and they find themselves at risk of relapsing, they come back in and see me.”

There’s also some evidence that contingency management might be helpful, both in terms of opioid negative urines, and retention and treatment. Meanwhile, extended-release forms of buprenorphine are emerging.

In 2017, the Food and Drug Administration approved Sublocade, the first once-monthly injectable buprenorphine product for the treatment of moderate-to-severe OUD in adult patients who have initiated treatment with a transmucosal buprenorphine-containing product. “The recommendations are that you have about a 7-day lead-in of sublingual buprenorphine, and then 2 months of a 300-mg IV injection,” Dr. Hartwell said. “This is followed by either 100-mg injections monthly or 300-mg maintenance in select cases. There is some pain at the injection site. Some clinicians are getting around this by using a little bit of lidocaine prior to giving the injection.”

Another product, Brixadi, is an extended-release weekly (8 mg, 16 mg, 24 mg, 32 mg) and monthly (64 mg, 96 mg, 128 mg) buprenorphine injection used for the treatment of moderate to severe OUD. It is expected to be available in December 2020.

In 2016, the FDA approved Probuphine, the first buprenorphine implant for the maintenance treatment of opioid dependence. Probuphine is designed to provide a constant, low-level dose of buprenorphine for 6 months in patients who are already stable on low to moderate doses of other forms of buprenorphine, as part of a complete treatment program. “The 6-month duration kind of takes the issue of adherence off the table,” Dr. Hartwell said. “The caveat with this is that you have to be stable on 8 mg of buprenorphine per day or less. The majority of my patients require much higher doses.”

Dr. Hartwell reported having no relevant disclosures.

[email protected]

LAS VEGAS – For Karen J. Hartwell, MD, few things in her clinical work bring more reward than providing medication-assisted treatment (MAT) to patients with opioid use disorder.

Doug Brunk/MDedge News

“Seeing people get into recovery on buprenorphine is as exciting as seeing your first person respond to clozapine, or to see a depression remit on your selection of an antidepressant,” she said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “We know that medication-assisted treatment is underused and, sadly, relapse rates remain high.”

According to the Centers for Disease Control and Prevention, there were 70,237 drug-related overdose deaths in 2017 – 47,600 from prescription and illicit opioids. “This is being driven predominately by fentanyl and other high-potency synthetic opioids, followed by prescription opioids and heroin,” said Dr. Hartwell, an associate professor in the addiction sciences division in the department of psychiatry and behavioral sciences at the Medical University of South Carolina, Charleston.

There were an estimated 2 million Americans with an opioid use disorder (OUD) in 2018, she said, and more than 10 million misused prescription opioids. At the same time, prescriptions for opioids have dropped to lowest level in 10 years from a peak in 2012 of 81.3 prescriptions per 100 persons to 58.7 prescriptions per 100 persons in 2017 – total of more than 191 million scripts. “There is a decline in the number of opioid prescriptions, but there is still a lot of diversion, and there are some prescription ‘hot spots’ in the Southeast,” Dr. Hartwell said. “Heroin is a very low cost, and we’re wrestling with the issue of fentanyl.”

To complicate matters, most Americans with opioid use disorder are not in treatment. “In many people, the disorder is never diagnosed, and even fewer engage in care,” she said. “There are challenges with treatment retention, and even fewer achieve remission. There’s a lot of work to be done. One of which is the availability of medication-assisted treatment.”

Dr. Hartwell said that she knows of physician colleagues who have obtained a waiver to prescribe buprenorphine but have yet to prescribe it. “Some people may prefer to avoid the dance [of buprenorphine prescribing],” she said. “I’m here to advise you to dance.” Clinicians can learn about MAT waiver training opportunities by visiting the website of the Providers Clinical Support System, a program funded by the Substance Abuse and Mental Health Services Administration (SAMHSA).

Another option is to join a telementoring session on the topic facilitated by Project ECHO, or Extension for Community Healthcare Outcomes, which is being used by the University of New Mexico, Albuquerque. The goal of this model is to break down the walls between specialty and primary care by linking experts at an academic “hub” with primary care doctors and nurses in nearby communities.

“Our Project ECHO at the Medical University of South Carolina is twice a month on Fridays,” Dr. Hartwell said. “The first half is a case. The second half is a didactic [session], and you get a free hour of CME.”

The most common drugs used for medication-assisted treatment of opioid disorder are buprenorphine (a partial agonist), naltrexone (an antagonist), and methadone (a full agonist). Methadone retention generally is better than buprenorphine or naltrexone. The recommended treatment duration is 6-12 months, yet many studies demonstrate that many only stay on treatment for 30-60 days.

“You want to keep patients on treatment as long as they benefit from the medication,” Dr. Hartwell said. One large study of Medicaid claims data found that the risk of acute care service use and overdose were high following buprenorphine discontinuation, regardless of treatment duration. Superior outcomes became significant with treatment duration beyond 15 months, although rates of the primary adverse outcomes remained high (Am J Psychiatry. 2020 Feb 1;177[2]:117-24). About 5% of patients across all cohorts experienced one or more medically treated overdoses.

“One thing I don’t want is for people to drop out of treatment and not come back to see me,” Dr. Hartwell said. “This is a time for us to use our shared decision-making skills. I like to use the Tapering Readiness Inventory, a list of 16 questions. It asks such things as ‘Are you able to cope with difficult situations without using?’ and ‘Do you have all of the [drug] paraphernalia out of the house?’ We then have a discussion. If the patient decides to go ahead and do a taper, I always leave the door open. So, as that taper persists and someone says, ‘I’m starting to think about using, Doctor,’ I’ll put them back on [buprenorphine]. Or, if they come off the drug and they find themselves at risk of relapsing, they come back in and see me.”

There’s also some evidence that contingency management might be helpful, both in terms of opioid negative urines, and retention and treatment. Meanwhile, extended-release forms of buprenorphine are emerging.

In 2017, the Food and Drug Administration approved Sublocade, the first once-monthly injectable buprenorphine product for the treatment of moderate-to-severe OUD in adult patients who have initiated treatment with a transmucosal buprenorphine-containing product. “The recommendations are that you have about a 7-day lead-in of sublingual buprenorphine, and then 2 months of a 300-mg IV injection,” Dr. Hartwell said. “This is followed by either 100-mg injections monthly or 300-mg maintenance in select cases. There is some pain at the injection site. Some clinicians are getting around this by using a little bit of lidocaine prior to giving the injection.”

Another product, Brixadi, is an extended-release weekly (8 mg, 16 mg, 24 mg, 32 mg) and monthly (64 mg, 96 mg, 128 mg) buprenorphine injection used for the treatment of moderate to severe OUD. It is expected to be available in December 2020.

In 2016, the FDA approved Probuphine, the first buprenorphine implant for the maintenance treatment of opioid dependence. Probuphine is designed to provide a constant, low-level dose of buprenorphine for 6 months in patients who are already stable on low to moderate doses of other forms of buprenorphine, as part of a complete treatment program. “The 6-month duration kind of takes the issue of adherence off the table,” Dr. Hartwell said. “The caveat with this is that you have to be stable on 8 mg of buprenorphine per day or less. The majority of my patients require much higher doses.”

Dr. Hartwell reported having no relevant disclosures.

[email protected]

Rheumatologists may have a tough time in the office, but they know how to enjoy themselves once the workday ends, according to Medscape’s 2020 Lifestyle, Happiness, & Burnout Report.

In the Medscape survey, less than one-quarter of rheumatologists reported being happy at work, the same as internal medicine, with only neurologists reporting worse at-work happiness rates. While all measured specialties were happier outside of work than at work, no specialty had more of a gap than rheumatologists, rising from 22% at work to 60% outside of work.

The rate of burnout in rheumatologists was slightly higher than that seen in physicians overall (45% vs. 41%), with 78% of rheumatologists reporting that the growing number of bureaucratic tasks contributed most to burnout, followed by increased time devoted to EHRs (43%) and spending too much time at work (40%).

Rheumatologists most commonly dealt with burnout through exercise (46%), isolating themselves from others (45%), and talking with family/friends (44%). Rheumatologists were about average when it came to taking vacation, with 47% taking 3-4 weeks off of work, compared with 44% of all physicians; only 29% took less than 3 weeks’ vacation.

More than 90% of rheumatologists reported that they’d never contemplated suicide, with only 6% reported that they’d thought about it and none reporting that they’d attempted suicide. Similarly, 79% of rheumatologists reported that they are not and do not plan to seek professional help for symptoms of burnout and/or depression, with 10% saying they were currently seeing professional help and 8% saying they had been to therapy but were not anymore.

The Medscape survey was conducted from June 25 to Sept. 19, 2019, and involved 15,181 physicians.

[email protected]

Rheumatologists may have a tough time in the office, but they know how to enjoy themselves once the workday ends, according to Medscape’s 2020 Lifestyle, Happiness, & Burnout Report.

In the Medscape survey, less than one-quarter of rheumatologists reported being happy at work, the same as internal medicine, with only neurologists reporting worse at-work happiness rates. While all measured specialties were happier outside of work than at work, no specialty had more of a gap than rheumatologists, rising from 22% at work to 60% outside of work.

The rate of burnout in rheumatologists was slightly higher than that seen in physicians overall (45% vs. 41%), with 78% of rheumatologists reporting that the growing number of bureaucratic tasks contributed most to burnout, followed by increased time devoted to EHRs (43%) and spending too much time at work (40%).

Rheumatologists most commonly dealt with burnout through exercise (46%), isolating themselves from others (45%), and talking with family/friends (44%). Rheumatologists were about average when it came to taking vacation, with 47% taking 3-4 weeks off of work, compared with 44% of all physicians; only 29% took less than 3 weeks’ vacation.

More than 90% of rheumatologists reported that they’d never contemplated suicide, with only 6% reported that they’d thought about it and none reporting that they’d attempted suicide. Similarly, 79% of rheumatologists reported that they are not and do not plan to seek professional help for symptoms of burnout and/or depression, with 10% saying they were currently seeing professional help and 8% saying they had been to therapy but were not anymore.

The Medscape survey was conducted from June 25 to Sept. 19, 2019, and involved 15,181 physicians.

[email protected]

Rheumatologists may have a tough time in the office, but they know how to enjoy themselves once the workday ends, according to Medscape’s 2020 Lifestyle, Happiness, & Burnout Report.

In the Medscape survey, less than one-quarter of rheumatologists reported being happy at work, the same as internal medicine, with only neurologists reporting worse at-work happiness rates. While all measured specialties were happier outside of work than at work, no specialty had more of a gap than rheumatologists, rising from 22% at work to 60% outside of work.

The rate of burnout in rheumatologists was slightly higher than that seen in physicians overall (45% vs. 41%), with 78% of rheumatologists reporting that the growing number of bureaucratic tasks contributed most to burnout, followed by increased time devoted to EHRs (43%) and spending too much time at work (40%).

Rheumatologists most commonly dealt with burnout through exercise (46%), isolating themselves from others (45%), and talking with family/friends (44%). Rheumatologists were about average when it came to taking vacation, with 47% taking 3-4 weeks off of work, compared with 44% of all physicians; only 29% took less than 3 weeks’ vacation.

More than 90% of rheumatologists reported that they’d never contemplated suicide, with only 6% reported that they’d thought about it and none reporting that they’d attempted suicide. Similarly, 79% of rheumatologists reported that they are not and do not plan to seek professional help for symptoms of burnout and/or depression, with 10% saying they were currently seeing professional help and 8% saying they had been to therapy but were not anymore.

The Medscape survey was conducted from June 25 to Sept. 19, 2019, and involved 15,181 physicians.

[email protected]

MAUI, HAWAII – If an intra-abdominal abscess in a recently diagnosed Crohn’s disease patient is less than 6 cm across with no downstream stenosis, involves only a short segment of bowel, and the patient has no perianal disease, then infliximab and azathioprine after drainage and antibiotics might be enough to heal it, according to Miguel Regueiro, MD, chair of the department of gastroenterology, hepatology, and nutrition at the Cleveland Clinic.

M. Alexander Otto/MDedge News

That will work in about 30% of patients who hit the mark; the rest will eventually need surgery, said Dr. Regueiro, a clinical researcher who has worked extensively with surgical GI patients and is also a coauthor on the American College of Gastroenterology 2018 Crohn’s disease guidelines (Am J Gastroenterol. 2018 Apr;113[4]:481-517).

Intra-abdominal abscesses are common in Crohn’s, usually from an inflammation-induced fistula or sinus in the small intestines that spills luminal contents into the abdominal cavity. Drainage and antibiotics are first line, but then there’s the question of who needs to go to the operating room and who doesn’t.

It has to do with “how much the hole in the intestines is actually reversible. Evidence of a stricture is of paramount importance. If you have a stricture below a fistula and prestenotic dilatation, that’s a high-pressure zone.” It’s a “fixed complication that, in my opinion, no medication is ever going to treat,” he said at the Gastroenterology Updates, IBD, Liver Disease Conference.

Most patients will need surgery, but for smaller abscesses in qualifying patients, medical treatment can work. “Infliximab is still probably the best medicine for fistulizing disease,” so Dr. Regueiro opts for that if patients haven’t been on it before, in combination with an immunomodulator, generally azathioprine at half the standard dose, to prevent patients from forming antibodies to the infliximab.

When patients do go to the operating room, there is a good chance they will end up with a temporary ostomy, and definitely so if the abscess can’t be drained completely to prevent spillage. The risk of dehiscence and other complications is too great for primary anastomosis.

“I mentally prepare my patients for that; I tell them up front. I never guarantee that they are not going to have an ostomy bag,” Dr. Regueiro said.

He also said abscess formation isn’t necessarily a sign the biologic patients were on before has failed, especially if they were only on it for 6 months or so. More likely, “the disease was too far gone at that point” for short-term treatment to have much of an effect.

So he’s often likely to continue patients on the same biologic after surgery. “We’ve done a lot of study on” this and have “actually found that” patients do well with the approach. He will switch treatment, however, if they otherwise no longer seem to respond to a biologic they have been taking a while, despite adequate serum levels.

There’s no need to delay surgery for patients on biologics. “If they get a biologic the day before, they can still go to the [operating room]. We are not seeing increased postop complications, infections, or wound dehiscence,” he said.

Dr. Regueiro generally restarts biologics 2-4 weeks after surgery, which is enough time to know if there is going to be a surgical complication but not so long that patients will have a Crohn’s relapse. He restarts the maintenance dose, as “it’s not necessary to reinduct patients after such a short break,” he said.

He also noted that opioids and steroids should be avoided with Crohn’s abscesses. Opioids increase the risk of ileus, and steroids the risk of sepsis.

Dr. Regueiro reported no relevant disclosures.

[email protected]

MAUI, HAWAII – If an intra-abdominal abscess in a recently diagnosed Crohn’s disease patient is less than 6 cm across with no downstream stenosis, involves only a short segment of bowel, and the patient has no perianal disease, then infliximab and azathioprine after drainage and antibiotics might be enough to heal it, according to Miguel Regueiro, MD, chair of the department of gastroenterology, hepatology, and nutrition at the Cleveland Clinic.

M. Alexander Otto/MDedge News

That will work in about 30% of patients who hit the mark; the rest will eventually need surgery, said Dr. Regueiro, a clinical researcher who has worked extensively with surgical GI patients and is also a coauthor on the American College of Gastroenterology 2018 Crohn’s disease guidelines (Am J Gastroenterol. 2018 Apr;113[4]:481-517).

Intra-abdominal abscesses are common in Crohn’s, usually from an inflammation-induced fistula or sinus in the small intestines that spills luminal contents into the abdominal cavity. Drainage and antibiotics are first line, but then there’s the question of who needs to go to the operating room and who doesn’t.

It has to do with “how much the hole in the intestines is actually reversible. Evidence of a stricture is of paramount importance. If you have a stricture below a fistula and prestenotic dilatation, that’s a high-pressure zone.” It’s a “fixed complication that, in my opinion, no medication is ever going to treat,” he said at the Gastroenterology Updates, IBD, Liver Disease Conference.

Most patients will need surgery, but for smaller abscesses in qualifying patients, medical treatment can work. “Infliximab is still probably the best medicine for fistulizing disease,” so Dr. Regueiro opts for that if patients haven’t been on it before, in combination with an immunomodulator, generally azathioprine at half the standard dose, to prevent patients from forming antibodies to the infliximab.

When patients do go to the operating room, there is a good chance they will end up with a temporary ostomy, and definitely so if the abscess can’t be drained completely to prevent spillage. The risk of dehiscence and other complications is too great for primary anastomosis.

“I mentally prepare my patients for that; I tell them up front. I never guarantee that they are not going to have an ostomy bag,” Dr. Regueiro said.

He also said abscess formation isn’t necessarily a sign the biologic patients were on before has failed, especially if they were only on it for 6 months or so. More likely, “the disease was too far gone at that point” for short-term treatment to have much of an effect.

So he’s often likely to continue patients on the same biologic after surgery. “We’ve done a lot of study on” this and have “actually found that” patients do well with the approach. He will switch treatment, however, if they otherwise no longer seem to respond to a biologic they have been taking a while, despite adequate serum levels.

There’s no need to delay surgery for patients on biologics. “If they get a biologic the day before, they can still go to the [operating room]. We are not seeing increased postop complications, infections, or wound dehiscence,” he said.

Dr. Regueiro generally restarts biologics 2-4 weeks after surgery, which is enough time to know if there is going to be a surgical complication but not so long that patients will have a Crohn’s relapse. He restarts the maintenance dose, as “it’s not necessary to reinduct patients after such a short break,” he said.

He also noted that opioids and steroids should be avoided with Crohn’s abscesses. Opioids increase the risk of ileus, and steroids the risk of sepsis.

Dr. Regueiro reported no relevant disclosures.

[email protected]

MAUI, HAWAII – If an intra-abdominal abscess in a recently diagnosed Crohn’s disease patient is less than 6 cm across with no downstream stenosis, involves only a short segment of bowel, and the patient has no perianal disease, then infliximab and azathioprine after drainage and antibiotics might be enough to heal it, according to Miguel Regueiro, MD, chair of the department of gastroenterology, hepatology, and nutrition at the Cleveland Clinic.

M. Alexander Otto/MDedge News

That will work in about 30% of patients who hit the mark; the rest will eventually need surgery, said Dr. Regueiro, a clinical researcher who has worked extensively with surgical GI patients and is also a coauthor on the American College of Gastroenterology 2018 Crohn’s disease guidelines (Am J Gastroenterol. 2018 Apr;113[4]:481-517).

Intra-abdominal abscesses are common in Crohn’s, usually from an inflammation-induced fistula or sinus in the small intestines that spills luminal contents into the abdominal cavity. Drainage and antibiotics are first line, but then there’s the question of who needs to go to the operating room and who doesn’t.

It has to do with “how much the hole in the intestines is actually reversible. Evidence of a stricture is of paramount importance. If you have a stricture below a fistula and prestenotic dilatation, that’s a high-pressure zone.” It’s a “fixed complication that, in my opinion, no medication is ever going to treat,” he said at the Gastroenterology Updates, IBD, Liver Disease Conference.

Most patients will need surgery, but for smaller abscesses in qualifying patients, medical treatment can work. “Infliximab is still probably the best medicine for fistulizing disease,” so Dr. Regueiro opts for that if patients haven’t been on it before, in combination with an immunomodulator, generally azathioprine at half the standard dose, to prevent patients from forming antibodies to the infliximab.

When patients do go to the operating room, there is a good chance they will end up with a temporary ostomy, and definitely so if the abscess can’t be drained completely to prevent spillage. The risk of dehiscence and other complications is too great for primary anastomosis.

“I mentally prepare my patients for that; I tell them up front. I never guarantee that they are not going to have an ostomy bag,” Dr. Regueiro said.

He also said abscess formation isn’t necessarily a sign the biologic patients were on before has failed, especially if they were only on it for 6 months or so. More likely, “the disease was too far gone at that point” for short-term treatment to have much of an effect.

So he’s often likely to continue patients on the same biologic after surgery. “We’ve done a lot of study on” this and have “actually found that” patients do well with the approach. He will switch treatment, however, if they otherwise no longer seem to respond to a biologic they have been taking a while, despite adequate serum levels.

There’s no need to delay surgery for patients on biologics. “If they get a biologic the day before, they can still go to the [operating room]. We are not seeing increased postop complications, infections, or wound dehiscence,” he said.

Dr. Regueiro generally restarts biologics 2-4 weeks after surgery, which is enough time to know if there is going to be a surgical complication but not so long that patients will have a Crohn’s relapse. He restarts the maintenance dose, as “it’s not necessary to reinduct patients after such a short break,” he said.

He also noted that opioids and steroids should be avoided with Crohn’s abscesses. Opioids increase the risk of ileus, and steroids the risk of sepsis.

Dr. Regueiro reported no relevant disclosures.

[email protected]

Hospitalists encounter troponin elevations daily, but we have to use clinical judgment to determine if the troponin elevation represents either a myocardial infarction (MI), or a non-MI troponin elevation (i.e. a , nonischemic myocardial injury).

©decade3d/Thinkstock.com

It is important to remember that an MI specifically refers to myocardial injury due to acute myocardial ischemia to the myocardium. This lack of blood supply can be due to an acute absolute or relative deficiency in coronary artery blood flow. However, there are also many mechanisms of myocardial injury unrelated to reduced coronary artery blood flow, and these should be more appropriately termed non-MI troponin elevations.

Historically, when an ischemic mechanism of myocardial injury was suspected, providers would categorize troponin elevations into ST-elevation MI (STEMI) versus non-ST-elevation MI (NSTEMI) based on the electrocardiogram (ECG). We would further classify the NSTEMI into type 1 or type 2, depending on the mechanism of injury. The term “NSTEMI” served as a “catch-all” term to describe both type 1 NSTEMIs and type 2 MIs, but that classification system is no longer valid.

Classification of MI types

The Fourth Universal Definition of MI published in August 2018 further updated the definitions of MI (summarized in Figure 1).² This review focuses on type 1 and type 2 MIs, which are the most common types encountered by hospitalists. Types 3-5 MI (grouped under a common ICD-10 diagnosis code for “Other MI Types,” or I21.A9) would rarely be diagnosed by hospitalists.



Figure 1: Classification of MI
 

The diagnosis of a type 1 MIs (STEMI and NSTEMI) is supported by the presence of an acute coronary thrombus or plaque rupture/erosion on coronary angiography or a strong suspicion for these when angiography is unavailable or contraindicated. Type 1 MI (also referred to as spontaneous MI) is generally a primary reason (or “principal” diagnosis) for a patient’s presentation to a hospital.³ Please note that a very high or rising troponin level alone is not diagnostic for a type 1 or type 2 NSTEMI. The lab has to be taken in the context of the patient’s presentation and other supporting findings.

In contrast to a type 1 MI (STEMI and NSTEMI), at type 2 MI results from an imbalance between myocardial oxygen supply and demand unrelated to acute coronary artery thrombosis or plaque rupture. A type 2 MI is a relative (as opposed to an absolute) deficiency in coronary artery blood flow triggered by an abrupt increase in myocardial oxygen demand, drop in myocardial blood supply, or both. In type 2 MI, myocardial injury occurs secondary to an underlying process, and therefore requires correct documentation of the underlying cause as well. 

Common examples of underlying causes of type 2 MI include acute blood loss anemia (e.g. GI bleed), acute hypoxia (e.g. COPD exacerbation), shock states (cardiogenic, hypovolemic, hemorrhagic, or septic), coronary vasospasm (e.g. spontaneous), and bradyarrhythmias. Patients with type 2 MI often have a history of fixed obstructive coronary disease, which when coupled with the acute trigger facilitates the type 2 MI; however, underlying CAD is not always present. 

Diagnosing a type 2 MI requires evidence of acute myocardial ischemia (Figure 2) with an elevated troponin but must also have at least one of the following:²

• Symptoms of acute myocardial ischemia such as typical chest pain.
• New ischemic ECG changes.
• Development of pathological Q waves.
• Imaging evidence of new loss of viable myocardium, significant reversible perfusion defect on nuclear imaging, or new regional wall motion abnormality in a pattern consistent with an ischemic etiology.

Distinguishing a type 1 NSTEMI from a type 2 MI depends mainly on the clinical context and clinical judgment. A patient whose presenting symptoms include acute chest discomfort, acute ST-T wave changes, and a rise in troponin would be suspected of having a type 1 NSTEMI. However, in a patient presenting with other or vague complaints where an elevated troponin was found amongst a battery of tests, a type 2 MI may be favored, particularly if there is evidence of an underlying trigger for a supply-demand mismatch. In challenging cases, cardiology consultation can help determine the MI type and/or the next diagnostic and treatment considerations.

When there is only elevated troponin levels (or even a rise and fall in troponin) without new symptoms or ECG/imaging evidence of myocardial ischemia, it is most appropriate to document a non-MI troponin elevation due to a nonischemic mechanism of myocardial injury.
 

Non-MI troponin elevation (nonischemic myocardial injury)

The number of conditions known to cause myocardial injury through mechanisms other than myocardial ischemia (see Figure 2) is growing, especially in the current era of high-sensitivity troponin assays.⁴

Common examples of underlying causes of non-MI troponin elevation include:

• Acute (on chronic) systolic or diastolic heart failure: Usually due to acute ventricular wall stretch/strain. Troponin elevations tend to be mild, with more indolent (or even flat) troponin trajectories.
• Pericarditis and myocarditis: Due to direct injury from myocardial inflammation.
• Cardiopulmonary resuscitation (CPR): Due to physical injury to the heart from mechanical chest compressions and from electrical shocks of external defibrillation.
• Stress-induced (takotsubo) cardiomyopathy: Stress-induced release of neurohormonal factors and catecholamines that cause direct myocyte injury and transient dilatation of the ventricle.
• Acute pulmonary embolism: Result of acute right ventricular wall stretch/strain, not from myocardial ischemia.
• Sepsis without shock: Direct toxicity of circulating cytokines to cardiac myocytes. In the absence of evidence of shock and symptoms/signs of myocardial ischemia, do not document type 2 MI.
• Renal failure (acute kidney injury or chronic kidney disease): Multiple etiologies, but at least partially related to reduced renal clearance of troponin. In general, renal failure in the absence of symptoms/signs of ischemia is best classified as a non-MI troponin elevation. ESRD patients who present with volume overload due to missed dialysis also typically have a non-MI troponin elevation.
• Stroke/intracranial hemorrhage: Mechanisms of myocardial injury and troponin elevation are incompletely understood, but may include catecholamine surges that injure the heart.

Some underlying conditions can cause a type 2 MI or a non-MI troponin elevation depending on the clinical context. For example, hypertensive emergency, severe aortic valve stenosis, hypertrophic cardiomyopathy, and tachyarrhythmias (including atrial fibrillation with rapid ventricular response) may cause increased myocardial oxygen demand, and in patients with underlying CAD, could precipitate a type 2 MI.

However, these same conditions could cause a non-MI troponin elevation in patients without CAD and could also cause myocardial injury and troponin release by causing acute left ventricular stretch/strain. Distinguishing the diagnose of type 2 MI vs. non-MI troponin elevation depends on documenting whether there are ancillary ischemic symptoms, ECG findings, imaging, and/or cath findings of acute myocardial ischemia.
 

Case examples 

1. A 60-year-old male presents with fever, cough, shortness of breath, and an infiltrate on CXR and is diagnosed with sepsis secondary to pneumonia. His initial troponin of 0.07 (normal < 0.05) rises to 0.11, peaks at 0.23, then subsequently trends down.

While some may be tempted to diagnose a type 2 MI, remember that sepsis can cause direct myocardial cell injury via direct cell toxicity. Unless this patient had at least one additional criteria (anginal chest pain, new ischemic ECG changes, or imaging evidence of new loss of viable myocardium, which does not recover with treatment of sepsis), this was most likely myocardial injury via direct cell toxicity, and should be documented as a non-MI troponin elevation due to sepsis without shock.

If there were ischemic ECG changes and the patient had chest pain, one would have to use clinical suspicion to differentiate between a type 1 NSTEMI and a type 2 MI. If there is a high clinical suspicion for an acute plaque rupture/thrombus, one would call it an NSTEMI and would have to document treatment as such (e.g. start heparin drip). Again, cardiology consultation can be helpful in cases where it may be hard to decide how to manage. Many times, the true mechanism is not determined until the patient is taken to the cath lab and if no acute plaque rupture is seen, then it was likely a type 2 MI.

2. A 70-year-old male with chronic systolic heart failure, noncompliant with medications, presents with 3 days of dyspnea on exertion and lower extremity edema. He had no chest discomfort. Exam shows bibasilar crackles and hepatojugular reflux. ECG shows no ischemic changes. Serial troponin values over 48 hours were: 0.48, 0.58, 0.51. A transthoracic echocardiogram reveals an LVEF of 40% with poor movement in the apex, similar to his prior echo.

This patient had no overt evidence of ischemia (no chest pain, ischemic ECG, or imaging changes) so the troponin elevation was most likely a non-MI troponin elevation secondary to acute on chronic systolic heart failure (in which the mechanism of troponin elevation is left ventricular chamber stretch from volume overload, and not demand ischemia). Generally, it is uncommon for a heart failure exacerbation to cause a type 2 MI.
 

Why is it so important to get this diagnosis right?

Misdiagnosing an MI when the patient does not have one can have multiple downstream repercussions. Because it stays on their medical record, it impacts their ability to get insurance and their premium costs. We expose patients to additional medications (e.g. dual antiplatelet therapy, statins), which can have adverse effects. As a result, it is very important to classify the etiology of the troponin elevation and treat accordingly.

Finally, when we incorrectly label a patient as having an MI, this can impact billing and reimbursement, DRG denials, insurance premiums, and quality metrics for both the hospital and the physicians. Hospitals’ 30-day readmission rates for AMI will suffer and quality metrics can be significantly impacted. We must be diligent and as precise as possible with our diagnoses and documentation to ensure the maximum benefit for our patients and our health care system.
 

Dr. Nave is assistant professor of medicine in the division of hospital medicine at Emory University, Atlanta. Dr. Goyal is associate professor of medicine (cardiology), at Emory University, and chief quality officer, Emory Heart and Vascular Center, Emory Healthcare. He is also codirector of nuclear cardiology at Emory University Hospital.

Key points

• A diagnosis of a type 1 MI is supported by evidence or strong suspicion of acute coronary artery thrombus or plaque rupture/erosion.
• A very high troponin level alone is not diagnostic for a type 1 or type 2 MI. It has to be contextualized with the patient’s presentation and other supporting findings.
• Type 2 MI is a mismatch between myocardial oxygen supply and demand unrelated to acute coronary thrombosis or plaque rupture triggered by an abrupt increase in myocardial oxygen demand, drop in myocardial blood supply, or both. Type 2 MI should be documented along with its underlying cause.
• To diagnose an MI (either type 1 or type 2 MI), in addition to the troponin elevation, the patient must have symptoms of acute ischemia, ischemic ECG findings, and/or imaging suggestive of new ischemia.
• An elevated troponin level without new symptoms or ECG/imaging evidence of myocardial ischemia should be documented as a non-MI troponin elevation secondary to an underlying cause.

References

1. Goyal A, Gluckman TJ, Tcheng JE. What’s in a name? The new ICD-10 (10th revision of the international statistical classification of diseases and related health problems) codes and type 2 myocardial infarction. Circulation. 2017;136:1180-2.

2. Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal definition of myocardial infarction (2018). J Am Coll Cardiol. 2018;Aug 25:[Epub ahead of print].

3. Goyal, et al. Translating the Fourth Universal Definition of Myocardial Infarction into Clinical Documentation: Ten Pearls For Frontline Clinicians. Cardiology Magazine. Nov 2018.

4. Roongsritong C, Warraich I, Bradley C. Common causes of troponin elevations in the absence of acute myocardial infarction: incidence and clinical significance. Chest. 2004;125:1877-84.

Hospitalists encounter troponin elevations daily, but we have to use clinical judgment to determine if the troponin elevation represents either a myocardial infarction (MI), or a non-MI troponin elevation (i.e. a , nonischemic myocardial injury).

©decade3d/Thinkstock.com

It is important to remember that an MI specifically refers to myocardial injury due to acute myocardial ischemia to the myocardium. This lack of blood supply can be due to an acute absolute or relative deficiency in coronary artery blood flow. However, there are also many mechanisms of myocardial injury unrelated to reduced coronary artery blood flow, and these should be more appropriately termed non-MI troponin elevations.

Historically, when an ischemic mechanism of myocardial injury was suspected, providers would categorize troponin elevations into ST-elevation MI (STEMI) versus non-ST-elevation MI (NSTEMI) based on the electrocardiogram (ECG). We would further classify the NSTEMI into type 1 or type 2, depending on the mechanism of injury. The term “NSTEMI” served as a “catch-all” term to describe both type 1 NSTEMIs and type 2 MIs, but that classification system is no longer valid.

Classification of MI types

The Fourth Universal Definition of MI published in August 2018 further updated the definitions of MI (summarized in Figure 1).² This review focuses on type 1 and type 2 MIs, which are the most common types encountered by hospitalists. Types 3-5 MI (grouped under a common ICD-10 diagnosis code for “Other MI Types,” or I21.A9) would rarely be diagnosed by hospitalists.



Figure 1: Classification of MI
 

The diagnosis of a type 1 MIs (STEMI and NSTEMI) is supported by the presence of an acute coronary thrombus or plaque rupture/erosion on coronary angiography or a strong suspicion for these when angiography is unavailable or contraindicated. Type 1 MI (also referred to as spontaneous MI) is generally a primary reason (or “principal” diagnosis) for a patient’s presentation to a hospital.³ Please note that a very high or rising troponin level alone is not diagnostic for a type 1 or type 2 NSTEMI. The lab has to be taken in the context of the patient’s presentation and other supporting findings.

In contrast to a type 1 MI (STEMI and NSTEMI), at type 2 MI results from an imbalance between myocardial oxygen supply and demand unrelated to acute coronary artery thrombosis or plaque rupture. A type 2 MI is a relative (as opposed to an absolute) deficiency in coronary artery blood flow triggered by an abrupt increase in myocardial oxygen demand, drop in myocardial blood supply, or both. In type 2 MI, myocardial injury occurs secondary to an underlying process, and therefore requires correct documentation of the underlying cause as well. 

Common examples of underlying causes of type 2 MI include acute blood loss anemia (e.g. GI bleed), acute hypoxia (e.g. COPD exacerbation), shock states (cardiogenic, hypovolemic, hemorrhagic, or septic), coronary vasospasm (e.g. spontaneous), and bradyarrhythmias. Patients with type 2 MI often have a history of fixed obstructive coronary disease, which when coupled with the acute trigger facilitates the type 2 MI; however, underlying CAD is not always present. 

Diagnosing a type 2 MI requires evidence of acute myocardial ischemia (Figure 2) with an elevated troponin but must also have at least one of the following:²

• Symptoms of acute myocardial ischemia such as typical chest pain.
• New ischemic ECG changes.
• Development of pathological Q waves.
• Imaging evidence of new loss of viable myocardium, significant reversible perfusion defect on nuclear imaging, or new regional wall motion abnormality in a pattern consistent with an ischemic etiology.

Distinguishing a type 1 NSTEMI from a type 2 MI depends mainly on the clinical context and clinical judgment. A patient whose presenting symptoms include acute chest discomfort, acute ST-T wave changes, and a rise in troponin would be suspected of having a type 1 NSTEMI. However, in a patient presenting with other or vague complaints where an elevated troponin was found amongst a battery of tests, a type 2 MI may be favored, particularly if there is evidence of an underlying trigger for a supply-demand mismatch. In challenging cases, cardiology consultation can help determine the MI type and/or the next diagnostic and treatment considerations.

When there is only elevated troponin levels (or even a rise and fall in troponin) without new symptoms or ECG/imaging evidence of myocardial ischemia, it is most appropriate to document a non-MI troponin elevation due to a nonischemic mechanism of myocardial injury.
 

Non-MI troponin elevation (nonischemic myocardial injury)

The number of conditions known to cause myocardial injury through mechanisms other than myocardial ischemia (see Figure 2) is growing, especially in the current era of high-sensitivity troponin assays.⁴

Common examples of underlying causes of non-MI troponin elevation include:

• Acute (on chronic) systolic or diastolic heart failure: Usually due to acute ventricular wall stretch/strain. Troponin elevations tend to be mild, with more indolent (or even flat) troponin trajectories.
• Pericarditis and myocarditis: Due to direct injury from myocardial inflammation.
• Cardiopulmonary resuscitation (CPR): Due to physical injury to the heart from mechanical chest compressions and from electrical shocks of external defibrillation.
• Stress-induced (takotsubo) cardiomyopathy: Stress-induced release of neurohormonal factors and catecholamines that cause direct myocyte injury and transient dilatation of the ventricle.
• Acute pulmonary embolism: Result of acute right ventricular wall stretch/strain, not from myocardial ischemia.
• Sepsis without shock: Direct toxicity of circulating cytokines to cardiac myocytes. In the absence of evidence of shock and symptoms/signs of myocardial ischemia, do not document type 2 MI.
• Renal failure (acute kidney injury or chronic kidney disease): Multiple etiologies, but at least partially related to reduced renal clearance of troponin. In general, renal failure in the absence of symptoms/signs of ischemia is best classified as a non-MI troponin elevation. ESRD patients who present with volume overload due to missed dialysis also typically have a non-MI troponin elevation.
• Stroke/intracranial hemorrhage: Mechanisms of myocardial injury and troponin elevation are incompletely understood, but may include catecholamine surges that injure the heart.

Some underlying conditions can cause a type 2 MI or a non-MI troponin elevation depending on the clinical context. For example, hypertensive emergency, severe aortic valve stenosis, hypertrophic cardiomyopathy, and tachyarrhythmias (including atrial fibrillation with rapid ventricular response) may cause increased myocardial oxygen demand, and in patients with underlying CAD, could precipitate a type 2 MI.

However, these same conditions could cause a non-MI troponin elevation in patients without CAD and could also cause myocardial injury and troponin release by causing acute left ventricular stretch/strain. Distinguishing the diagnose of type 2 MI vs. non-MI troponin elevation depends on documenting whether there are ancillary ischemic symptoms, ECG findings, imaging, and/or cath findings of acute myocardial ischemia.
 

Case examples 

1. A 60-year-old male presents with fever, cough, shortness of breath, and an infiltrate on CXR and is diagnosed with sepsis secondary to pneumonia. His initial troponin of 0.07 (normal < 0.05) rises to 0.11, peaks at 0.23, then subsequently trends down.

While some may be tempted to diagnose a type 2 MI, remember that sepsis can cause direct myocardial cell injury via direct cell toxicity. Unless this patient had at least one additional criteria (anginal chest pain, new ischemic ECG changes, or imaging evidence of new loss of viable myocardium, which does not recover with treatment of sepsis), this was most likely myocardial injury via direct cell toxicity, and should be documented as a non-MI troponin elevation due to sepsis without shock.

If there were ischemic ECG changes and the patient had chest pain, one would have to use clinical suspicion to differentiate between a type 1 NSTEMI and a type 2 MI. If there is a high clinical suspicion for an acute plaque rupture/thrombus, one would call it an NSTEMI and would have to document treatment as such (e.g. start heparin drip). Again, cardiology consultation can be helpful in cases where it may be hard to decide how to manage. Many times, the true mechanism is not determined until the patient is taken to the cath lab and if no acute plaque rupture is seen, then it was likely a type 2 MI.

2. A 70-year-old male with chronic systolic heart failure, noncompliant with medications, presents with 3 days of dyspnea on exertion and lower extremity edema. He had no chest discomfort. Exam shows bibasilar crackles and hepatojugular reflux. ECG shows no ischemic changes. Serial troponin values over 48 hours were: 0.48, 0.58, 0.51. A transthoracic echocardiogram reveals an LVEF of 40% with poor movement in the apex, similar to his prior echo.

This patient had no overt evidence of ischemia (no chest pain, ischemic ECG, or imaging changes) so the troponin elevation was most likely a non-MI troponin elevation secondary to acute on chronic systolic heart failure (in which the mechanism of troponin elevation is left ventricular chamber stretch from volume overload, and not demand ischemia). Generally, it is uncommon for a heart failure exacerbation to cause a type 2 MI.
 

Why is it so important to get this diagnosis right?

Misdiagnosing an MI when the patient does not have one can have multiple downstream repercussions. Because it stays on their medical record, it impacts their ability to get insurance and their premium costs. We expose patients to additional medications (e.g. dual antiplatelet therapy, statins), which can have adverse effects. As a result, it is very important to classify the etiology of the troponin elevation and treat accordingly.

Finally, when we incorrectly label a patient as having an MI, this can impact billing and reimbursement, DRG denials, insurance premiums, and quality metrics for both the hospital and the physicians. Hospitals’ 30-day readmission rates for AMI will suffer and quality metrics can be significantly impacted. We must be diligent and as precise as possible with our diagnoses and documentation to ensure the maximum benefit for our patients and our health care system.
 

Dr. Nave is assistant professor of medicine in the division of hospital medicine at Emory University, Atlanta. Dr. Goyal is associate professor of medicine (cardiology), at Emory University, and chief quality officer, Emory Heart and Vascular Center, Emory Healthcare. He is also codirector of nuclear cardiology at Emory University Hospital.

Key points

• A diagnosis of a type 1 MI is supported by evidence or strong suspicion of acute coronary artery thrombus or plaque rupture/erosion.
• A very high troponin level alone is not diagnostic for a type 1 or type 2 MI. It has to be contextualized with the patient’s presentation and other supporting findings.
• Type 2 MI is a mismatch between myocardial oxygen supply and demand unrelated to acute coronary thrombosis or plaque rupture triggered by an abrupt increase in myocardial oxygen demand, drop in myocardial blood supply, or both. Type 2 MI should be documented along with its underlying cause.
• To diagnose an MI (either type 1 or type 2 MI), in addition to the troponin elevation, the patient must have symptoms of acute ischemia, ischemic ECG findings, and/or imaging suggestive of new ischemia.
• An elevated troponin level without new symptoms or ECG/imaging evidence of myocardial ischemia should be documented as a non-MI troponin elevation secondary to an underlying cause.

References

1. Goyal A, Gluckman TJ, Tcheng JE. What’s in a name? The new ICD-10 (10th revision of the international statistical classification of diseases and related health problems) codes and type 2 myocardial infarction. Circulation. 2017;136:1180-2.

2. Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal definition of myocardial infarction (2018). J Am Coll Cardiol. 2018;Aug 25:[Epub ahead of print].

3. Goyal, et al. Translating the Fourth Universal Definition of Myocardial Infarction into Clinical Documentation: Ten Pearls For Frontline Clinicians. Cardiology Magazine. Nov 2018.

4. Roongsritong C, Warraich I, Bradley C. Common causes of troponin elevations in the absence of acute myocardial infarction: incidence and clinical significance. Chest. 2004;125:1877-84.

Hospitalists encounter troponin elevations daily, but we have to use clinical judgment to determine if the troponin elevation represents either a myocardial infarction (MI), or a non-MI troponin elevation (i.e. a , nonischemic myocardial injury).

©decade3d/Thinkstock.com

It is important to remember that an MI specifically refers to myocardial injury due to acute myocardial ischemia to the myocardium. This lack of blood supply can be due to an acute absolute or relative deficiency in coronary artery blood flow. However, there are also many mechanisms of myocardial injury unrelated to reduced coronary artery blood flow, and these should be more appropriately termed non-MI troponin elevations.

Historically, when an ischemic mechanism of myocardial injury was suspected, providers would categorize troponin elevations into ST-elevation MI (STEMI) versus non-ST-elevation MI (NSTEMI) based on the electrocardiogram (ECG). We would further classify the NSTEMI into type 1 or type 2, depending on the mechanism of injury. The term “NSTEMI” served as a “catch-all” term to describe both type 1 NSTEMIs and type 2 MIs, but that classification system is no longer valid.

Classification of MI types

The Fourth Universal Definition of MI published in August 2018 further updated the definitions of MI (summarized in Figure 1).² This review focuses on type 1 and type 2 MIs, which are the most common types encountered by hospitalists. Types 3-5 MI (grouped under a common ICD-10 diagnosis code for “Other MI Types,” or I21.A9) would rarely be diagnosed by hospitalists.



Figure 1: Classification of MI
 

The diagnosis of a type 1 MIs (STEMI and NSTEMI) is supported by the presence of an acute coronary thrombus or plaque rupture/erosion on coronary angiography or a strong suspicion for these when angiography is unavailable or contraindicated. Type 1 MI (also referred to as spontaneous MI) is generally a primary reason (or “principal” diagnosis) for a patient’s presentation to a hospital.³ Please note that a very high or rising troponin level alone is not diagnostic for a type 1 or type 2 NSTEMI. The lab has to be taken in the context of the patient’s presentation and other supporting findings.

In contrast to a type 1 MI (STEMI and NSTEMI), at type 2 MI results from an imbalance between myocardial oxygen supply and demand unrelated to acute coronary artery thrombosis or plaque rupture. A type 2 MI is a relative (as opposed to an absolute) deficiency in coronary artery blood flow triggered by an abrupt increase in myocardial oxygen demand, drop in myocardial blood supply, or both. In type 2 MI, myocardial injury occurs secondary to an underlying process, and therefore requires correct documentation of the underlying cause as well. 

Common examples of underlying causes of type 2 MI include acute blood loss anemia (e.g. GI bleed), acute hypoxia (e.g. COPD exacerbation), shock states (cardiogenic, hypovolemic, hemorrhagic, or septic), coronary vasospasm (e.g. spontaneous), and bradyarrhythmias. Patients with type 2 MI often have a history of fixed obstructive coronary disease, which when coupled with the acute trigger facilitates the type 2 MI; however, underlying CAD is not always present. 

Diagnosing a type 2 MI requires evidence of acute myocardial ischemia (Figure 2) with an elevated troponin but must also have at least one of the following:²

• Symptoms of acute myocardial ischemia such as typical chest pain.
• New ischemic ECG changes.
• Development of pathological Q waves.
• Imaging evidence of new loss of viable myocardium, significant reversible perfusion defect on nuclear imaging, or new regional wall motion abnormality in a pattern consistent with an ischemic etiology.

Distinguishing a type 1 NSTEMI from a type 2 MI depends mainly on the clinical context and clinical judgment. A patient whose presenting symptoms include acute chest discomfort, acute ST-T wave changes, and a rise in troponin would be suspected of having a type 1 NSTEMI. However, in a patient presenting with other or vague complaints where an elevated troponin was found amongst a battery of tests, a type 2 MI may be favored, particularly if there is evidence of an underlying trigger for a supply-demand mismatch. In challenging cases, cardiology consultation can help determine the MI type and/or the next diagnostic and treatment considerations.

When there is only elevated troponin levels (or even a rise and fall in troponin) without new symptoms or ECG/imaging evidence of myocardial ischemia, it is most appropriate to document a non-MI troponin elevation due to a nonischemic mechanism of myocardial injury.
 

Non-MI troponin elevation (nonischemic myocardial injury)

The number of conditions known to cause myocardial injury through mechanisms other than myocardial ischemia (see Figure 2) is growing, especially in the current era of high-sensitivity troponin assays.⁴

Common examples of underlying causes of non-MI troponin elevation include:

• Acute (on chronic) systolic or diastolic heart failure: Usually due to acute ventricular wall stretch/strain. Troponin elevations tend to be mild, with more indolent (or even flat) troponin trajectories.
• Pericarditis and myocarditis: Due to direct injury from myocardial inflammation.
• Cardiopulmonary resuscitation (CPR): Due to physical injury to the heart from mechanical chest compressions and from electrical shocks of external defibrillation.
• Stress-induced (takotsubo) cardiomyopathy: Stress-induced release of neurohormonal factors and catecholamines that cause direct myocyte injury and transient dilatation of the ventricle.
• Acute pulmonary embolism: Result of acute right ventricular wall stretch/strain, not from myocardial ischemia.
• Sepsis without shock: Direct toxicity of circulating cytokines to cardiac myocytes. In the absence of evidence of shock and symptoms/signs of myocardial ischemia, do not document type 2 MI.
• Renal failure (acute kidney injury or chronic kidney disease): Multiple etiologies, but at least partially related to reduced renal clearance of troponin. In general, renal failure in the absence of symptoms/signs of ischemia is best classified as a non-MI troponin elevation. ESRD patients who present with volume overload due to missed dialysis also typically have a non-MI troponin elevation.
• Stroke/intracranial hemorrhage: Mechanisms of myocardial injury and troponin elevation are incompletely understood, but may include catecholamine surges that injure the heart.

Some underlying conditions can cause a type 2 MI or a non-MI troponin elevation depending on the clinical context. For example, hypertensive emergency, severe aortic valve stenosis, hypertrophic cardiomyopathy, and tachyarrhythmias (including atrial fibrillation with rapid ventricular response) may cause increased myocardial oxygen demand, and in patients with underlying CAD, could precipitate a type 2 MI.

However, these same conditions could cause a non-MI troponin elevation in patients without CAD and could also cause myocardial injury and troponin release by causing acute left ventricular stretch/strain. Distinguishing the diagnose of type 2 MI vs. non-MI troponin elevation depends on documenting whether there are ancillary ischemic symptoms, ECG findings, imaging, and/or cath findings of acute myocardial ischemia.
 

Case examples 

1. A 60-year-old male presents with fever, cough, shortness of breath, and an infiltrate on CXR and is diagnosed with sepsis secondary to pneumonia. His initial troponin of 0.07 (normal < 0.05) rises to 0.11, peaks at 0.23, then subsequently trends down.

While some may be tempted to diagnose a type 2 MI, remember that sepsis can cause direct myocardial cell injury via direct cell toxicity. Unless this patient had at least one additional criteria (anginal chest pain, new ischemic ECG changes, or imaging evidence of new loss of viable myocardium, which does not recover with treatment of sepsis), this was most likely myocardial injury via direct cell toxicity, and should be documented as a non-MI troponin elevation due to sepsis without shock.

If there were ischemic ECG changes and the patient had chest pain, one would have to use clinical suspicion to differentiate between a type 1 NSTEMI and a type 2 MI. If there is a high clinical suspicion for an acute plaque rupture/thrombus, one would call it an NSTEMI and would have to document treatment as such (e.g. start heparin drip). Again, cardiology consultation can be helpful in cases where it may be hard to decide how to manage. Many times, the true mechanism is not determined until the patient is taken to the cath lab and if no acute plaque rupture is seen, then it was likely a type 2 MI.

2. A 70-year-old male with chronic systolic heart failure, noncompliant with medications, presents with 3 days of dyspnea on exertion and lower extremity edema. He had no chest discomfort. Exam shows bibasilar crackles and hepatojugular reflux. ECG shows no ischemic changes. Serial troponin values over 48 hours were: 0.48, 0.58, 0.51. A transthoracic echocardiogram reveals an LVEF of 40% with poor movement in the apex, similar to his prior echo.

This patient had no overt evidence of ischemia (no chest pain, ischemic ECG, or imaging changes) so the troponin elevation was most likely a non-MI troponin elevation secondary to acute on chronic systolic heart failure (in which the mechanism of troponin elevation is left ventricular chamber stretch from volume overload, and not demand ischemia). Generally, it is uncommon for a heart failure exacerbation to cause a type 2 MI.
 

Why is it so important to get this diagnosis right?

Misdiagnosing an MI when the patient does not have one can have multiple downstream repercussions. Because it stays on their medical record, it impacts their ability to get insurance and their premium costs. We expose patients to additional medications (e.g. dual antiplatelet therapy, statins), which can have adverse effects. As a result, it is very important to classify the etiology of the troponin elevation and treat accordingly.

Finally, when we incorrectly label a patient as having an MI, this can impact billing and reimbursement, DRG denials, insurance premiums, and quality metrics for both the hospital and the physicians. Hospitals’ 30-day readmission rates for AMI will suffer and quality metrics can be significantly impacted. We must be diligent and as precise as possible with our diagnoses and documentation to ensure the maximum benefit for our patients and our health care system.
 

Dr. Nave is assistant professor of medicine in the division of hospital medicine at Emory University, Atlanta. Dr. Goyal is associate professor of medicine (cardiology), at Emory University, and chief quality officer, Emory Heart and Vascular Center, Emory Healthcare. He is also codirector of nuclear cardiology at Emory University Hospital.

Key points

• A diagnosis of a type 1 MI is supported by evidence or strong suspicion of acute coronary artery thrombus or plaque rupture/erosion.
• A very high troponin level alone is not diagnostic for a type 1 or type 2 MI. It has to be contextualized with the patient’s presentation and other supporting findings.
• Type 2 MI is a mismatch between myocardial oxygen supply and demand unrelated to acute coronary thrombosis or plaque rupture triggered by an abrupt increase in myocardial oxygen demand, drop in myocardial blood supply, or both. Type 2 MI should be documented along with its underlying cause.
• To diagnose an MI (either type 1 or type 2 MI), in addition to the troponin elevation, the patient must have symptoms of acute ischemia, ischemic ECG findings, and/or imaging suggestive of new ischemia.
• An elevated troponin level without new symptoms or ECG/imaging evidence of myocardial ischemia should be documented as a non-MI troponin elevation secondary to an underlying cause.

References

1. Goyal A, Gluckman TJ, Tcheng JE. What’s in a name? The new ICD-10 (10th revision of the international statistical classification of diseases and related health problems) codes and type 2 myocardial infarction. Circulation. 2017;136:1180-2.

2. Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal definition of myocardial infarction (2018). J Am Coll Cardiol. 2018;Aug 25:[Epub ahead of print].

3. Goyal, et al. Translating the Fourth Universal Definition of Myocardial Infarction into Clinical Documentation: Ten Pearls For Frontline Clinicians. Cardiology Magazine. Nov 2018.

4. Roongsritong C, Warraich I, Bradley C. Common causes of troponin elevations in the absence of acute myocardial infarction: incidence and clinical significance. Chest. 2004;125:1877-84.

Private equity firms are increasingly acquiring physician practices across a range of specialties, a recent analysis shows.

Lead author Jane M. Zhu, MD, of Oregon Health & Science University, Portland, and colleagues examined physician group practice acquisitions by private equity firms using the Irving Levin Associates Health Care M&A data set, which includes manually collected and verified transactional information on health care mergers and acquisitions. Investigators linked acquisitions to the SK&A data set, a commercial data set of verified physicians and practice-level characteristics of U.S. office-based practices.

Of about 18,000 unique group medical practices, private equity firms acquired 355 physician practice acquisitions from 2013 to 2016, a trend that rose from 59 practices in 2013 to 136 practices in 2016, Dr. Zhu and colleagues reported on Feb. 18 , 2020, in a research letter published in JAMA.

Acquired practices had a mean of four sites, 16 physicians in each practice, and 6 physicians affiliated with each site, the data found. Overall, 81% of these medical practices reported accepting new patients, 83% accepted Medicare, and 60% accepted Medicaid. The majority of acquired practices were in the South (44%).

Anesthesiology (19%) and multispecialty (19%) were the most commonly represented medical groups in the acquisitions, followed by emergency medicine (12%), family practice (11%), and dermatology (10%). In addition, from 2015 to 2016, the number of acquired cardiology, ophthalmology, radiology, and ob.gyn. practices increased. Within acquired practices, anesthesiologists represented the majority of all physicians, followed by emergency medicine specialists, family physicians, and dermatologists.

Dr. Zhu and colleagues cited a key limitation: Because the data are based on transactions that have been publicly announced, the acquisition of smaller practices might have been underestimated.

Still, the findings demonstrate that private equity acquisitions of physician medical groups are accelerating across multiple specialties, Dr. Zhu said in an interview.

“From our data, acquired medical groups seem to have relatively large footprints with multiple office sites and multiple physicians, which mirrors a typical investment strategy for these firms,” she said.

Dr. Zhu said that more research is needed about how these purchases affect practice patterns, delivery of care, and clinician behavior. Private equity firms expect greater than 20% annual returns, and such financial incentives may conflict with the need for longer-term investments in practice stability, physician recruitment, quality, and safety, according to the study.

“In theory, there may be greater efficiencies introduced from private equity investment – for example, through administrative and billing efficiencies, reorganizing practice structures, or strengthening technology supports,” Dr. Zhu said. “But because of private equity firms’ emphasis on return on investment, there may be unintended consequences of these purchases on practice stability and patient care. We don’t yet know what these effects will be, and we need robust, longitudinal data to investigate this question.”

Dr. Zhu and colleagues reported that they had no disclosures.

SOURCE: Zhu JM et al. JAMA. 2020 Feb 18;323(17):663-5.

Private equity firms are increasingly acquiring physician practices across a range of specialties, a recent analysis shows.

Lead author Jane M. Zhu, MD, of Oregon Health & Science University, Portland, and colleagues examined physician group practice acquisitions by private equity firms using the Irving Levin Associates Health Care M&A data set, which includes manually collected and verified transactional information on health care mergers and acquisitions. Investigators linked acquisitions to the SK&A data set, a commercial data set of verified physicians and practice-level characteristics of U.S. office-based practices.

Of about 18,000 unique group medical practices, private equity firms acquired 355 physician practice acquisitions from 2013 to 2016, a trend that rose from 59 practices in 2013 to 136 practices in 2016, Dr. Zhu and colleagues reported on Feb. 18 , 2020, in a research letter published in JAMA.

Acquired practices had a mean of four sites, 16 physicians in each practice, and 6 physicians affiliated with each site, the data found. Overall, 81% of these medical practices reported accepting new patients, 83% accepted Medicare, and 60% accepted Medicaid. The majority of acquired practices were in the South (44%).

Anesthesiology (19%) and multispecialty (19%) were the most commonly represented medical groups in the acquisitions, followed by emergency medicine (12%), family practice (11%), and dermatology (10%). In addition, from 2015 to 2016, the number of acquired cardiology, ophthalmology, radiology, and ob.gyn. practices increased. Within acquired practices, anesthesiologists represented the majority of all physicians, followed by emergency medicine specialists, family physicians, and dermatologists.

Dr. Zhu and colleagues cited a key limitation: Because the data are based on transactions that have been publicly announced, the acquisition of smaller practices might have been underestimated.

Still, the findings demonstrate that private equity acquisitions of physician medical groups are accelerating across multiple specialties, Dr. Zhu said in an interview.

“From our data, acquired medical groups seem to have relatively large footprints with multiple office sites and multiple physicians, which mirrors a typical investment strategy for these firms,” she said.

Dr. Zhu said that more research is needed about how these purchases affect practice patterns, delivery of care, and clinician behavior. Private equity firms expect greater than 20% annual returns, and such financial incentives may conflict with the need for longer-term investments in practice stability, physician recruitment, quality, and safety, according to the study.

“In theory, there may be greater efficiencies introduced from private equity investment – for example, through administrative and billing efficiencies, reorganizing practice structures, or strengthening technology supports,” Dr. Zhu said. “But because of private equity firms’ emphasis on return on investment, there may be unintended consequences of these purchases on practice stability and patient care. We don’t yet know what these effects will be, and we need robust, longitudinal data to investigate this question.”

Dr. Zhu and colleagues reported that they had no disclosures.

SOURCE: Zhu JM et al. JAMA. 2020 Feb 18;323(17):663-5.

Private equity firms are increasingly acquiring physician practices across a range of specialties, a recent analysis shows.

Lead author Jane M. Zhu, MD, of Oregon Health & Science University, Portland, and colleagues examined physician group practice acquisitions by private equity firms using the Irving Levin Associates Health Care M&A data set, which includes manually collected and verified transactional information on health care mergers and acquisitions. Investigators linked acquisitions to the SK&A data set, a commercial data set of verified physicians and practice-level characteristics of U.S. office-based practices.

Of about 18,000 unique group medical practices, private equity firms acquired 355 physician practice acquisitions from 2013 to 2016, a trend that rose from 59 practices in 2013 to 136 practices in 2016, Dr. Zhu and colleagues reported on Feb. 18 , 2020, in a research letter published in JAMA.

Acquired practices had a mean of four sites, 16 physicians in each practice, and 6 physicians affiliated with each site, the data found. Overall, 81% of these medical practices reported accepting new patients, 83% accepted Medicare, and 60% accepted Medicaid. The majority of acquired practices were in the South (44%).

Anesthesiology (19%) and multispecialty (19%) were the most commonly represented medical groups in the acquisitions, followed by emergency medicine (12%), family practice (11%), and dermatology (10%). In addition, from 2015 to 2016, the number of acquired cardiology, ophthalmology, radiology, and ob.gyn. practices increased. Within acquired practices, anesthesiologists represented the majority of all physicians, followed by emergency medicine specialists, family physicians, and dermatologists.

Dr. Zhu and colleagues cited a key limitation: Because the data are based on transactions that have been publicly announced, the acquisition of smaller practices might have been underestimated.

Still, the findings demonstrate that private equity acquisitions of physician medical groups are accelerating across multiple specialties, Dr. Zhu said in an interview.

“From our data, acquired medical groups seem to have relatively large footprints with multiple office sites and multiple physicians, which mirrors a typical investment strategy for these firms,” she said.

Dr. Zhu said that more research is needed about how these purchases affect practice patterns, delivery of care, and clinician behavior. Private equity firms expect greater than 20% annual returns, and such financial incentives may conflict with the need for longer-term investments in practice stability, physician recruitment, quality, and safety, according to the study.

“In theory, there may be greater efficiencies introduced from private equity investment – for example, through administrative and billing efficiencies, reorganizing practice structures, or strengthening technology supports,” Dr. Zhu said. “But because of private equity firms’ emphasis on return on investment, there may be unintended consequences of these purchases on practice stability and patient care. We don’t yet know what these effects will be, and we need robust, longitudinal data to investigate this question.”

Dr. Zhu and colleagues reported that they had no disclosures.

SOURCE: Zhu JM et al. JAMA. 2020 Feb 18;323(17):663-5.