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.

aotto@mdedge.com

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.

aotto@mdedge.com

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.

aotto@mdedge.com

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.

Nine infants younger than 1 year of age were infected with the virus that causes COVID-19 and hospitalized in China between Dec. 8, 2019, and Feb. 6, 2020, based on data from the Chinese central government and local health departments.

Courtesy NIAID-RML

“As of February 6, 2020, China reported 31,211 confirmed cases of COVID-19 and 637 fatalities,” wrote Min Wei, MD, of Wuhan University, China, and colleagues. However, “few infections in children have been reported.”

In a research letter published in JAMA, the investigators reviewed data from nine infants aged 28 days to 1 year who were hospitalized with a diagnosis of COVID-19 between Dec. 8, 2019, and Feb. 6, 2020. The ages of the infants ranged from 1 month to 11 months, and seven were female. The patients included two children from Beijing, two from Hainan, and one each from the areas of Guangdong, Anhui, Shanghai, Zhejiang, and Guizhou.

All infected infants had at least one infected family member, and the infants’ infections occurred after the family members’ infections; seven infants lived in Wuhan or had family members who had visited Wuhan.

One of the infants had no symptoms but tested positive for the 2019 novel coronavirus, and two others had a diagnosis but missing information on any symptoms. Fever occurred in four patients, and mild upper respiratory tract symptoms occurred in two patients.

None of the infants died, and none reported severe complications or the need for intensive care or mechanical ventilation, the investigators said. The fact that most of the infants were female might suggest that they are more susceptible to the virus than males, although overall COVID-19 viral infections have been more common in adult men, especially those with chronic comorbidities, Dr. Wei and associates noted.

The study findings were limited by the small sample size and lack of symptom data for some patients, the researchers said. However, the results confirm that the COVID-19 virus is transmissible to infants younger than 1 year, and adult caregivers should exercise protective measures including wearing masks, washing hands before contact with infants, and routinely sterilizing toys and tableware, they emphasized.

The study was supported by the National Natural Science Foundation of China and the Fundamental Research Funds for the Central Universities. The researchers had no financial conflicts to disclose.

SOURCE: Wei M et al. JAMA. 2020 Feb 14. doi:10.1001/jama.2020.2131.

Nine infants younger than 1 year of age were infected with the virus that causes COVID-19 and hospitalized in China between Dec. 8, 2019, and Feb. 6, 2020, based on data from the Chinese central government and local health departments.

Courtesy NIAID-RML

“As of February 6, 2020, China reported 31,211 confirmed cases of COVID-19 and 637 fatalities,” wrote Min Wei, MD, of Wuhan University, China, and colleagues. However, “few infections in children have been reported.”

In a research letter published in JAMA, the investigators reviewed data from nine infants aged 28 days to 1 year who were hospitalized with a diagnosis of COVID-19 between Dec. 8, 2019, and Feb. 6, 2020. The ages of the infants ranged from 1 month to 11 months, and seven were female. The patients included two children from Beijing, two from Hainan, and one each from the areas of Guangdong, Anhui, Shanghai, Zhejiang, and Guizhou.

All infected infants had at least one infected family member, and the infants’ infections occurred after the family members’ infections; seven infants lived in Wuhan or had family members who had visited Wuhan.

One of the infants had no symptoms but tested positive for the 2019 novel coronavirus, and two others had a diagnosis but missing information on any symptoms. Fever occurred in four patients, and mild upper respiratory tract symptoms occurred in two patients.

None of the infants died, and none reported severe complications or the need for intensive care or mechanical ventilation, the investigators said. The fact that most of the infants were female might suggest that they are more susceptible to the virus than males, although overall COVID-19 viral infections have been more common in adult men, especially those with chronic comorbidities, Dr. Wei and associates noted.

The study findings were limited by the small sample size and lack of symptom data for some patients, the researchers said. However, the results confirm that the COVID-19 virus is transmissible to infants younger than 1 year, and adult caregivers should exercise protective measures including wearing masks, washing hands before contact with infants, and routinely sterilizing toys and tableware, they emphasized.

The study was supported by the National Natural Science Foundation of China and the Fundamental Research Funds for the Central Universities. The researchers had no financial conflicts to disclose.

SOURCE: Wei M et al. JAMA. 2020 Feb 14. doi:10.1001/jama.2020.2131.

Nine infants younger than 1 year of age were infected with the virus that causes COVID-19 and hospitalized in China between Dec. 8, 2019, and Feb. 6, 2020, based on data from the Chinese central government and local health departments.

Courtesy NIAID-RML

“As of February 6, 2020, China reported 31,211 confirmed cases of COVID-19 and 637 fatalities,” wrote Min Wei, MD, of Wuhan University, China, and colleagues. However, “few infections in children have been reported.”

In a research letter published in JAMA, the investigators reviewed data from nine infants aged 28 days to 1 year who were hospitalized with a diagnosis of COVID-19 between Dec. 8, 2019, and Feb. 6, 2020. The ages of the infants ranged from 1 month to 11 months, and seven were female. The patients included two children from Beijing, two from Hainan, and one each from the areas of Guangdong, Anhui, Shanghai, Zhejiang, and Guizhou.

All infected infants had at least one infected family member, and the infants’ infections occurred after the family members’ infections; seven infants lived in Wuhan or had family members who had visited Wuhan.

One of the infants had no symptoms but tested positive for the 2019 novel coronavirus, and two others had a diagnosis but missing information on any symptoms. Fever occurred in four patients, and mild upper respiratory tract symptoms occurred in two patients.

None of the infants died, and none reported severe complications or the need for intensive care or mechanical ventilation, the investigators said. The fact that most of the infants were female might suggest that they are more susceptible to the virus than males, although overall COVID-19 viral infections have been more common in adult men, especially those with chronic comorbidities, Dr. Wei and associates noted.

The study findings were limited by the small sample size and lack of symptom data for some patients, the researchers said. However, the results confirm that the COVID-19 virus is transmissible to infants younger than 1 year, and adult caregivers should exercise protective measures including wearing masks, washing hands before contact with infants, and routinely sterilizing toys and tableware, they emphasized.

The study was supported by the National Natural Science Foundation of China and the Fundamental Research Funds for the Central Universities. The researchers had no financial conflicts to disclose.

SOURCE: Wei M et al. JAMA. 2020 Feb 14. doi:10.1001/jama.2020.2131.

A 13-year-old boy with ADHD, combined type, presents to his family physician with his parents. His parents called for an appointment outside of his routine follow-up care to discuss what they should do to address their son’s new “aggressive behaviors.” He will throw objects when angry, yell, and slam doors at home when he is told to turn off video games. He used to play soccer but doesn’t anymore. He has maintained very good grades and friends. There is not a concern for substance abuse at this time.He speaks in curt sentences during the appointment, and he has his arms crossed or is looking out of the window the entire time.

His parents share in front on him that he has always been a “difficult child” (their words), but they now are struggling to adjust to his aggressive tendencies as he ages. He is growing bigger and angrier. He will not attend therapy and will not see a consultation psychiatrist in the office. A variety of stimulant trials including Ritalin and amphetamine preparations to manage impulsivity in ADHD were ineffective to curb his aggression, and he doesn’t want to take any medication.

They ask, what do we do? They are not worried for their safety but living like this is eroding their quality of life as a family, and the dynamic seems destined to get worse before it gets better.

They wonder, is there a next medication step to manage his aggression?

A family physician presented the above situation to me in my role as a child and adolescent psychiatrist in the medical home. It led us to a fruitful discussion of aggression and what can be done to help families who are all too often in situations like the above, then in your office looking for immediate solutions. The questions are, what can be done with an aggressive child, even and especially without the child’s buy-in to work on that as a problem?

Markus Wegmann/Thinkstock

Psychoeducation can go a long way in helping families rethink aggression as a symptom of something deeper, either in the environment or a diagnosis, although we all can empathize with the desire to reconcile the above behavior immediately.
 

Characterize the aggression

First, it can be helpful to identify a child’s aggression type. There are two types of aggression, reactive and proactive. We most often see reactive aggression in our clinics, which is aggression as a defensive and impulsive response to something in the environment (often limit-setting, as above). Proactive aggression is premeditated and may appear as aggression for aggression’s sake without the emotional drive behind it.

Secondly, it also can be helpful to know that externalizing and internalizing symptoms can represent different sides of the same coin, with the proverbial “coin” as “emotion” and the associated behaviors (throwing objects, in the above example) as the “signs” that there is a complex difficulty in managing painful emotions. Some children (and adults too!) tend to “externalize” strong emotions as aggression or irritability with others, while others “internalize” them by retreating with internal suffering such as “anxiety and depression.” These styles also can be similar among children and their parents.

With those two points in mind, it’s important to consider the diagnosis, which would guide treatment. It’s generally agreed upon that “reactive aggression” is more likely to be related to underlying untreated ADHD, or a depressive or anxiety disorder. This is much more amenable to treatment than aggression related to oppositional defiant disorder or conduct disorder, which are more defined by proactive forms of aggression.

You can pick up on family dynamics that may inadvertently reinforce the same behaviors they so wish to change. In the above example, the parents have clearly identified their son as “the problem.” You can imagine the difficulty of going to school and being a “problem,” and then coming home and feeling the same way. This negative perception can erode a child’s self-esteem over time, which may appear as disengagement or simply not caring in an appointment. It may become harder and harder to engage the child in psychotherapy or even in taking a medication as their only means of resistance to that painful notion about oneself as the “problem.”

It can be useful to begin appointments with “what is going well?” (in the example above, he “has friends and is maintaining grades”) and “what do you like most about your child?” As we all know, positive reinforcement is more powerful than its counterpart. Also problems in a family often are complex, and may involve many family members needing to change to meet their goals, not just the child.
 

Why you should try behavioral interventions first

Behavioral interventions are the first step always. Parents can do behavioral interventions and change their parenting and family environment through their own behavioral changes – commonly called parent management training. They can assess antecedents of aggression and their own responses, which may contribute or perpetuate a cycle of the aggression – such as giving attention or giving in to fewer limitations to avoid a fight. This small but important point can help protect against a feeling of helplessness that a child will not engage in therapy or skills-building.

In answering the clinician’s question about what to do next, I often feel like the question embedded in this is “what medication is next?” There is a felt pressure to do something “right now” conveyed to a clinician. This drives the impulse to prescribe something immediately – and likely more risky and with less of an evidence base – even before trying the known psychotherapy interventions that have the most evidence to change aggressive tendencies.

In looking deeper into this consultation case, I also found more “food for thought” for one’s thinking about aggression and psychopharmacology in cases like the above: Aggression isn’t an uncomplicated symptom that one can address immediately, and therefore we cannot rely on symptom-specific management to eradicate it. This is similar to prescribing Tylenol to manage a general ache or pain; if the pain persists, we want to know the “whys” of the pain persisting.

Thankfully, there are ways that a parent can better understand behaviors with this philosophy in mind. Applied Behavioral Analysis¹ offers some helpful ideas, not only for children with autism spectrum disorder, but that can be applied to one’s understanding of other’s behavior in general. ABA pays attention to antecedents, perpetuating factors, and consequences as well as their interplay in understanding behaviors. You can encourage a family – rather than wanting to “get rid of a problem behavior” – to try to understand it and come up, with help from a psychotherapist or other professional, with a deeper evaluation of the behavior and a specific, collaborative plan.

Most experts see that ADHD, anxiety disorders, depressive disorders, and unrecognized learning disabilities, in sum, are more common underpinnings than not with aggressive children. This also can be confounded by an environment with parents who have those diagnoses untreated as well. Aggression should raise a red flag in our clinics to consider the above even if a family or child simply says aggression is the one issue, and it’s only the child with the issue.

While there have been attempts to find a “spot treatment” for aggression in a medication, medications not only fail to address the underlying issues many times, but have little evidence that support them and may do more harm long term than good.²

Kids need outlets for “normal aggressive drives.” And puberty, as in the case above, is a time of intense emotions of all varieties. In the example above, you may notice that the child is no longer playing soccer, which was likely serving some protective function in many ways for him and as a positive outlet for aggression. In the same way, you may see that kids who are more sedentary or idle (playing unrestricted video games now instead of sports, ) would benefit from revisiting outlets or finding new ones as a family.
 

Consider medications if the underlying diagnosis merits it

We generally seek to find and treat the underlying diagnosis, if it exists, in the following ways.

If a child has ADHD, as in the case above, you can trial a stimulant or an alpha-adrenergic agent to target impulsivity if that is suspected as the driver of aggression. This may include guanfacine (long-acting Intuniv at night, but I would choose lower dosing such as 0.5 mg to 1 mg at bedtime) to manage ADHD. However, the evidence base that management of ADHD improves aggressive behaviors at all or on their own, is scant. In addition, these medications can represent more harm than good as well, although they are perceived as more innocuous than their antipsychotic counterparts. For example, some patients can begin to have bed-wetting accidents in the evening or become sleepy in classes, which can further erode their sense of self-confidence even if this is clearly attributable to a medication side effect and resolves once the agent is reduced or removed.

In the same way to reorient to diagnosis with children with aggression, you can consider an SSRI for an anxiety disorder or irritable depression. But know that it’s a rare thing for children to say specifically that they are struggling with their emotions, whether they are angry, sad, or nervous and that a deeper dive into this may be warranted. Data by Connor DF et al.³ may indicate anxiety disorders should be highest on one’s differential diagnosis in aggression, followed by consideration for ADHD, which may be a different assumption than one would expect.

Mood stabilizers –lamotrigine (Lamictal), divalproex sodium (Depakote), and lithium – and antipsychotics – aripiprazole (Abilify) and risperidone (Risperdal) – are risky medications and the use of them contradicts the first point, agreed upon by most experts, that diagnosis should drive treatment. One is hardly ever treating a young child for psychosis or bipolar disorder in these circumstances of episodic, reactive aggression. Antipsychotics also carry the notorious risks of metabolic syndrome, among other risks to overall health, which becomes an additive risk over time and potentially into adulthood. I once heard in my child adolescent psychiatry training the haunting phase, “yes, they can ‘work’ quickly but they can work ‘almost too well,’ ” meaning they can sedate or tranquilize an aggressive child when the real goal should be to understand, diagnose, and intervene in ways that see the “big picture” of aggression.

Benzodiazepines generally are avoided in children due to disinhibition and often not even considered, in these circumstances, as they are in adults to manage agitation or aggression, due to this fact.

In many instances in working with families, our role in primary care can be one of illuminating children’s behaviors not just as symptoms to treat, but to understand deeply. This is as true for aggression as it is for anxiety.

Finally, I am reminded of the common question I receive from adult patients in primary care who ask me if anyone has yet made a medication to lose weight that’s safe and effective. Then the counseling commences on our fantasies, from our patients and ourselves, about what medications can do for us and our risks therein.
 

Dr. Pawlowski is an adult, adolescent, and child psychiatrist at the University of Vermont Medical Center and assistant professor of psychiatry at the Larner College of Medicine at UVM in Burlington. Email her at pdnews@mdedge.com.
 

References

1. ABA in the Treatment of Aggressive Behavior Disorder and Lack of Impulse Control.

2. Managing Aggression in Children: A Practical Approach, The Carlat Child Psychiatry Report, May 2010, The Explosive Child.

3. Child Psychiatry Hum Dev. 2006 May;37[1]:1-14.

A 13-year-old boy with ADHD, combined type, presents to his family physician with his parents. His parents called for an appointment outside of his routine follow-up care to discuss what they should do to address their son’s new “aggressive behaviors.” He will throw objects when angry, yell, and slam doors at home when he is told to turn off video games. He used to play soccer but doesn’t anymore. He has maintained very good grades and friends. There is not a concern for substance abuse at this time.He speaks in curt sentences during the appointment, and he has his arms crossed or is looking out of the window the entire time.

His parents share in front on him that he has always been a “difficult child” (their words), but they now are struggling to adjust to his aggressive tendencies as he ages. He is growing bigger and angrier. He will not attend therapy and will not see a consultation psychiatrist in the office. A variety of stimulant trials including Ritalin and amphetamine preparations to manage impulsivity in ADHD were ineffective to curb his aggression, and he doesn’t want to take any medication.

They ask, what do we do? They are not worried for their safety but living like this is eroding their quality of life as a family, and the dynamic seems destined to get worse before it gets better.

They wonder, is there a next medication step to manage his aggression?

A family physician presented the above situation to me in my role as a child and adolescent psychiatrist in the medical home. It led us to a fruitful discussion of aggression and what can be done to help families who are all too often in situations like the above, then in your office looking for immediate solutions. The questions are, what can be done with an aggressive child, even and especially without the child’s buy-in to work on that as a problem?

Markus Wegmann/Thinkstock

Psychoeducation can go a long way in helping families rethink aggression as a symptom of something deeper, either in the environment or a diagnosis, although we all can empathize with the desire to reconcile the above behavior immediately.
 

Characterize the aggression

First, it can be helpful to identify a child’s aggression type. There are two types of aggression, reactive and proactive. We most often see reactive aggression in our clinics, which is aggression as a defensive and impulsive response to something in the environment (often limit-setting, as above). Proactive aggression is premeditated and may appear as aggression for aggression’s sake without the emotional drive behind it.

Secondly, it also can be helpful to know that externalizing and internalizing symptoms can represent different sides of the same coin, with the proverbial “coin” as “emotion” and the associated behaviors (throwing objects, in the above example) as the “signs” that there is a complex difficulty in managing painful emotions. Some children (and adults too!) tend to “externalize” strong emotions as aggression or irritability with others, while others “internalize” them by retreating with internal suffering such as “anxiety and depression.” These styles also can be similar among children and their parents.

With those two points in mind, it’s important to consider the diagnosis, which would guide treatment. It’s generally agreed upon that “reactive aggression” is more likely to be related to underlying untreated ADHD, or a depressive or anxiety disorder. This is much more amenable to treatment than aggression related to oppositional defiant disorder or conduct disorder, which are more defined by proactive forms of aggression.

You can pick up on family dynamics that may inadvertently reinforce the same behaviors they so wish to change. In the above example, the parents have clearly identified their son as “the problem.” You can imagine the difficulty of going to school and being a “problem,” and then coming home and feeling the same way. This negative perception can erode a child’s self-esteem over time, which may appear as disengagement or simply not caring in an appointment. It may become harder and harder to engage the child in psychotherapy or even in taking a medication as their only means of resistance to that painful notion about oneself as the “problem.”

It can be useful to begin appointments with “what is going well?” (in the example above, he “has friends and is maintaining grades”) and “what do you like most about your child?” As we all know, positive reinforcement is more powerful than its counterpart. Also problems in a family often are complex, and may involve many family members needing to change to meet their goals, not just the child.
 

Why you should try behavioral interventions first

Behavioral interventions are the first step always. Parents can do behavioral interventions and change their parenting and family environment through their own behavioral changes – commonly called parent management training. They can assess antecedents of aggression and their own responses, which may contribute or perpetuate a cycle of the aggression – such as giving attention or giving in to fewer limitations to avoid a fight. This small but important point can help protect against a feeling of helplessness that a child will not engage in therapy or skills-building.

In answering the clinician’s question about what to do next, I often feel like the question embedded in this is “what medication is next?” There is a felt pressure to do something “right now” conveyed to a clinician. This drives the impulse to prescribe something immediately – and likely more risky and with less of an evidence base – even before trying the known psychotherapy interventions that have the most evidence to change aggressive tendencies.

In looking deeper into this consultation case, I also found more “food for thought” for one’s thinking about aggression and psychopharmacology in cases like the above: Aggression isn’t an uncomplicated symptom that one can address immediately, and therefore we cannot rely on symptom-specific management to eradicate it. This is similar to prescribing Tylenol to manage a general ache or pain; if the pain persists, we want to know the “whys” of the pain persisting.

Thankfully, there are ways that a parent can better understand behaviors with this philosophy in mind. Applied Behavioral Analysis¹ offers some helpful ideas, not only for children with autism spectrum disorder, but that can be applied to one’s understanding of other’s behavior in general. ABA pays attention to antecedents, perpetuating factors, and consequences as well as their interplay in understanding behaviors. You can encourage a family – rather than wanting to “get rid of a problem behavior” – to try to understand it and come up, with help from a psychotherapist or other professional, with a deeper evaluation of the behavior and a specific, collaborative plan.

Most experts see that ADHD, anxiety disorders, depressive disorders, and unrecognized learning disabilities, in sum, are more common underpinnings than not with aggressive children. This also can be confounded by an environment with parents who have those diagnoses untreated as well. Aggression should raise a red flag in our clinics to consider the above even if a family or child simply says aggression is the one issue, and it’s only the child with the issue.

While there have been attempts to find a “spot treatment” for aggression in a medication, medications not only fail to address the underlying issues many times, but have little evidence that support them and may do more harm long term than good.²

Kids need outlets for “normal aggressive drives.” And puberty, as in the case above, is a time of intense emotions of all varieties. In the example above, you may notice that the child is no longer playing soccer, which was likely serving some protective function in many ways for him and as a positive outlet for aggression. In the same way, you may see that kids who are more sedentary or idle (playing unrestricted video games now instead of sports, ) would benefit from revisiting outlets or finding new ones as a family.
 

Consider medications if the underlying diagnosis merits it

We generally seek to find and treat the underlying diagnosis, if it exists, in the following ways.

If a child has ADHD, as in the case above, you can trial a stimulant or an alpha-adrenergic agent to target impulsivity if that is suspected as the driver of aggression. This may include guanfacine (long-acting Intuniv at night, but I would choose lower dosing such as 0.5 mg to 1 mg at bedtime) to manage ADHD. However, the evidence base that management of ADHD improves aggressive behaviors at all or on their own, is scant. In addition, these medications can represent more harm than good as well, although they are perceived as more innocuous than their antipsychotic counterparts. For example, some patients can begin to have bed-wetting accidents in the evening or become sleepy in classes, which can further erode their sense of self-confidence even if this is clearly attributable to a medication side effect and resolves once the agent is reduced or removed.

In the same way to reorient to diagnosis with children with aggression, you can consider an SSRI for an anxiety disorder or irritable depression. But know that it’s a rare thing for children to say specifically that they are struggling with their emotions, whether they are angry, sad, or nervous and that a deeper dive into this may be warranted. Data by Connor DF et al.³ may indicate anxiety disorders should be highest on one’s differential diagnosis in aggression, followed by consideration for ADHD, which may be a different assumption than one would expect.

Mood stabilizers –lamotrigine (Lamictal), divalproex sodium (Depakote), and lithium – and antipsychotics – aripiprazole (Abilify) and risperidone (Risperdal) – are risky medications and the use of them contradicts the first point, agreed upon by most experts, that diagnosis should drive treatment. One is hardly ever treating a young child for psychosis or bipolar disorder in these circumstances of episodic, reactive aggression. Antipsychotics also carry the notorious risks of metabolic syndrome, among other risks to overall health, which becomes an additive risk over time and potentially into adulthood. I once heard in my child adolescent psychiatry training the haunting phase, “yes, they can ‘work’ quickly but they can work ‘almost too well,’ ” meaning they can sedate or tranquilize an aggressive child when the real goal should be to understand, diagnose, and intervene in ways that see the “big picture” of aggression.

Benzodiazepines generally are avoided in children due to disinhibition and often not even considered, in these circumstances, as they are in adults to manage agitation or aggression, due to this fact.

In many instances in working with families, our role in primary care can be one of illuminating children’s behaviors not just as symptoms to treat, but to understand deeply. This is as true for aggression as it is for anxiety.

Finally, I am reminded of the common question I receive from adult patients in primary care who ask me if anyone has yet made a medication to lose weight that’s safe and effective. Then the counseling commences on our fantasies, from our patients and ourselves, about what medications can do for us and our risks therein.
 

Dr. Pawlowski is an adult, adolescent, and child psychiatrist at the University of Vermont Medical Center and assistant professor of psychiatry at the Larner College of Medicine at UVM in Burlington. Email her at pdnews@mdedge.com.
 

References

1. ABA in the Treatment of Aggressive Behavior Disorder and Lack of Impulse Control.

2. Managing Aggression in Children: A Practical Approach, The Carlat Child Psychiatry Report, May 2010, The Explosive Child.

3. Child Psychiatry Hum Dev. 2006 May;37[1]:1-14.

A 13-year-old boy with ADHD, combined type, presents to his family physician with his parents. His parents called for an appointment outside of his routine follow-up care to discuss what they should do to address their son’s new “aggressive behaviors.” He will throw objects when angry, yell, and slam doors at home when he is told to turn off video games. He used to play soccer but doesn’t anymore. He has maintained very good grades and friends. There is not a concern for substance abuse at this time.He speaks in curt sentences during the appointment, and he has his arms crossed or is looking out of the window the entire time.

His parents share in front on him that he has always been a “difficult child” (their words), but they now are struggling to adjust to his aggressive tendencies as he ages. He is growing bigger and angrier. He will not attend therapy and will not see a consultation psychiatrist in the office. A variety of stimulant trials including Ritalin and amphetamine preparations to manage impulsivity in ADHD were ineffective to curb his aggression, and he doesn’t want to take any medication.

They ask, what do we do? They are not worried for their safety but living like this is eroding their quality of life as a family, and the dynamic seems destined to get worse before it gets better.

They wonder, is there a next medication step to manage his aggression?

A family physician presented the above situation to me in my role as a child and adolescent psychiatrist in the medical home. It led us to a fruitful discussion of aggression and what can be done to help families who are all too often in situations like the above, then in your office looking for immediate solutions. The questions are, what can be done with an aggressive child, even and especially without the child’s buy-in to work on that as a problem?

Markus Wegmann/Thinkstock

Psychoeducation can go a long way in helping families rethink aggression as a symptom of something deeper, either in the environment or a diagnosis, although we all can empathize with the desire to reconcile the above behavior immediately.
 

Characterize the aggression

First, it can be helpful to identify a child’s aggression type. There are two types of aggression, reactive and proactive. We most often see reactive aggression in our clinics, which is aggression as a defensive and impulsive response to something in the environment (often limit-setting, as above). Proactive aggression is premeditated and may appear as aggression for aggression’s sake without the emotional drive behind it.

Secondly, it also can be helpful to know that externalizing and internalizing symptoms can represent different sides of the same coin, with the proverbial “coin” as “emotion” and the associated behaviors (throwing objects, in the above example) as the “signs” that there is a complex difficulty in managing painful emotions. Some children (and adults too!) tend to “externalize” strong emotions as aggression or irritability with others, while others “internalize” them by retreating with internal suffering such as “anxiety and depression.” These styles also can be similar among children and their parents.

With those two points in mind, it’s important to consider the diagnosis, which would guide treatment. It’s generally agreed upon that “reactive aggression” is more likely to be related to underlying untreated ADHD, or a depressive or anxiety disorder. This is much more amenable to treatment than aggression related to oppositional defiant disorder or conduct disorder, which are more defined by proactive forms of aggression.

You can pick up on family dynamics that may inadvertently reinforce the same behaviors they so wish to change. In the above example, the parents have clearly identified their son as “the problem.” You can imagine the difficulty of going to school and being a “problem,” and then coming home and feeling the same way. This negative perception can erode a child’s self-esteem over time, which may appear as disengagement or simply not caring in an appointment. It may become harder and harder to engage the child in psychotherapy or even in taking a medication as their only means of resistance to that painful notion about oneself as the “problem.”

It can be useful to begin appointments with “what is going well?” (in the example above, he “has friends and is maintaining grades”) and “what do you like most about your child?” As we all know, positive reinforcement is more powerful than its counterpart. Also problems in a family often are complex, and may involve many family members needing to change to meet their goals, not just the child.
 

Why you should try behavioral interventions first

Behavioral interventions are the first step always. Parents can do behavioral interventions and change their parenting and family environment through their own behavioral changes – commonly called parent management training. They can assess antecedents of aggression and their own responses, which may contribute or perpetuate a cycle of the aggression – such as giving attention or giving in to fewer limitations to avoid a fight. This small but important point can help protect against a feeling of helplessness that a child will not engage in therapy or skills-building.

In answering the clinician’s question about what to do next, I often feel like the question embedded in this is “what medication is next?” There is a felt pressure to do something “right now” conveyed to a clinician. This drives the impulse to prescribe something immediately – and likely more risky and with less of an evidence base – even before trying the known psychotherapy interventions that have the most evidence to change aggressive tendencies.

In looking deeper into this consultation case, I also found more “food for thought” for one’s thinking about aggression and psychopharmacology in cases like the above: Aggression isn’t an uncomplicated symptom that one can address immediately, and therefore we cannot rely on symptom-specific management to eradicate it. This is similar to prescribing Tylenol to manage a general ache or pain; if the pain persists, we want to know the “whys” of the pain persisting.

Thankfully, there are ways that a parent can better understand behaviors with this philosophy in mind. Applied Behavioral Analysis¹ offers some helpful ideas, not only for children with autism spectrum disorder, but that can be applied to one’s understanding of other’s behavior in general. ABA pays attention to antecedents, perpetuating factors, and consequences as well as their interplay in understanding behaviors. You can encourage a family – rather than wanting to “get rid of a problem behavior” – to try to understand it and come up, with help from a psychotherapist or other professional, with a deeper evaluation of the behavior and a specific, collaborative plan.

Most experts see that ADHD, anxiety disorders, depressive disorders, and unrecognized learning disabilities, in sum, are more common underpinnings than not with aggressive children. This also can be confounded by an environment with parents who have those diagnoses untreated as well. Aggression should raise a red flag in our clinics to consider the above even if a family or child simply says aggression is the one issue, and it’s only the child with the issue.

While there have been attempts to find a “spot treatment” for aggression in a medication, medications not only fail to address the underlying issues many times, but have little evidence that support them and may do more harm long term than good.²

Kids need outlets for “normal aggressive drives.” And puberty, as in the case above, is a time of intense emotions of all varieties. In the example above, you may notice that the child is no longer playing soccer, which was likely serving some protective function in many ways for him and as a positive outlet for aggression. In the same way, you may see that kids who are more sedentary or idle (playing unrestricted video games now instead of sports, ) would benefit from revisiting outlets or finding new ones as a family.
 

Consider medications if the underlying diagnosis merits it

We generally seek to find and treat the underlying diagnosis, if it exists, in the following ways.

If a child has ADHD, as in the case above, you can trial a stimulant or an alpha-adrenergic agent to target impulsivity if that is suspected as the driver of aggression. This may include guanfacine (long-acting Intuniv at night, but I would choose lower dosing such as 0.5 mg to 1 mg at bedtime) to manage ADHD. However, the evidence base that management of ADHD improves aggressive behaviors at all or on their own, is scant. In addition, these medications can represent more harm than good as well, although they are perceived as more innocuous than their antipsychotic counterparts. For example, some patients can begin to have bed-wetting accidents in the evening or become sleepy in classes, which can further erode their sense of self-confidence even if this is clearly attributable to a medication side effect and resolves once the agent is reduced or removed.

In the same way to reorient to diagnosis with children with aggression, you can consider an SSRI for an anxiety disorder or irritable depression. But know that it’s a rare thing for children to say specifically that they are struggling with their emotions, whether they are angry, sad, or nervous and that a deeper dive into this may be warranted. Data by Connor DF et al.³ may indicate anxiety disorders should be highest on one’s differential diagnosis in aggression, followed by consideration for ADHD, which may be a different assumption than one would expect.

Mood stabilizers –lamotrigine (Lamictal), divalproex sodium (Depakote), and lithium – and antipsychotics – aripiprazole (Abilify) and risperidone (Risperdal) – are risky medications and the use of them contradicts the first point, agreed upon by most experts, that diagnosis should drive treatment. One is hardly ever treating a young child for psychosis or bipolar disorder in these circumstances of episodic, reactive aggression. Antipsychotics also carry the notorious risks of metabolic syndrome, among other risks to overall health, which becomes an additive risk over time and potentially into adulthood. I once heard in my child adolescent psychiatry training the haunting phase, “yes, they can ‘work’ quickly but they can work ‘almost too well,’ ” meaning they can sedate or tranquilize an aggressive child when the real goal should be to understand, diagnose, and intervene in ways that see the “big picture” of aggression.

Benzodiazepines generally are avoided in children due to disinhibition and often not even considered, in these circumstances, as they are in adults to manage agitation or aggression, due to this fact.

In many instances in working with families, our role in primary care can be one of illuminating children’s behaviors not just as symptoms to treat, but to understand deeply. This is as true for aggression as it is for anxiety.

Finally, I am reminded of the common question I receive from adult patients in primary care who ask me if anyone has yet made a medication to lose weight that’s safe and effective. Then the counseling commences on our fantasies, from our patients and ourselves, about what medications can do for us and our risks therein.
 

Dr. Pawlowski is an adult, adolescent, and child psychiatrist at the University of Vermont Medical Center and assistant professor of psychiatry at the Larner College of Medicine at UVM in Burlington. Email her at pdnews@mdedge.com.
 

References

1. ABA in the Treatment of Aggressive Behavior Disorder and Lack of Impulse Control.

2. Managing Aggression in Children: A Practical Approach, The Carlat Child Psychiatry Report, May 2010, The Explosive Child.

3. Child Psychiatry Hum Dev. 2006 May;37[1]:1-14.

LAS VEGAS – The risk-benefit ratio of new and emerging drugs for depression is going to be under the spotlight more than ever before, according to an expert in mood disorders.

Doug Brunk/MDedge News

“We’ve seen a shift in the landscape,” Alan F. Schatzberg, MD, said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “We’ve gone from the development of ‘me too’ agents such as venlafaxine and fluoxetine to developing drugs that may have more dramatic effects, but they also may have more baggage in terms of risks. The risk-benefit ratio is going to become increasingly more of a focus in drug development, in terms of increasing risk.”

The development of the SSRIs, he continued, led to the introduction of agents that were generally effective and well tolerated.

“Particularly, they were well tolerated in terms of their wide safety margin,” said Dr. Schatzberg, who directs the Mood Disorders Center at Stanford (Calif.) University. “It’s difficult to [die by suicide] on an SSRI. Because of that, we had greater numbers of individuals treated than we did with the tricyclics.” The introduction of SSRIs led to “widening of the net in terms of the numbers of depressed patients,” he said. “Combine that with DSM-III, and DSM-IV having relatively easy criteria to obtain a diagnosis [of depression, and] you see a large group of subjects who are exposed to treatment. But a lot of those people may not respond to a particular agent. As new treatments are promulgated and tried, what you find is [that] a reasonable number of subjects are, in fact, truly resistant. That becomes a tough nut to crack for all of us who treat depression.”

Drugs for depression that clinicians commonly have in their armamentarium commonly revolve around monoaminergic function. New and emerging agents include hallucinatory serotonin 2a agonists, glutamatergic drugs such as ketamine, GABAergic neurosteroids, opioid modulators, and onabotulinumtoxinA.

In 2013, the Food and Drug Administration approved the multimodal agent vortioxetine for the treatment of major depressive disorder. The recommended dosing is 20 mg/day, and the drug appears to have a positive effect on cognition. A meta-analysis of vortioxetine, duloxetine, and placebo comparison trials evaluated the effect of each treatment on the Digit Symbol Substitution Test (Int J Neuropsychopharmacol. 2016 Jun 15;19[10]). Vortioxetine was superior to placebo in all three trials and was superior to duloxetine in two trials. Duloxetine was not superior to placebo in two trials.

In two double-blind studies, researchers evaluated the effects of psilocybin in cancer patients with comorbid depression and anxiety. Full doses of psilocybin were 0.3 mg/kg or 22-30 mg per 70 kg. Both studies demonstrated sustained responses at full doses (J Psychopharmacol. 2016 Nov 30;30[12]:1181-97 and J Psychopharmacol. 2016 Nov 30;30[12]:1165-80).

In an open label study of psilocybin in refractory major depression, 12 patients received 10 mg on day 1 and 25 mg on day 8. Eight of 12 patients responded at 1 week, and 7 of the 12 maintained response at 3 months (Lancet Psychiatry. 2016 Jul;3[7]:619-27). According to Dr. Schatzberg, this trial became the basis for a blinded study that Compass is conducting in the United States and in the United Kingdom in which refractory patients are going to be randomized to 1 mg, 10 mg, or 25 mg psilocybin using an independent rater. “These patients are accompanied during this experience by two therapists for up to 8 hours. It’s not quite a guided therapy; it’s kind of a safety net therapy if the patient needs [help]. We’ll see what happens.”

Another agent being studied is ketamine, which works on the glutamate system, an excitatory neurotransmitter. “Glutamate is the juice that keeps us going,” said Dr. Schatzberg, who is also the Kenneth T. Norris Jr. professor of psychiatry and behavioral sciences at the university. “We can’t live without glutamate.” An anesthetic agent that has been used for 50 years, ketamine is a N-methyl-d-aspartate antagonist that has mu opioid agonist effects and stimulant properties. “It causes a psychotomimetic dissociative kind of reaction,” he said. “The doses used in depression are subanesthetic. They may put the patient asleep, but they usually don’t. The problem with the antidepressant effect is that 70% of people who initially respond don’t continue to respond beyond 1 week.”

In a randomized, placebo-controlled, double-blind crossover study of patients with treatment-resistant depression, subjects who received ketamine showed significant improvement in depression, compared with subjects who received placebo within 110 minutes after injection, which remained significant throughout the following week (Arch Gen Psychiatry. 2006;63:856-64). Specifically, of the 17 subjects treated with ketamine, 71% met response and 29% met remission criteria the day following ketamine infusion. Thirty-five percent of subjects maintained response for at least 1 week.

In an effort to further evaluate the antidepressive effects of ketamine, researchers conducted a two-site, parallel-arm, randomized, controlled trial of a single infusion of ketamine, compared with an active placebo control condition, the anesthetic midazolam (Am J Psychiatry. 2013 Oct;170[10]:1134-42). After adjustment for baseline scores and site, the Montgomery-Åsberg Depression Rating Scale score was lower in the ketamine group than in the midazolam group by 7.95 points. The likelihood of response at 24 hours was greater with ketamine than with midazolam (odds ratio, 2.18), with response rates of 64% and 28%, respectively.

In 2019, the FDA approved esketamine nasal spray, in conjunction with an oral antidepressant, for the treatment of depression in adults with treatment-resistant depression. In three phase 3 double-blind studies of esketamine in treatment-refractory depression, one was positive, two were nearly positive, and the effect sizes were mild. One maintenance discontinuation trial was positive. Based on this data, Dr. Schatzberg said, there “is not much evidence” that patients get further gain beyond an antidepressant alone in the first 24-48 hours following ketamine administration. “It makes me wonder: Should we be continuing to give this drug intranasally beyond 48 hours?” he asked. “The reason I have concern is that in certain cultures, ketamine is a highly abusable drug.”

He and Gerard Sanacora, PhD, MD, addressed the topic in a 2015 opinion piece entitled, “Ketamine: Promising path or false prophecy in the development of novel therapeutics for mood disorders?”

“If we step back for a moment and look at where we are – an intravenously administered agent that is a street drug of abuse, works rapidly, and whose enantiomers are being studied by industry for intranasal use – we should be anxious, “ they wrote (Neuropsychopharmacology. 2015 Jan;40[2]:259-67). “We need to be as careful and conservative as possible and understand how it is acting and rule out the possibility of whether it acts as an opioid.”

Dr. Schatzberg disclosed that he has served a consultant to Alkermes, Avanir, Bracket, Compass, Delpor, Epiodyne, Janssen, Jazz, Lundbeck, McKinsey, Merck, Myriad Genetics, Owl, Neuronetics, Pfizer, Sage, and Sunovion. He has received research funding from Janssen and also holds an ownership interest in Corcept, Dermira, Delpor, Epiodyne, Incyte Genetics, Madrigal, Maerck, Owl Analytics, Seattle Genetics, Titan, and Xhale.

dbrunk@mdedge.com

LAS VEGAS – The risk-benefit ratio of new and emerging drugs for depression is going to be under the spotlight more than ever before, according to an expert in mood disorders.

Doug Brunk/MDedge News

“We’ve seen a shift in the landscape,” Alan F. Schatzberg, MD, said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “We’ve gone from the development of ‘me too’ agents such as venlafaxine and fluoxetine to developing drugs that may have more dramatic effects, but they also may have more baggage in terms of risks. The risk-benefit ratio is going to become increasingly more of a focus in drug development, in terms of increasing risk.”

The development of the SSRIs, he continued, led to the introduction of agents that were generally effective and well tolerated.

“Particularly, they were well tolerated in terms of their wide safety margin,” said Dr. Schatzberg, who directs the Mood Disorders Center at Stanford (Calif.) University. “It’s difficult to [die by suicide] on an SSRI. Because of that, we had greater numbers of individuals treated than we did with the tricyclics.” The introduction of SSRIs led to “widening of the net in terms of the numbers of depressed patients,” he said. “Combine that with DSM-III, and DSM-IV having relatively easy criteria to obtain a diagnosis [of depression, and] you see a large group of subjects who are exposed to treatment. But a lot of those people may not respond to a particular agent. As new treatments are promulgated and tried, what you find is [that] a reasonable number of subjects are, in fact, truly resistant. That becomes a tough nut to crack for all of us who treat depression.”

Drugs for depression that clinicians commonly have in their armamentarium commonly revolve around monoaminergic function. New and emerging agents include hallucinatory serotonin 2a agonists, glutamatergic drugs such as ketamine, GABAergic neurosteroids, opioid modulators, and onabotulinumtoxinA.

In 2013, the Food and Drug Administration approved the multimodal agent vortioxetine for the treatment of major depressive disorder. The recommended dosing is 20 mg/day, and the drug appears to have a positive effect on cognition. A meta-analysis of vortioxetine, duloxetine, and placebo comparison trials evaluated the effect of each treatment on the Digit Symbol Substitution Test (Int J Neuropsychopharmacol. 2016 Jun 15;19[10]). Vortioxetine was superior to placebo in all three trials and was superior to duloxetine in two trials. Duloxetine was not superior to placebo in two trials.

In two double-blind studies, researchers evaluated the effects of psilocybin in cancer patients with comorbid depression and anxiety. Full doses of psilocybin were 0.3 mg/kg or 22-30 mg per 70 kg. Both studies demonstrated sustained responses at full doses (J Psychopharmacol. 2016 Nov 30;30[12]:1181-97 and J Psychopharmacol. 2016 Nov 30;30[12]:1165-80).

In an open label study of psilocybin in refractory major depression, 12 patients received 10 mg on day 1 and 25 mg on day 8. Eight of 12 patients responded at 1 week, and 7 of the 12 maintained response at 3 months (Lancet Psychiatry. 2016 Jul;3[7]:619-27). According to Dr. Schatzberg, this trial became the basis for a blinded study that Compass is conducting in the United States and in the United Kingdom in which refractory patients are going to be randomized to 1 mg, 10 mg, or 25 mg psilocybin using an independent rater. “These patients are accompanied during this experience by two therapists for up to 8 hours. It’s not quite a guided therapy; it’s kind of a safety net therapy if the patient needs [help]. We’ll see what happens.”

Another agent being studied is ketamine, which works on the glutamate system, an excitatory neurotransmitter. “Glutamate is the juice that keeps us going,” said Dr. Schatzberg, who is also the Kenneth T. Norris Jr. professor of psychiatry and behavioral sciences at the university. “We can’t live without glutamate.” An anesthetic agent that has been used for 50 years, ketamine is a N-methyl-d-aspartate antagonist that has mu opioid agonist effects and stimulant properties. “It causes a psychotomimetic dissociative kind of reaction,” he said. “The doses used in depression are subanesthetic. They may put the patient asleep, but they usually don’t. The problem with the antidepressant effect is that 70% of people who initially respond don’t continue to respond beyond 1 week.”

In a randomized, placebo-controlled, double-blind crossover study of patients with treatment-resistant depression, subjects who received ketamine showed significant improvement in depression, compared with subjects who received placebo within 110 minutes after injection, which remained significant throughout the following week (Arch Gen Psychiatry. 2006;63:856-64). Specifically, of the 17 subjects treated with ketamine, 71% met response and 29% met remission criteria the day following ketamine infusion. Thirty-five percent of subjects maintained response for at least 1 week.

In an effort to further evaluate the antidepressive effects of ketamine, researchers conducted a two-site, parallel-arm, randomized, controlled trial of a single infusion of ketamine, compared with an active placebo control condition, the anesthetic midazolam (Am J Psychiatry. 2013 Oct;170[10]:1134-42). After adjustment for baseline scores and site, the Montgomery-Åsberg Depression Rating Scale score was lower in the ketamine group than in the midazolam group by 7.95 points. The likelihood of response at 24 hours was greater with ketamine than with midazolam (odds ratio, 2.18), with response rates of 64% and 28%, respectively.

In 2019, the FDA approved esketamine nasal spray, in conjunction with an oral antidepressant, for the treatment of depression in adults with treatment-resistant depression. In three phase 3 double-blind studies of esketamine in treatment-refractory depression, one was positive, two were nearly positive, and the effect sizes were mild. One maintenance discontinuation trial was positive. Based on this data, Dr. Schatzberg said, there “is not much evidence” that patients get further gain beyond an antidepressant alone in the first 24-48 hours following ketamine administration. “It makes me wonder: Should we be continuing to give this drug intranasally beyond 48 hours?” he asked. “The reason I have concern is that in certain cultures, ketamine is a highly abusable drug.”

He and Gerard Sanacora, PhD, MD, addressed the topic in a 2015 opinion piece entitled, “Ketamine: Promising path or false prophecy in the development of novel therapeutics for mood disorders?”

“If we step back for a moment and look at where we are – an intravenously administered agent that is a street drug of abuse, works rapidly, and whose enantiomers are being studied by industry for intranasal use – we should be anxious, “ they wrote (Neuropsychopharmacology. 2015 Jan;40[2]:259-67). “We need to be as careful and conservative as possible and understand how it is acting and rule out the possibility of whether it acts as an opioid.”

Dr. Schatzberg disclosed that he has served a consultant to Alkermes, Avanir, Bracket, Compass, Delpor, Epiodyne, Janssen, Jazz, Lundbeck, McKinsey, Merck, Myriad Genetics, Owl, Neuronetics, Pfizer, Sage, and Sunovion. He has received research funding from Janssen and also holds an ownership interest in Corcept, Dermira, Delpor, Epiodyne, Incyte Genetics, Madrigal, Maerck, Owl Analytics, Seattle Genetics, Titan, and Xhale.

dbrunk@mdedge.com

LAS VEGAS – The risk-benefit ratio of new and emerging drugs for depression is going to be under the spotlight more than ever before, according to an expert in mood disorders.

Doug Brunk/MDedge News

“We’ve seen a shift in the landscape,” Alan F. Schatzberg, MD, said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “We’ve gone from the development of ‘me too’ agents such as venlafaxine and fluoxetine to developing drugs that may have more dramatic effects, but they also may have more baggage in terms of risks. The risk-benefit ratio is going to become increasingly more of a focus in drug development, in terms of increasing risk.”

The development of the SSRIs, he continued, led to the introduction of agents that were generally effective and well tolerated.

“Particularly, they were well tolerated in terms of their wide safety margin,” said Dr. Schatzberg, who directs the Mood Disorders Center at Stanford (Calif.) University. “It’s difficult to [die by suicide] on an SSRI. Because of that, we had greater numbers of individuals treated than we did with the tricyclics.” The introduction of SSRIs led to “widening of the net in terms of the numbers of depressed patients,” he said. “Combine that with DSM-III, and DSM-IV having relatively easy criteria to obtain a diagnosis [of depression, and] you see a large group of subjects who are exposed to treatment. But a lot of those people may not respond to a particular agent. As new treatments are promulgated and tried, what you find is [that] a reasonable number of subjects are, in fact, truly resistant. That becomes a tough nut to crack for all of us who treat depression.”

Drugs for depression that clinicians commonly have in their armamentarium commonly revolve around monoaminergic function. New and emerging agents include hallucinatory serotonin 2a agonists, glutamatergic drugs such as ketamine, GABAergic neurosteroids, opioid modulators, and onabotulinumtoxinA.

In 2013, the Food and Drug Administration approved the multimodal agent vortioxetine for the treatment of major depressive disorder. The recommended dosing is 20 mg/day, and the drug appears to have a positive effect on cognition. A meta-analysis of vortioxetine, duloxetine, and placebo comparison trials evaluated the effect of each treatment on the Digit Symbol Substitution Test (Int J Neuropsychopharmacol. 2016 Jun 15;19[10]). Vortioxetine was superior to placebo in all three trials and was superior to duloxetine in two trials. Duloxetine was not superior to placebo in two trials.

In two double-blind studies, researchers evaluated the effects of psilocybin in cancer patients with comorbid depression and anxiety. Full doses of psilocybin were 0.3 mg/kg or 22-30 mg per 70 kg. Both studies demonstrated sustained responses at full doses (J Psychopharmacol. 2016 Nov 30;30[12]:1181-97 and J Psychopharmacol. 2016 Nov 30;30[12]:1165-80).

In an open label study of psilocybin in refractory major depression, 12 patients received 10 mg on day 1 and 25 mg on day 8. Eight of 12 patients responded at 1 week, and 7 of the 12 maintained response at 3 months (Lancet Psychiatry. 2016 Jul;3[7]:619-27). According to Dr. Schatzberg, this trial became the basis for a blinded study that Compass is conducting in the United States and in the United Kingdom in which refractory patients are going to be randomized to 1 mg, 10 mg, or 25 mg psilocybin using an independent rater. “These patients are accompanied during this experience by two therapists for up to 8 hours. It’s not quite a guided therapy; it’s kind of a safety net therapy if the patient needs [help]. We’ll see what happens.”

Another agent being studied is ketamine, which works on the glutamate system, an excitatory neurotransmitter. “Glutamate is the juice that keeps us going,” said Dr. Schatzberg, who is also the Kenneth T. Norris Jr. professor of psychiatry and behavioral sciences at the university. “We can’t live without glutamate.” An anesthetic agent that has been used for 50 years, ketamine is a N-methyl-d-aspartate antagonist that has mu opioid agonist effects and stimulant properties. “It causes a psychotomimetic dissociative kind of reaction,” he said. “The doses used in depression are subanesthetic. They may put the patient asleep, but they usually don’t. The problem with the antidepressant effect is that 70% of people who initially respond don’t continue to respond beyond 1 week.”

In a randomized, placebo-controlled, double-blind crossover study of patients with treatment-resistant depression, subjects who received ketamine showed significant improvement in depression, compared with subjects who received placebo within 110 minutes after injection, which remained significant throughout the following week (Arch Gen Psychiatry. 2006;63:856-64). Specifically, of the 17 subjects treated with ketamine, 71% met response and 29% met remission criteria the day following ketamine infusion. Thirty-five percent of subjects maintained response for at least 1 week.

In an effort to further evaluate the antidepressive effects of ketamine, researchers conducted a two-site, parallel-arm, randomized, controlled trial of a single infusion of ketamine, compared with an active placebo control condition, the anesthetic midazolam (Am J Psychiatry. 2013 Oct;170[10]:1134-42). After adjustment for baseline scores and site, the Montgomery-Åsberg Depression Rating Scale score was lower in the ketamine group than in the midazolam group by 7.95 points. The likelihood of response at 24 hours was greater with ketamine than with midazolam (odds ratio, 2.18), with response rates of 64% and 28%, respectively.

In 2019, the FDA approved esketamine nasal spray, in conjunction with an oral antidepressant, for the treatment of depression in adults with treatment-resistant depression. In three phase 3 double-blind studies of esketamine in treatment-refractory depression, one was positive, two were nearly positive, and the effect sizes were mild. One maintenance discontinuation trial was positive. Based on this data, Dr. Schatzberg said, there “is not much evidence” that patients get further gain beyond an antidepressant alone in the first 24-48 hours following ketamine administration. “It makes me wonder: Should we be continuing to give this drug intranasally beyond 48 hours?” he asked. “The reason I have concern is that in certain cultures, ketamine is a highly abusable drug.”

He and Gerard Sanacora, PhD, MD, addressed the topic in a 2015 opinion piece entitled, “Ketamine: Promising path or false prophecy in the development of novel therapeutics for mood disorders?”

“If we step back for a moment and look at where we are – an intravenously administered agent that is a street drug of abuse, works rapidly, and whose enantiomers are being studied by industry for intranasal use – we should be anxious, “ they wrote (Neuropsychopharmacology. 2015 Jan;40[2]:259-67). “We need to be as careful and conservative as possible and understand how it is acting and rule out the possibility of whether it acts as an opioid.”

Dr. Schatzberg disclosed that he has served a consultant to Alkermes, Avanir, Bracket, Compass, Delpor, Epiodyne, Janssen, Jazz, Lundbeck, McKinsey, Merck, Myriad Genetics, Owl, Neuronetics, Pfizer, Sage, and Sunovion. He has received research funding from Janssen and also holds an ownership interest in Corcept, Dermira, Delpor, Epiodyne, Incyte Genetics, Madrigal, Maerck, Owl Analytics, Seattle Genetics, Titan, and Xhale.

dbrunk@mdedge.com

LAS VEGAS – No evidence-based medications are approved for the treatment of avoidant/restrictive food intake disorder, but olanzapine is a sensible option to consider, according to Timothy D. Brewerton, MD.

Doug Brunk/MDedge News

A newly classified disorder in the DSM-5, avoidant/restrictive food intake disorder (ARFID) is an eating/feeding disturbance manifested by the persistent failure to meet appropriate nutritional energy needs associated with one or more of the following factors: significant weight loss or failure to achieve expected growth, significant nutritional deficiency, dependence on enteral feeding or oral nutritional supplements to survive, and marked interference with psychosocial functioning. ARFID “is not better explained by lack of available food or by culturally sanctioned practices,” Dr. Brewerton, an affiliate professor of psychiatry and behavioral sciences at the Medical University of South Carolina, Charleston, said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “It does not occur during the course of anorexia nervosa or bulimia nervosa, and there is no evidence of a disturbance in the way in which one’s body weight or shape is experienced. That’s what distinguishes it from anorexia nervosa.”

He added that, although many cases of ARFID have autism spectrum disorder traits, ARFID “is not attributable to a concurrent medical condition or to mental disorder.” When it does occur, the severity of the feeding disorder far outweighs that of the medical condition.”

Several ARFID case reports have been published in the medical literature, yet no randomized controlled trials exist to date. “Treatment is multidisciplinary and involves cognitive-behavioral therapy, sometimes occupational therapy,” said Dr. Brewerton, who is a founding fellow and former board member of the Academy for Eating Disorders.

He and his colleagues published a report on nine ARFID cases treated in an eating disorders program (J Child Adolesc Psychopharmacol. 2017;27[10]:920-2). The patients were treated with adjunctive olanzapine at a starting dose of 0.9 mg/day and discharge dose 2.8 mg/day. For the starting dose, “you have to break the [olanzapine pills] in pieces,” he said. “You have to have a pill cutter. What you don’t want to do is overwhelm the patient or their family members with oversedation. Too often, people start them with 2.5 mg or 5 mg [of olanzapine] right off the bat.”

The researchers found a significant increase in weight gain pre- versus post-olanzapine treatment (a mean of 3.3 pounds vs. 13.1 pounds, respectively; P less than .04) and BMI-for-weight percentiles (P less than .009). “Patients also had improvements in their Clinical Global Impressions Scale scores and a reduction in their associated anxious, depressive, and cognitive symptoms,” Dr. Brewerton said.

Similar findings were observed in a subsequent Canadian study of six ARFID cases (J Eat Disord. 2018;6:20). Five females and one male were treated with a combination of medical monitoring, family therapy, medication (including olanzapine, fluoxetine and in two cases, cyproheptadine), and CBT. At treatment termination, all six patients had achieved their goal weight.

At the University of California, San Diego, researchers led by Emily Gray, MD, conducted a retrospective chart review of six females and eight males with ARFID who ranged in age from 7 to 23 years. All but one of the 14 patients had a co-occurring diagnosis, including general anxiety disorder, social anxiety, unspecified anxiety, ADHD, major depressive disorder, and autism spectrum disorder (J Am Acad Child Adoles Psychiatry. 2018;57[4]:288-9). They were treated with mirtazapine at a dosing range of 7.5-45 mg per day. The average change in BMI per week rose from 0.10 BMI points per week pretreatment to 0.23 BMI points per week post-treatment (P less than .05).

“These cases illustrate that the judicious use of low-dose olanzapine, when used as an adjunct to other treatment modalities, may facilitate eating, weight gain, and the reduction of anxious, depressive, and cognitive symptoms,” said Dr. Brewerton, who also has a private practice in Charleston.

Dr. Brewerton disclosed that he is a consultant to Monte Nido & Affiliates and Sunovion. He receives royalties from Taylor & Francis and Springer-Verlag, and holds ownership interest in Monte Nido & Affiliates.

dbrunk@mdedge.com

LAS VEGAS – No evidence-based medications are approved for the treatment of avoidant/restrictive food intake disorder, but olanzapine is a sensible option to consider, according to Timothy D. Brewerton, MD.

Doug Brunk/MDedge News

A newly classified disorder in the DSM-5, avoidant/restrictive food intake disorder (ARFID) is an eating/feeding disturbance manifested by the persistent failure to meet appropriate nutritional energy needs associated with one or more of the following factors: significant weight loss or failure to achieve expected growth, significant nutritional deficiency, dependence on enteral feeding or oral nutritional supplements to survive, and marked interference with psychosocial functioning. ARFID “is not better explained by lack of available food or by culturally sanctioned practices,” Dr. Brewerton, an affiliate professor of psychiatry and behavioral sciences at the Medical University of South Carolina, Charleston, said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “It does not occur during the course of anorexia nervosa or bulimia nervosa, and there is no evidence of a disturbance in the way in which one’s body weight or shape is experienced. That’s what distinguishes it from anorexia nervosa.”

He added that, although many cases of ARFID have autism spectrum disorder traits, ARFID “is not attributable to a concurrent medical condition or to mental disorder.” When it does occur, the severity of the feeding disorder far outweighs that of the medical condition.”

Several ARFID case reports have been published in the medical literature, yet no randomized controlled trials exist to date. “Treatment is multidisciplinary and involves cognitive-behavioral therapy, sometimes occupational therapy,” said Dr. Brewerton, who is a founding fellow and former board member of the Academy for Eating Disorders.

He and his colleagues published a report on nine ARFID cases treated in an eating disorders program (J Child Adolesc Psychopharmacol. 2017;27[10]:920-2). The patients were treated with adjunctive olanzapine at a starting dose of 0.9 mg/day and discharge dose 2.8 mg/day. For the starting dose, “you have to break the [olanzapine pills] in pieces,” he said. “You have to have a pill cutter. What you don’t want to do is overwhelm the patient or their family members with oversedation. Too often, people start them with 2.5 mg or 5 mg [of olanzapine] right off the bat.”

The researchers found a significant increase in weight gain pre- versus post-olanzapine treatment (a mean of 3.3 pounds vs. 13.1 pounds, respectively; P less than .04) and BMI-for-weight percentiles (P less than .009). “Patients also had improvements in their Clinical Global Impressions Scale scores and a reduction in their associated anxious, depressive, and cognitive symptoms,” Dr. Brewerton said.

Similar findings were observed in a subsequent Canadian study of six ARFID cases (J Eat Disord. 2018;6:20). Five females and one male were treated with a combination of medical monitoring, family therapy, medication (including olanzapine, fluoxetine and in two cases, cyproheptadine), and CBT. At treatment termination, all six patients had achieved their goal weight.

At the University of California, San Diego, researchers led by Emily Gray, MD, conducted a retrospective chart review of six females and eight males with ARFID who ranged in age from 7 to 23 years. All but one of the 14 patients had a co-occurring diagnosis, including general anxiety disorder, social anxiety, unspecified anxiety, ADHD, major depressive disorder, and autism spectrum disorder (J Am Acad Child Adoles Psychiatry. 2018;57[4]:288-9). They were treated with mirtazapine at a dosing range of 7.5-45 mg per day. The average change in BMI per week rose from 0.10 BMI points per week pretreatment to 0.23 BMI points per week post-treatment (P less than .05).

“These cases illustrate that the judicious use of low-dose olanzapine, when used as an adjunct to other treatment modalities, may facilitate eating, weight gain, and the reduction of anxious, depressive, and cognitive symptoms,” said Dr. Brewerton, who also has a private practice in Charleston.

Dr. Brewerton disclosed that he is a consultant to Monte Nido & Affiliates and Sunovion. He receives royalties from Taylor & Francis and Springer-Verlag, and holds ownership interest in Monte Nido & Affiliates.

dbrunk@mdedge.com

LAS VEGAS – No evidence-based medications are approved for the treatment of avoidant/restrictive food intake disorder, but olanzapine is a sensible option to consider, according to Timothy D. Brewerton, MD.

Doug Brunk/MDedge News

A newly classified disorder in the DSM-5, avoidant/restrictive food intake disorder (ARFID) is an eating/feeding disturbance manifested by the persistent failure to meet appropriate nutritional energy needs associated with one or more of the following factors: significant weight loss or failure to achieve expected growth, significant nutritional deficiency, dependence on enteral feeding or oral nutritional supplements to survive, and marked interference with psychosocial functioning. ARFID “is not better explained by lack of available food or by culturally sanctioned practices,” Dr. Brewerton, an affiliate professor of psychiatry and behavioral sciences at the Medical University of South Carolina, Charleston, said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “It does not occur during the course of anorexia nervosa or bulimia nervosa, and there is no evidence of a disturbance in the way in which one’s body weight or shape is experienced. That’s what distinguishes it from anorexia nervosa.”

He added that, although many cases of ARFID have autism spectrum disorder traits, ARFID “is not attributable to a concurrent medical condition or to mental disorder.” When it does occur, the severity of the feeding disorder far outweighs that of the medical condition.”

Several ARFID case reports have been published in the medical literature, yet no randomized controlled trials exist to date. “Treatment is multidisciplinary and involves cognitive-behavioral therapy, sometimes occupational therapy,” said Dr. Brewerton, who is a founding fellow and former board member of the Academy for Eating Disorders.

He and his colleagues published a report on nine ARFID cases treated in an eating disorders program (J Child Adolesc Psychopharmacol. 2017;27[10]:920-2). The patients were treated with adjunctive olanzapine at a starting dose of 0.9 mg/day and discharge dose 2.8 mg/day. For the starting dose, “you have to break the [olanzapine pills] in pieces,” he said. “You have to have a pill cutter. What you don’t want to do is overwhelm the patient or their family members with oversedation. Too often, people start them with 2.5 mg or 5 mg [of olanzapine] right off the bat.”

The researchers found a significant increase in weight gain pre- versus post-olanzapine treatment (a mean of 3.3 pounds vs. 13.1 pounds, respectively; P less than .04) and BMI-for-weight percentiles (P less than .009). “Patients also had improvements in their Clinical Global Impressions Scale scores and a reduction in their associated anxious, depressive, and cognitive symptoms,” Dr. Brewerton said.

Similar findings were observed in a subsequent Canadian study of six ARFID cases (J Eat Disord. 2018;6:20). Five females and one male were treated with a combination of medical monitoring, family therapy, medication (including olanzapine, fluoxetine and in two cases, cyproheptadine), and CBT. At treatment termination, all six patients had achieved their goal weight.

At the University of California, San Diego, researchers led by Emily Gray, MD, conducted a retrospective chart review of six females and eight males with ARFID who ranged in age from 7 to 23 years. All but one of the 14 patients had a co-occurring diagnosis, including general anxiety disorder, social anxiety, unspecified anxiety, ADHD, major depressive disorder, and autism spectrum disorder (J Am Acad Child Adoles Psychiatry. 2018;57[4]:288-9). They were treated with mirtazapine at a dosing range of 7.5-45 mg per day. The average change in BMI per week rose from 0.10 BMI points per week pretreatment to 0.23 BMI points per week post-treatment (P less than .05).

“These cases illustrate that the judicious use of low-dose olanzapine, when used as an adjunct to other treatment modalities, may facilitate eating, weight gain, and the reduction of anxious, depressive, and cognitive symptoms,” said Dr. Brewerton, who also has a private practice in Charleston.

Dr. Brewerton disclosed that he is a consultant to Monte Nido & Affiliates and Sunovion. He receives royalties from Taylor & Francis and Springer-Verlag, and holds ownership interest in Monte Nido & Affiliates.

dbrunk@mdedge.com

The first quarterly meeting of your CHEST Board of Regents for the 2019-2020 CHEST year occurred from January 30 to February 1. We were welcomed to Coronado, California, by CHEST's new President Stephanie M. Levine, MD, FCCP, who began by reviewing the success of the CHEST 2019 Annual Meeting. The meeting had both the highest attendance of medical professionals and the highest total attendance in CHEST history, as well as CHEST's largest Fellow-in-Training attendance. There was also a significant increase in the number of international colleagues who attended the meeting. Dr. Levine next reported on upcoming CHEST activities including six live-learning courses scheduled to occur before May, the CHEST Congress in collaboration with the Italian delegation in Bologna, Italy in June, ongoing planning for CHEST 2020, the next volume of SEEK Critical Care and two additional cough guidelines. 
 

The first quarterly meeting of your CHEST Board of Regents for the 2019-2020 CHEST year occurred from January 30 to February 1. We were welcomed to Coronado, California, by CHEST's new President Stephanie M. Levine, MD, FCCP, who began by reviewing the success of the CHEST 2019 Annual Meeting. The meeting had both the highest attendance of medical professionals and the highest total attendance in CHEST history, as well as CHEST's largest Fellow-in-Training attendance. There was also a significant increase in the number of international colleagues who attended the meeting. Dr. Levine next reported on upcoming CHEST activities including six live-learning courses scheduled to occur before May, the CHEST Congress in collaboration with the Italian delegation in Bologna, Italy in June, ongoing planning for CHEST 2020, the next volume of SEEK Critical Care and two additional cough guidelines. 
 

The first quarterly meeting of your CHEST Board of Regents for the 2019-2020 CHEST year occurred from January 30 to February 1. We were welcomed to Coronado, California, by CHEST's new President Stephanie M. Levine, MD, FCCP, who began by reviewing the success of the CHEST 2019 Annual Meeting. The meeting had both the highest attendance of medical professionals and the highest total attendance in CHEST history, as well as CHEST's largest Fellow-in-Training attendance. There was also a significant increase in the number of international colleagues who attended the meeting. Dr. Levine next reported on upcoming CHEST activities including six live-learning courses scheduled to occur before May, the CHEST Congress in collaboration with the Italian delegation in Bologna, Italy in June, ongoing planning for CHEST 2020, the next volume of SEEK Critical Care and two additional cough guidelines. 
 

LAHAINA, HAWAII – The pathophysiology of rosacea is complicated, which is why “we try to target our treatments to various areas in this pathogenic pathway” to achieve optimal results, according to Linda Stein Gold, MD, director of dermatology research at the Henry Ford Health System in Detroit.

For example, in a patient with papules and pustules, a topical or oral anti-inflammatory agent is needed “to calm that down.” If background erythema is present, separate from papules and pustules, use a topical alpha-adrenergic agonist, she advised. For telangiectasias, consider a device-based treatment, and for a phyma, a surgical approach, she recommended at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.

For the background erythema of rosacea, which she described as “that pink face that’s always there,” the two alpha-adrenergic receptor agonists available, brimonidine gel 0.33%, approved by the Food and Drug Administration in 2013, and oxymetazoline cream 1%, approved in 2017, both work on the neurovascular junction, but on different receptors.

Brimonidine “kicks in very, very rapidly,” with a significant decrease in background erythema evident within 30 minutes and improvements that last over a 12-hour day, she said. It is effective over a year, but in longterm and postmarketing studies, about 20% of patients experienced exacerbation of erythema, with two peaks of redness. “One occurs at 3-6 hours,” and the other peak occurs when the drug is wearing off later in the day, Dr. Stein Gold said.

A study that sought to identify factors that might make patients more prone to this adverse effect found that “less is better” regarding brimonidine application, with an optimal application of one to three pea-sized dollops on the face, not five as instructed in the package insert. In addition, patients with more than five flushing episodes a week, particularly women, “tend to have more labile disease and [are] more likely to get that rebound erythema,” the study found.

Oxymetazoline 1% in a cream formulation has a “slightly more gentle onset of action and a more gentle offset of action,” without exacerbation of erythema and has been shown to have sustained efficacy over 52 weeks. In a yearlong safety study, there were “no new red flags and we weren’t seeing that redness at hours 3 to 6, or even when you take the patient off the drug,” she noted.

Dr. Stein Gold reported that she has served as a consultant, investigator, or speaker for Galderma, Dermira, Foamix Pharmaceuticals, Valeant, Allergan, Actavis, and Roche.

SDEF/Global Academy for Medical Education and this news organization are owned by the same parent company.

emechcatie@mdedge.com

LAHAINA, HAWAII – The pathophysiology of rosacea is complicated, which is why “we try to target our treatments to various areas in this pathogenic pathway” to achieve optimal results, according to Linda Stein Gold, MD, director of dermatology research at the Henry Ford Health System in Detroit.

For example, in a patient with papules and pustules, a topical or oral anti-inflammatory agent is needed “to calm that down.” If background erythema is present, separate from papules and pustules, use a topical alpha-adrenergic agonist, she advised. For telangiectasias, consider a device-based treatment, and for a phyma, a surgical approach, she recommended at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.

For the background erythema of rosacea, which she described as “that pink face that’s always there,” the two alpha-adrenergic receptor agonists available, brimonidine gel 0.33%, approved by the Food and Drug Administration in 2013, and oxymetazoline cream 1%, approved in 2017, both work on the neurovascular junction, but on different receptors.

Brimonidine “kicks in very, very rapidly,” with a significant decrease in background erythema evident within 30 minutes and improvements that last over a 12-hour day, she said. It is effective over a year, but in longterm and postmarketing studies, about 20% of patients experienced exacerbation of erythema, with two peaks of redness. “One occurs at 3-6 hours,” and the other peak occurs when the drug is wearing off later in the day, Dr. Stein Gold said.

A study that sought to identify factors that might make patients more prone to this adverse effect found that “less is better” regarding brimonidine application, with an optimal application of one to three pea-sized dollops on the face, not five as instructed in the package insert. In addition, patients with more than five flushing episodes a week, particularly women, “tend to have more labile disease and [are] more likely to get that rebound erythema,” the study found.

Oxymetazoline 1% in a cream formulation has a “slightly more gentle onset of action and a more gentle offset of action,” without exacerbation of erythema and has been shown to have sustained efficacy over 52 weeks. In a yearlong safety study, there were “no new red flags and we weren’t seeing that redness at hours 3 to 6, or even when you take the patient off the drug,” she noted.

Dr. Stein Gold reported that she has served as a consultant, investigator, or speaker for Galderma, Dermira, Foamix Pharmaceuticals, Valeant, Allergan, Actavis, and Roche.

SDEF/Global Academy for Medical Education and this news organization are owned by the same parent company.

emechcatie@mdedge.com

LAHAINA, HAWAII – The pathophysiology of rosacea is complicated, which is why “we try to target our treatments to various areas in this pathogenic pathway” to achieve optimal results, according to Linda Stein Gold, MD, director of dermatology research at the Henry Ford Health System in Detroit.

For example, in a patient with papules and pustules, a topical or oral anti-inflammatory agent is needed “to calm that down.” If background erythema is present, separate from papules and pustules, use a topical alpha-adrenergic agonist, she advised. For telangiectasias, consider a device-based treatment, and for a phyma, a surgical approach, she recommended at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.

For the background erythema of rosacea, which she described as “that pink face that’s always there,” the two alpha-adrenergic receptor agonists available, brimonidine gel 0.33%, approved by the Food and Drug Administration in 2013, and oxymetazoline cream 1%, approved in 2017, both work on the neurovascular junction, but on different receptors.

Brimonidine “kicks in very, very rapidly,” with a significant decrease in background erythema evident within 30 minutes and improvements that last over a 12-hour day, she said. It is effective over a year, but in longterm and postmarketing studies, about 20% of patients experienced exacerbation of erythema, with two peaks of redness. “One occurs at 3-6 hours,” and the other peak occurs when the drug is wearing off later in the day, Dr. Stein Gold said.

A study that sought to identify factors that might make patients more prone to this adverse effect found that “less is better” regarding brimonidine application, with an optimal application of one to three pea-sized dollops on the face, not five as instructed in the package insert. In addition, patients with more than five flushing episodes a week, particularly women, “tend to have more labile disease and [are] more likely to get that rebound erythema,” the study found.

Oxymetazoline 1% in a cream formulation has a “slightly more gentle onset of action and a more gentle offset of action,” without exacerbation of erythema and has been shown to have sustained efficacy over 52 weeks. In a yearlong safety study, there were “no new red flags and we weren’t seeing that redness at hours 3 to 6, or even when you take the patient off the drug,” she noted.

Dr. Stein Gold reported that she has served as a consultant, investigator, or speaker for Galderma, Dermira, Foamix Pharmaceuticals, Valeant, Allergan, Actavis, and Roche.

SDEF/Global Academy for Medical Education and this news organization are owned by the same parent company.

emechcatie@mdedge.com

Only 26% of pulmonologists report that they are happy at work, with about twice as many happy outside of work, according to Medscape’s Pulmonologist Lifestyle, Happiness & Burnout Report 2020. Dermatologists are the happiest at work, at 41%, and neurologists are the least happy, at 18%.

According to the report, which surveyed more than 15,000 physicians from various specialties, 29% of pulmonologists report feeling burned out, with 5% reporting feeling depressed and 12% both depressed and burned out. An overabundance of bureaucratic tasks is the lead contributor to burnout (52%), according to pulmonologists, followed by lack of respect from administrators, employers, colleagues, and staff (38%) and spending too many hours at work (35%).

Pulmonologists report that exercise is the biggest way they cope with burnout (47%), compared with neurologists, for example, who ranked it third at 40%. Other ways they deal with burnout include isolating themselves from others (43%) and playing or listening to music (38%).

Among depressed or burned-out pulmonologists, 70% reported not planning to seek professional help or seeking it in the past, while 12% reported currently seeking professional help. Furthermore, almost half of pulmonologists (48%) say they’re unlikely to participate in workplace programs.

When asked for reasons they wouldn’t seek professional help, 60% said they deal with it without professional help and 49% didn’t think their symptoms were severe enough, while 31% were simply too busy.

The slideshow of the full report is available on Medscape.com.

cpalmer@mdedge.com

Only 26% of pulmonologists report that they are happy at work, with about twice as many happy outside of work, according to Medscape’s Pulmonologist Lifestyle, Happiness & Burnout Report 2020. Dermatologists are the happiest at work, at 41%, and neurologists are the least happy, at 18%.

According to the report, which surveyed more than 15,000 physicians from various specialties, 29% of pulmonologists report feeling burned out, with 5% reporting feeling depressed and 12% both depressed and burned out. An overabundance of bureaucratic tasks is the lead contributor to burnout (52%), according to pulmonologists, followed by lack of respect from administrators, employers, colleagues, and staff (38%) and spending too many hours at work (35%).

Pulmonologists report that exercise is the biggest way they cope with burnout (47%), compared with neurologists, for example, who ranked it third at 40%. Other ways they deal with burnout include isolating themselves from others (43%) and playing or listening to music (38%).

Among depressed or burned-out pulmonologists, 70% reported not planning to seek professional help or seeking it in the past, while 12% reported currently seeking professional help. Furthermore, almost half of pulmonologists (48%) say they’re unlikely to participate in workplace programs.

When asked for reasons they wouldn’t seek professional help, 60% said they deal with it without professional help and 49% didn’t think their symptoms were severe enough, while 31% were simply too busy.

The slideshow of the full report is available on Medscape.com.

cpalmer@mdedge.com

Only 26% of pulmonologists report that they are happy at work, with about twice as many happy outside of work, according to Medscape’s Pulmonologist Lifestyle, Happiness & Burnout Report 2020. Dermatologists are the happiest at work, at 41%, and neurologists are the least happy, at 18%.

According to the report, which surveyed more than 15,000 physicians from various specialties, 29% of pulmonologists report feeling burned out, with 5% reporting feeling depressed and 12% both depressed and burned out. An overabundance of bureaucratic tasks is the lead contributor to burnout (52%), according to pulmonologists, followed by lack of respect from administrators, employers, colleagues, and staff (38%) and spending too many hours at work (35%).

Pulmonologists report that exercise is the biggest way they cope with burnout (47%), compared with neurologists, for example, who ranked it third at 40%. Other ways they deal with burnout include isolating themselves from others (43%) and playing or listening to music (38%).

Among depressed or burned-out pulmonologists, 70% reported not planning to seek professional help or seeking it in the past, while 12% reported currently seeking professional help. Furthermore, almost half of pulmonologists (48%) say they’re unlikely to participate in workplace programs.

When asked for reasons they wouldn’t seek professional help, 60% said they deal with it without professional help and 49% didn’t think their symptoms were severe enough, while 31% were simply too busy.

The slideshow of the full report is available on Medscape.com.

cpalmer@mdedge.com