Commentary

A 53-year-old woman presents for evaluation of persistent abdominal pain over the past 6 months. She reports the pain is about a 7 out of 10, located in the right upper quadrant. The pain does not worsen with food and not relieved with bowel movements. She has no nausea or vomiting. She reports that the pain worsens when she is sitting or standing and is relieved by lying down. Her past medical history includes having had a cholecystectomy in 2016, having hypertension, and having type 2 diabetes mellitus.

The patient’s medications include metformin, lisinopril, and empagliflozin. Her blood pressure was 130/70, and her pulse was 80. An abdominal exam of her found tenderness to palpation in the right upper quadrant, and no rebound tenderness. Her labs found a white blood cell count of 5.4, a hematocrit of 44%, an erythrocyte sedimentation rate of 13, a C-reactive protein of 1.0, a bilirubin of .8, an alkaline phosphatase of 100, an aspartate aminotransferase of 30, and an alanine transaminase of 22.



What is the most appropriate next step?

A) Right side up oblique ultrasound.

B) Abdominal CT scan.

C) Upper endoscopy.

D) More detailed physical exam.



The correct answer here is D, a more detailed physical exam is needed. Given the positional nature of this patient’s abdominal pain, an evaluation for an abdominal wall cause is appropriate.

Abdominal wall pain as a cause of chronic abdominal pain is rarely considered, but it really should be. Costanza and colleagues looked at 2,709 patients referred to gastroenterologists for chronic abdominal pain.¹ Chronic abdominal wall pain was diagnosed in 137 patients, with the diagnosis unchanged in 97% of these patients after 4 years. Most of the patients were women (four to one), and the diagnosis was almost always unsuspected by the referring physician. Physical exam was helpful in suggesting the diagnosis of abdominal wall pain.

The use of Carnett sign can be helpful. A positive Carnett sign is when abdominal pain increases or remains unchanged with tensing abdomen or when the examiner palpates the tensed abdomen. Thompson and colleagues looked at the outcome of 72 patients with undiagnosed abdominal pain and a positive Carnett sign.² Despite multiple diagnostic tests and surgeries done on these patients, very few of them had serious underlying pathology.

Thompson and Frances published another study looking at 120 patients presenting to an ED with undiagnosed abdominal pain.³ Twenty-four of the patients had positive abdominal wall tenderness on exam, and of those, only 1 had intra-abdominal pathology.

In another study, 158 patients admitted to the hospital with abdominal pain were evaluated for the presence of abdominal wall pain.⁴ Fifty-three patients were diagnosed with appendicitis, and 5 had abdominal wall tenderness on exam. Thirty-eight patients had other intra-abdominal pathology, and none of those had abdominal wall tenderness on exam. Of the 67 patients in the study who had nonspecific abdominal pain, 19 had abdominal wall tenderness on exam.

Most physicians do not include evaluation for abdominal wall tenderness as part of their evaluation of patients with abdominal pain. I think looking for this is helpful and, if positive, may lead to a diagnosis, as well as reduce the likelihood of intra-abdominal diagnoses.
 

What can we do in regard to therapy for patients with an abdominal wall source of pain?

Many patients with abdominal wall pain have anterior cutaneous nerve entrapment syndrome (ACNES). Patient’s with this often have discrete areas of tenderness on exam, often on the lateral edge of the rectus sheath, frequently on the right side of the abdomen. Anesthetic injection at the point of tenderness provides immediate relief for patients with ACNES, and is helpful in confirming the diagnosis.

Boelens and colleagues did injections in 48 patients suspected of having ACNE, randomizing half to receive lidocaine and half to receive saline placebo.5The majority of the patients receiving lidocaine (54%) had a response, compared with 17% of placebo patients (P less than .007).

Greenbaum and colleagues studied 79 patients with chronic abdominal wall pain.⁶ In this study, 72 of 79 patients had greater than 50% pain relief with anesthetic injection and were followed for a mean of almost 14 months. Only four of these patients ended up having a visceral cause of pain.
 

Can using injections help pain from ACNES longer term?

Koop and colleagues looked at all published studies in regards to both immediate and longer-term pain relief with injections.⁷ Both lidocaine injections and injections with lidocaine plus steroids led to long-term pain relief (40%-50% of patients with multiple lidocaine injections and up to 80% with lidocaine plus steroid injections). I think that injections are certainly worth a try in patients with chronic abdominal wall pain.

Pearl

Consider chronic abdominal wall pain in your differential diagnoses for patients with chronic abdominal pain, and use Carnett sign to help with diagnosis.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.

References

1. Costanza CD et al. Clin Gastroenterol Hepatol. 2004 May;2(5):395-9.

2. Thomson WH et al. Br J Surg. 1991 Feb;78(2):223-5.

3. Thomson H, Francis DM. Lancet. 1977 Nov 19;2(8047):1053-4.

4. Gray DW et al. Ann R Coll Surg Engl. 1988 Jul;70(4):233-4.

5. Boelens OB et al. Br J Surg. 2013 Jan;100(2):217-21.

6. Greenbaum DS et al. Dig Dis Sci. 1994 Sep;39(9):1935-41.

7. Koop H et al. Dtsch Arztebl Int. 2016 Jan 29;113(4):51-7.


 

A 53-year-old woman presents for evaluation of persistent abdominal pain over the past 6 months. She reports the pain is about a 7 out of 10, located in the right upper quadrant. The pain does not worsen with food and not relieved with bowel movements. She has no nausea or vomiting. She reports that the pain worsens when she is sitting or standing and is relieved by lying down. Her past medical history includes having had a cholecystectomy in 2016, having hypertension, and having type 2 diabetes mellitus.

The patient’s medications include metformin, lisinopril, and empagliflozin. Her blood pressure was 130/70, and her pulse was 80. An abdominal exam of her found tenderness to palpation in the right upper quadrant, and no rebound tenderness. Her labs found a white blood cell count of 5.4, a hematocrit of 44%, an erythrocyte sedimentation rate of 13, a C-reactive protein of 1.0, a bilirubin of .8, an alkaline phosphatase of 100, an aspartate aminotransferase of 30, and an alanine transaminase of 22.



What is the most appropriate next step?

A) Right side up oblique ultrasound.

B) Abdominal CT scan.

C) Upper endoscopy.

D) More detailed physical exam.



The correct answer here is D, a more detailed physical exam is needed. Given the positional nature of this patient’s abdominal pain, an evaluation for an abdominal wall cause is appropriate.

Abdominal wall pain as a cause of chronic abdominal pain is rarely considered, but it really should be. Costanza and colleagues looked at 2,709 patients referred to gastroenterologists for chronic abdominal pain.¹ Chronic abdominal wall pain was diagnosed in 137 patients, with the diagnosis unchanged in 97% of these patients after 4 years. Most of the patients were women (four to one), and the diagnosis was almost always unsuspected by the referring physician. Physical exam was helpful in suggesting the diagnosis of abdominal wall pain.

The use of Carnett sign can be helpful. A positive Carnett sign is when abdominal pain increases or remains unchanged with tensing abdomen or when the examiner palpates the tensed abdomen. Thompson and colleagues looked at the outcome of 72 patients with undiagnosed abdominal pain and a positive Carnett sign.² Despite multiple diagnostic tests and surgeries done on these patients, very few of them had serious underlying pathology.

Thompson and Frances published another study looking at 120 patients presenting to an ED with undiagnosed abdominal pain.³ Twenty-four of the patients had positive abdominal wall tenderness on exam, and of those, only 1 had intra-abdominal pathology.

In another study, 158 patients admitted to the hospital with abdominal pain were evaluated for the presence of abdominal wall pain.⁴ Fifty-three patients were diagnosed with appendicitis, and 5 had abdominal wall tenderness on exam. Thirty-eight patients had other intra-abdominal pathology, and none of those had abdominal wall tenderness on exam. Of the 67 patients in the study who had nonspecific abdominal pain, 19 had abdominal wall tenderness on exam.

Most physicians do not include evaluation for abdominal wall tenderness as part of their evaluation of patients with abdominal pain. I think looking for this is helpful and, if positive, may lead to a diagnosis, as well as reduce the likelihood of intra-abdominal diagnoses.
 

What can we do in regard to therapy for patients with an abdominal wall source of pain?

Many patients with abdominal wall pain have anterior cutaneous nerve entrapment syndrome (ACNES). Patient’s with this often have discrete areas of tenderness on exam, often on the lateral edge of the rectus sheath, frequently on the right side of the abdomen. Anesthetic injection at the point of tenderness provides immediate relief for patients with ACNES, and is helpful in confirming the diagnosis.

Boelens and colleagues did injections in 48 patients suspected of having ACNE, randomizing half to receive lidocaine and half to receive saline placebo.5The majority of the patients receiving lidocaine (54%) had a response, compared with 17% of placebo patients (P less than .007).

Greenbaum and colleagues studied 79 patients with chronic abdominal wall pain.⁶ In this study, 72 of 79 patients had greater than 50% pain relief with anesthetic injection and were followed for a mean of almost 14 months. Only four of these patients ended up having a visceral cause of pain.
 

Can using injections help pain from ACNES longer term?

Koop and colleagues looked at all published studies in regards to both immediate and longer-term pain relief with injections.⁷ Both lidocaine injections and injections with lidocaine plus steroids led to long-term pain relief (40%-50% of patients with multiple lidocaine injections and up to 80% with lidocaine plus steroid injections). I think that injections are certainly worth a try in patients with chronic abdominal wall pain.

Pearl

Consider chronic abdominal wall pain in your differential diagnoses for patients with chronic abdominal pain, and use Carnett sign to help with diagnosis.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.

References

1. Costanza CD et al. Clin Gastroenterol Hepatol. 2004 May;2(5):395-9.

2. Thomson WH et al. Br J Surg. 1991 Feb;78(2):223-5.

3. Thomson H, Francis DM. Lancet. 1977 Nov 19;2(8047):1053-4.

4. Gray DW et al. Ann R Coll Surg Engl. 1988 Jul;70(4):233-4.

5. Boelens OB et al. Br J Surg. 2013 Jan;100(2):217-21.

6. Greenbaum DS et al. Dig Dis Sci. 1994 Sep;39(9):1935-41.

7. Koop H et al. Dtsch Arztebl Int. 2016 Jan 29;113(4):51-7.


 

A 53-year-old woman presents for evaluation of persistent abdominal pain over the past 6 months. She reports the pain is about a 7 out of 10, located in the right upper quadrant. The pain does not worsen with food and not relieved with bowel movements. She has no nausea or vomiting. She reports that the pain worsens when she is sitting or standing and is relieved by lying down. Her past medical history includes having had a cholecystectomy in 2016, having hypertension, and having type 2 diabetes mellitus.

The patient’s medications include metformin, lisinopril, and empagliflozin. Her blood pressure was 130/70, and her pulse was 80. An abdominal exam of her found tenderness to palpation in the right upper quadrant, and no rebound tenderness. Her labs found a white blood cell count of 5.4, a hematocrit of 44%, an erythrocyte sedimentation rate of 13, a C-reactive protein of 1.0, a bilirubin of .8, an alkaline phosphatase of 100, an aspartate aminotransferase of 30, and an alanine transaminase of 22.



What is the most appropriate next step?

A) Right side up oblique ultrasound.

B) Abdominal CT scan.

C) Upper endoscopy.

D) More detailed physical exam.



The correct answer here is D, a more detailed physical exam is needed. Given the positional nature of this patient’s abdominal pain, an evaluation for an abdominal wall cause is appropriate.

Abdominal wall pain as a cause of chronic abdominal pain is rarely considered, but it really should be. Costanza and colleagues looked at 2,709 patients referred to gastroenterologists for chronic abdominal pain.¹ Chronic abdominal wall pain was diagnosed in 137 patients, with the diagnosis unchanged in 97% of these patients after 4 years. Most of the patients were women (four to one), and the diagnosis was almost always unsuspected by the referring physician. Physical exam was helpful in suggesting the diagnosis of abdominal wall pain.

The use of Carnett sign can be helpful. A positive Carnett sign is when abdominal pain increases or remains unchanged with tensing abdomen or when the examiner palpates the tensed abdomen. Thompson and colleagues looked at the outcome of 72 patients with undiagnosed abdominal pain and a positive Carnett sign.² Despite multiple diagnostic tests and surgeries done on these patients, very few of them had serious underlying pathology.

Thompson and Frances published another study looking at 120 patients presenting to an ED with undiagnosed abdominal pain.³ Twenty-four of the patients had positive abdominal wall tenderness on exam, and of those, only 1 had intra-abdominal pathology.

In another study, 158 patients admitted to the hospital with abdominal pain were evaluated for the presence of abdominal wall pain.⁴ Fifty-three patients were diagnosed with appendicitis, and 5 had abdominal wall tenderness on exam. Thirty-eight patients had other intra-abdominal pathology, and none of those had abdominal wall tenderness on exam. Of the 67 patients in the study who had nonspecific abdominal pain, 19 had abdominal wall tenderness on exam.

Most physicians do not include evaluation for abdominal wall tenderness as part of their evaluation of patients with abdominal pain. I think looking for this is helpful and, if positive, may lead to a diagnosis, as well as reduce the likelihood of intra-abdominal diagnoses.
 

What can we do in regard to therapy for patients with an abdominal wall source of pain?

Many patients with abdominal wall pain have anterior cutaneous nerve entrapment syndrome (ACNES). Patient’s with this often have discrete areas of tenderness on exam, often on the lateral edge of the rectus sheath, frequently on the right side of the abdomen. Anesthetic injection at the point of tenderness provides immediate relief for patients with ACNES, and is helpful in confirming the diagnosis.

Boelens and colleagues did injections in 48 patients suspected of having ACNE, randomizing half to receive lidocaine and half to receive saline placebo.5The majority of the patients receiving lidocaine (54%) had a response, compared with 17% of placebo patients (P less than .007).

Greenbaum and colleagues studied 79 patients with chronic abdominal wall pain.⁶ In this study, 72 of 79 patients had greater than 50% pain relief with anesthetic injection and were followed for a mean of almost 14 months. Only four of these patients ended up having a visceral cause of pain.
 

Can using injections help pain from ACNES longer term?

Koop and colleagues looked at all published studies in regards to both immediate and longer-term pain relief with injections.⁷ Both lidocaine injections and injections with lidocaine plus steroids led to long-term pain relief (40%-50% of patients with multiple lidocaine injections and up to 80% with lidocaine plus steroid injections). I think that injections are certainly worth a try in patients with chronic abdominal wall pain.

Pearl

Consider chronic abdominal wall pain in your differential diagnoses for patients with chronic abdominal pain, and use Carnett sign to help with diagnosis.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.

References

1. Costanza CD et al. Clin Gastroenterol Hepatol. 2004 May;2(5):395-9.

2. Thomson WH et al. Br J Surg. 1991 Feb;78(2):223-5.

3. Thomson H, Francis DM. Lancet. 1977 Nov 19;2(8047):1053-4.

4. Gray DW et al. Ann R Coll Surg Engl. 1988 Jul;70(4):233-4.

5. Boelens OB et al. Br J Surg. 2013 Jan;100(2):217-21.

6. Greenbaum DS et al. Dig Dis Sci. 1994 Sep;39(9):1935-41.

7. Koop H et al. Dtsch Arztebl Int. 2016 Jan 29;113(4):51-7.


 

Asthma effects about 10% of pregnant women worldwide. About 10% of these will have severe disease requiring oral corticosteroids. Brief reviews of asthma drugs are shown below. Because asthma can be a serious disease, selective treatment should not be withheld in pregnancy.

The trade names (if available) and molecular weights (rounded to the nearest whole number) are shown in parentheses. Nearly all of these drugs will cross the placenta.
 

Beclomethasone (Beconase AQ) (539)

Either beclomethasone or budesonide was considered the inhaled steroids of choice for use during pregnancy, according to a position statement from a joint committee of the American College of Obstetricians and Gynecologists and the American College of Allergy, Asthma, and Immunology published in 2000. Although the drug is teratogenic in animals, no human reports associating the use of inhaled beclomethasone with human congenital anomalies have been found.

Benralizumab (Fasenra) (150,000)

There is no published human pregnancy data. Based on studies in monkeys, the drug crosses the placenta in the third trimester. It caused no fetal harm in monkeys when given throughout pregnancy. There is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to the drug during pregnancy. Health care providers can enroll patients or encourage patients to enroll themselves by calling 1-877-311-8972 or visiting mothertobaby.org/Fasenra.

Budesonide (Rhinocort) (431)

Either budesonide or beclomethasone was considered the inhaled steroids of choice for use during pregnancy in a position statement from a joint committee of ACOG and ACAAI published in 2000. Although the drug is teratogenic in animals, no human reports associating the use of inhaled beclomethasone with human congenital anomalies have been found.

Caffeine (194)

Although the amount of caffeine in commonly used beverages varies widely, caffeine consumption in pregnancy in moderate amounts does not pose a risk to the fetus. When used in moderation, no association with congenital malformations, spontaneous abortions, preterm birth, and low birth weight have been proven.

Ciclesonide (Alvesco) (541)

Ciclesonide is an inhaled corticosteroid. There is no published human pregnancy data but the molecular weight suggests that it will cross the placenta throughout pregnancy. The drug produced no defects in rats but caused fetal toxicity in rabbits. Although the risk may be low because it is inhaled, avoiding it in the first trimester should be considered (see dexamethasone).

Cromolyn sodium (490)

Cromolyn was available as a nasal spray and oral solution, but it is no longer available in the United States. It is poorly absorbed into the systemic circulation. Neither the human nor the animal data suggest a risk of embryo-fetal harm.

Dexamethasone (392)

This is a corticosteroid with potency similar to betamethasone. Because large epidemiologic studies have found positive associations between systemic corticosteroids and nonsyndromic orofacial clefts, it is best to avoid this agent in the first trimester. However, when used for the treatment of asthma, other studies have not found a significantly increased risk of maternal or fetal complications. The difference in these outcomes may be related to the systemic concentrations of the drug.

Dyphylline (254) + guaifenesin (198) (Difil-G Forte) (Dilex-G 400) (Dy-G)

This is an OTC liquid drug taken orally. It has not been studied in pregnant animals, and there is no published human pregnancy data. However, these bronchodilator agents probably can be classified as low risk for the embryo and fetus. Dyphylline alone has been removed from the market.

Fluticasone (539) + vilanterol (Breo Ellipta) (775)

Fluticasone is a corticosteroid and vilanterol is a long acting beta2-adrenergic agonist that are given by inhalation. The molecular weights suggest that the two agents will cross the placenta throughout pregnancy. The drug did not cause fetal harm in animals. There is no published human pregnancy data for this fixed combination.

Fluticasone (539) + umeclidinium (509) + vilanterol (Trelegy Ellipta) (776)

The combination of fluticasone (glucocorticoid), umeclidinium, and vilanterol (long-acting beta2-adrenergic agonists) is given by inhalation. The molecular weights suggest that the three agents will cross the placenta throughout pregnancy. Although the three-drug combination has not been studied in pregnant rats and rabbits, the individual agents did not cause embryo-fetal harm in these species. There is no evidence that these agents, when given by inhalation, will harm the human embryo and/or fetus. No published human pregnancy reports for this fixed combination have been located.

Formoterol + mometasone (Dulera Aerosol) (841 / 521)

This combination is an aerosol product. Formoterol is a long-acting beta2-adrenergic agonist and mometasone is a topical corticosteroid. There is no published human pregnancy data for this fixed combination. The molecular weights suggest that both drugs will cross the placenta throughout pregnancy. In animals given high oral doses, both were teratogenic.

Ipratropium (Atrovent) (430)

Inhaled ipratropium, an anticholinergic bronchodilator, is recommended for asthma in patients not responding adequately to other therapy. It was not teratogenic mice, rats, and rabbits. Although the human pregnancy data is limited, there is no evidence that the drug is hazardous to the fetus. It produces fewer systemic effects then atropine and may have an additive bronchodilatory effect to beta2 agonists.

Isoproterenol (211)

Isoproterenol is a sympathomimetic (bronchodilator) with beta-adrenergic effects that is given intravenously. No reports linking this agent with congenital defects have been located. The drug was not teratogenic in rats and rabbits but was in hamsters.

Levalbuterol (Xopenex HFA) (240)

Levalbuterol is the (R)-enantiomer of racemic albuterol. It is given by inhalation. No reports of its use in human pregnancy have been located. However, racemic albuterol is considered compatible in pregnancy, and there is no apparent reason not to classify levalbuterol the same way. The drug, when given orally, is teratogenic in animals. If levalbuterol is used in pregnancy for the treatment of asthma, health care professionals are encouraged to call the toll-free number (1-877-311-8972) for information about patient enrollment in an Organization of Teratology Specialists study.

Mepolizumab (Nucala) (149,000)

Mepolizumab is given by subcutaneous injection. It is not indicated for status asthmaticus. There is no published human pregnancy data but the molecular weight suggests that it will not cross the placenta in the first half of pregnancy. The drug did not cause defects in monkeys and mice. There is a pregnancy exposure registry that monitors pregnancy outcomes in women with asthma exposed to Nucala during pregnancy. Health care providers can enroll patients or encourage patients to enroll themselves by calling 1-877-311-8972 or visiting www.mothertobaby.org/asthma.

Metaproterenol (521)

Metaproterenol, a selective beta2-adrenergic agonist, is a respiratory (bronchodilator) that is given orally. Use of this agent in pregnancy has not been linked with congenital defects. However, the drug is teratogenic in animals.

Methylprednisolone (Medrol) (374)

This is an oral glucocorticoid. The molecular weight suggests that it will cross the placenta throughout pregnancy. No reports relating to its use in human pregnancy or in pregnant animals have been located. However, teratogenicity is a potential problem (see below). If high doses of the drug are used in pregnancy, the newborn infants should be carefully observed for signs of hypoadrenalism. In addition, all corticosteroids increase calcium excretion.

Methylprednisolone acetate (Depo-Medrol) (417)

This is an injectable glucocorticoid. See below.

Methylprednisolone sodium succinate (Solu-Medrol) (497)

Methylprednisolone is a glucocorticoid given parenterally. The molecular weight suggests that it will cross the placenta throughout pregnancy. As with other corticosteroids, the drug was teratogenic, at doses equivalent to the human dose, in mice, rats, and rabbits. If the drug is used in pregnancy, the newborn infant should be carefully observed for signs of hypoadrenalism. In addition, all corticosteroids increase calcium excretion.

Mometasone + formoterol (Dulera) (321 + 841)

Dulera is a combination product of mometasone (corticosteroid) and formoterol (beta2-adrenergic agonist). There is no published human data for Dulera but the molecular weights suggest that the drugs will cross the placenta. Oral doses of formoterol were not teratogenic in animals but were with mometasone. The limited human pregnancy data with formoterol did not suggest a risk of embryo/fetal harm, but there is no human pregnancy data for mometasone.

Montelukast (Singulair) (608)

Montelukast is a leukotriene receptor antagonist that is given orally. Although the human data are limited, the drug does not appear to cause harm to the embryo and/or fetus. The drug was not teratogenic in rats and rabbits. The manufacturer maintains a pregnancy registry for women exposed to montelukast. Health care professionals are encouraged to report pregnancy exposures to the registry by calling the toll-free number 1-800-986-8999.

Omalizumab (Xolair) (149,000)

Omalizumab is a recombinant DNA–derived humanized immunoglobulin (IgG1k) monoclonal antibody that is administered subcutaneously for patients with moderate to severe persistent asthma. In monkeys, the drug did not cause embryotoxicity or teratogenicity. The human pregnancy data is very limited but does not suggest an increased embryo-fetal risk.

Prednisone (Rayos) (358)

The use of oral prednisone appears to represent a small risk to the developing fetus. One of these risks appears to be orofacial clefts. The drug causes birth defects in rats, mice, rabbits, and hamsters. However, the available evidence supports its use to control various maternal diseases, one of which is asthma.
 

Reslizumab (Cinqair) (147,000)

Reslizumab is given intravenously. Even though the molecular weight is high, the drug crosses the placenta during pregnancy. In placebo-controlled studies, anaphylaxis occurred in 0.3% of patients receiving the drug. No adverse effects were observed when the drug was given to pregnant mice and rabbits.

Salmeterol (Serevent Diskus) (416)

Salmeterol is a long-acting beta2-adrenergic agonist that is given as an aerosol or dry powder for oral inhalation. Because the drug acts locally in the lung, plasma levels are very low or undetectable and are a result of swallowed salmeterol. The limited human pregnancy data does not suggest risk of embryo-fetal harm. High oral doses in animals were not teratogenic.

Theophylline (180)

Oral theophylline is a methylxanthine that is indicated for the treatment of symptoms of chronic asthma and other chronic lung diseases. According to ACOG, theophylline is not a preferred asthma therapy but considered an alternative agent. No published reports linking the use of theophylline with congenital defects have been located. However, the drug is teratogenic in mice, rats, and rabbits at doses close to the human dose.

Tiotropium (Spiriva Respimat) (490)

Tiotropium, an anticholinergic bronchodilator, is given by oral inhalation only. No reports describing the use of tiotropium during human pregnancy have been located. The animal data suggest low risk. However, because of its long elimination half-life (about 25 hours), use of tiotropium immediately before the diagnosis of an inadvertent pregnancy would most likely result in the exposure of a portion of organogenesis.

Triamcinolone (Kenalog-40) (435)

Triamcinolone is an inhaled corticosteroid with potency slightly greater than prednisone. Although the systemic use of the drug has a small absolute risk of oral clefts and fetal growth restriction, inhaled triamcinolone does not appear to cause embryo-fetal harm. The drug is teratogenic when given orally to animals.

Breastfeeding

It is not known if the above drugs are excreted into breast milk. Agents with relatively low molecular weights will probably be in milk. However, if the maternal levels are low, the amount in milk will probably be very small, if at all. Nevertheless, it is doubtful if any of these agents, even if they are excreted into milk, will have a harmful effect on a nursing infant.

Mr. Briggs is clinical professor of pharmacy at the University of California, San Francisco, and adjunct professor of pharmacy at the University of Southern California, Los Angeles, as well as at Washington State University, Spokane. Mr. Briggs said he had no relevant financial disclosures. Email him at obnews@mdedge.com.

Asthma effects about 10% of pregnant women worldwide. About 10% of these will have severe disease requiring oral corticosteroids. Brief reviews of asthma drugs are shown below. Because asthma can be a serious disease, selective treatment should not be withheld in pregnancy.

The trade names (if available) and molecular weights (rounded to the nearest whole number) are shown in parentheses. Nearly all of these drugs will cross the placenta.
 

Beclomethasone (Beconase AQ) (539)

Either beclomethasone or budesonide was considered the inhaled steroids of choice for use during pregnancy, according to a position statement from a joint committee of the American College of Obstetricians and Gynecologists and the American College of Allergy, Asthma, and Immunology published in 2000. Although the drug is teratogenic in animals, no human reports associating the use of inhaled beclomethasone with human congenital anomalies have been found.

Benralizumab (Fasenra) (150,000)

There is no published human pregnancy data. Based on studies in monkeys, the drug crosses the placenta in the third trimester. It caused no fetal harm in monkeys when given throughout pregnancy. There is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to the drug during pregnancy. Health care providers can enroll patients or encourage patients to enroll themselves by calling 1-877-311-8972 or visiting mothertobaby.org/Fasenra.

Budesonide (Rhinocort) (431)

Either budesonide or beclomethasone was considered the inhaled steroids of choice for use during pregnancy in a position statement from a joint committee of ACOG and ACAAI published in 2000. Although the drug is teratogenic in animals, no human reports associating the use of inhaled beclomethasone with human congenital anomalies have been found.

Caffeine (194)

Although the amount of caffeine in commonly used beverages varies widely, caffeine consumption in pregnancy in moderate amounts does not pose a risk to the fetus. When used in moderation, no association with congenital malformations, spontaneous abortions, preterm birth, and low birth weight have been proven.

Ciclesonide (Alvesco) (541)

Ciclesonide is an inhaled corticosteroid. There is no published human pregnancy data but the molecular weight suggests that it will cross the placenta throughout pregnancy. The drug produced no defects in rats but caused fetal toxicity in rabbits. Although the risk may be low because it is inhaled, avoiding it in the first trimester should be considered (see dexamethasone).

Cromolyn sodium (490)

Cromolyn was available as a nasal spray and oral solution, but it is no longer available in the United States. It is poorly absorbed into the systemic circulation. Neither the human nor the animal data suggest a risk of embryo-fetal harm.

Dexamethasone (392)

This is a corticosteroid with potency similar to betamethasone. Because large epidemiologic studies have found positive associations between systemic corticosteroids and nonsyndromic orofacial clefts, it is best to avoid this agent in the first trimester. However, when used for the treatment of asthma, other studies have not found a significantly increased risk of maternal or fetal complications. The difference in these outcomes may be related to the systemic concentrations of the drug.

Dyphylline (254) + guaifenesin (198) (Difil-G Forte) (Dilex-G 400) (Dy-G)

This is an OTC liquid drug taken orally. It has not been studied in pregnant animals, and there is no published human pregnancy data. However, these bronchodilator agents probably can be classified as low risk for the embryo and fetus. Dyphylline alone has been removed from the market.

Fluticasone (539) + vilanterol (Breo Ellipta) (775)

Fluticasone is a corticosteroid and vilanterol is a long acting beta2-adrenergic agonist that are given by inhalation. The molecular weights suggest that the two agents will cross the placenta throughout pregnancy. The drug did not cause fetal harm in animals. There is no published human pregnancy data for this fixed combination.

Fluticasone (539) + umeclidinium (509) + vilanterol (Trelegy Ellipta) (776)

The combination of fluticasone (glucocorticoid), umeclidinium, and vilanterol (long-acting beta2-adrenergic agonists) is given by inhalation. The molecular weights suggest that the three agents will cross the placenta throughout pregnancy. Although the three-drug combination has not been studied in pregnant rats and rabbits, the individual agents did not cause embryo-fetal harm in these species. There is no evidence that these agents, when given by inhalation, will harm the human embryo and/or fetus. No published human pregnancy reports for this fixed combination have been located.

Formoterol + mometasone (Dulera Aerosol) (841 / 521)

This combination is an aerosol product. Formoterol is a long-acting beta2-adrenergic agonist and mometasone is a topical corticosteroid. There is no published human pregnancy data for this fixed combination. The molecular weights suggest that both drugs will cross the placenta throughout pregnancy. In animals given high oral doses, both were teratogenic.

Ipratropium (Atrovent) (430)

Inhaled ipratropium, an anticholinergic bronchodilator, is recommended for asthma in patients not responding adequately to other therapy. It was not teratogenic mice, rats, and rabbits. Although the human pregnancy data is limited, there is no evidence that the drug is hazardous to the fetus. It produces fewer systemic effects then atropine and may have an additive bronchodilatory effect to beta2 agonists.

Isoproterenol (211)

Isoproterenol is a sympathomimetic (bronchodilator) with beta-adrenergic effects that is given intravenously. No reports linking this agent with congenital defects have been located. The drug was not teratogenic in rats and rabbits but was in hamsters.

Levalbuterol (Xopenex HFA) (240)

Levalbuterol is the (R)-enantiomer of racemic albuterol. It is given by inhalation. No reports of its use in human pregnancy have been located. However, racemic albuterol is considered compatible in pregnancy, and there is no apparent reason not to classify levalbuterol the same way. The drug, when given orally, is teratogenic in animals. If levalbuterol is used in pregnancy for the treatment of asthma, health care professionals are encouraged to call the toll-free number (1-877-311-8972) for information about patient enrollment in an Organization of Teratology Specialists study.

Mepolizumab (Nucala) (149,000)

Mepolizumab is given by subcutaneous injection. It is not indicated for status asthmaticus. There is no published human pregnancy data but the molecular weight suggests that it will not cross the placenta in the first half of pregnancy. The drug did not cause defects in monkeys and mice. There is a pregnancy exposure registry that monitors pregnancy outcomes in women with asthma exposed to Nucala during pregnancy. Health care providers can enroll patients or encourage patients to enroll themselves by calling 1-877-311-8972 or visiting www.mothertobaby.org/asthma.

Metaproterenol (521)

Metaproterenol, a selective beta2-adrenergic agonist, is a respiratory (bronchodilator) that is given orally. Use of this agent in pregnancy has not been linked with congenital defects. However, the drug is teratogenic in animals.

Methylprednisolone (Medrol) (374)

This is an oral glucocorticoid. The molecular weight suggests that it will cross the placenta throughout pregnancy. No reports relating to its use in human pregnancy or in pregnant animals have been located. However, teratogenicity is a potential problem (see below). If high doses of the drug are used in pregnancy, the newborn infants should be carefully observed for signs of hypoadrenalism. In addition, all corticosteroids increase calcium excretion.

Methylprednisolone acetate (Depo-Medrol) (417)

This is an injectable glucocorticoid. See below.

Methylprednisolone sodium succinate (Solu-Medrol) (497)

Methylprednisolone is a glucocorticoid given parenterally. The molecular weight suggests that it will cross the placenta throughout pregnancy. As with other corticosteroids, the drug was teratogenic, at doses equivalent to the human dose, in mice, rats, and rabbits. If the drug is used in pregnancy, the newborn infant should be carefully observed for signs of hypoadrenalism. In addition, all corticosteroids increase calcium excretion.

Mometasone + formoterol (Dulera) (321 + 841)

Dulera is a combination product of mometasone (corticosteroid) and formoterol (beta2-adrenergic agonist). There is no published human data for Dulera but the molecular weights suggest that the drugs will cross the placenta. Oral doses of formoterol were not teratogenic in animals but were with mometasone. The limited human pregnancy data with formoterol did not suggest a risk of embryo/fetal harm, but there is no human pregnancy data for mometasone.

Montelukast (Singulair) (608)

Montelukast is a leukotriene receptor antagonist that is given orally. Although the human data are limited, the drug does not appear to cause harm to the embryo and/or fetus. The drug was not teratogenic in rats and rabbits. The manufacturer maintains a pregnancy registry for women exposed to montelukast. Health care professionals are encouraged to report pregnancy exposures to the registry by calling the toll-free number 1-800-986-8999.

Omalizumab (Xolair) (149,000)

Omalizumab is a recombinant DNA–derived humanized immunoglobulin (IgG1k) monoclonal antibody that is administered subcutaneously for patients with moderate to severe persistent asthma. In monkeys, the drug did not cause embryotoxicity or teratogenicity. The human pregnancy data is very limited but does not suggest an increased embryo-fetal risk.

Prednisone (Rayos) (358)

The use of oral prednisone appears to represent a small risk to the developing fetus. One of these risks appears to be orofacial clefts. The drug causes birth defects in rats, mice, rabbits, and hamsters. However, the available evidence supports its use to control various maternal diseases, one of which is asthma.
 

Reslizumab (Cinqair) (147,000)

Reslizumab is given intravenously. Even though the molecular weight is high, the drug crosses the placenta during pregnancy. In placebo-controlled studies, anaphylaxis occurred in 0.3% of patients receiving the drug. No adverse effects were observed when the drug was given to pregnant mice and rabbits.

Salmeterol (Serevent Diskus) (416)

Salmeterol is a long-acting beta2-adrenergic agonist that is given as an aerosol or dry powder for oral inhalation. Because the drug acts locally in the lung, plasma levels are very low or undetectable and are a result of swallowed salmeterol. The limited human pregnancy data does not suggest risk of embryo-fetal harm. High oral doses in animals were not teratogenic.

Theophylline (180)

Oral theophylline is a methylxanthine that is indicated for the treatment of symptoms of chronic asthma and other chronic lung diseases. According to ACOG, theophylline is not a preferred asthma therapy but considered an alternative agent. No published reports linking the use of theophylline with congenital defects have been located. However, the drug is teratogenic in mice, rats, and rabbits at doses close to the human dose.

Tiotropium (Spiriva Respimat) (490)

Tiotropium, an anticholinergic bronchodilator, is given by oral inhalation only. No reports describing the use of tiotropium during human pregnancy have been located. The animal data suggest low risk. However, because of its long elimination half-life (about 25 hours), use of tiotropium immediately before the diagnosis of an inadvertent pregnancy would most likely result in the exposure of a portion of organogenesis.

Triamcinolone (Kenalog-40) (435)

Triamcinolone is an inhaled corticosteroid with potency slightly greater than prednisone. Although the systemic use of the drug has a small absolute risk of oral clefts and fetal growth restriction, inhaled triamcinolone does not appear to cause embryo-fetal harm. The drug is teratogenic when given orally to animals.

Breastfeeding

It is not known if the above drugs are excreted into breast milk. Agents with relatively low molecular weights will probably be in milk. However, if the maternal levels are low, the amount in milk will probably be very small, if at all. Nevertheless, it is doubtful if any of these agents, even if they are excreted into milk, will have a harmful effect on a nursing infant.

Mr. Briggs is clinical professor of pharmacy at the University of California, San Francisco, and adjunct professor of pharmacy at the University of Southern California, Los Angeles, as well as at Washington State University, Spokane. Mr. Briggs said he had no relevant financial disclosures. Email him at obnews@mdedge.com.

Asthma effects about 10% of pregnant women worldwide. About 10% of these will have severe disease requiring oral corticosteroids. Brief reviews of asthma drugs are shown below. Because asthma can be a serious disease, selective treatment should not be withheld in pregnancy.

The trade names (if available) and molecular weights (rounded to the nearest whole number) are shown in parentheses. Nearly all of these drugs will cross the placenta.
 

Beclomethasone (Beconase AQ) (539)

Either beclomethasone or budesonide was considered the inhaled steroids of choice for use during pregnancy, according to a position statement from a joint committee of the American College of Obstetricians and Gynecologists and the American College of Allergy, Asthma, and Immunology published in 2000. Although the drug is teratogenic in animals, no human reports associating the use of inhaled beclomethasone with human congenital anomalies have been found.

Benralizumab (Fasenra) (150,000)

There is no published human pregnancy data. Based on studies in monkeys, the drug crosses the placenta in the third trimester. It caused no fetal harm in monkeys when given throughout pregnancy. There is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to the drug during pregnancy. Health care providers can enroll patients or encourage patients to enroll themselves by calling 1-877-311-8972 or visiting mothertobaby.org/Fasenra.

Budesonide (Rhinocort) (431)

Either budesonide or beclomethasone was considered the inhaled steroids of choice for use during pregnancy in a position statement from a joint committee of ACOG and ACAAI published in 2000. Although the drug is teratogenic in animals, no human reports associating the use of inhaled beclomethasone with human congenital anomalies have been found.

Caffeine (194)

Although the amount of caffeine in commonly used beverages varies widely, caffeine consumption in pregnancy in moderate amounts does not pose a risk to the fetus. When used in moderation, no association with congenital malformations, spontaneous abortions, preterm birth, and low birth weight have been proven.

Ciclesonide (Alvesco) (541)

Ciclesonide is an inhaled corticosteroid. There is no published human pregnancy data but the molecular weight suggests that it will cross the placenta throughout pregnancy. The drug produced no defects in rats but caused fetal toxicity in rabbits. Although the risk may be low because it is inhaled, avoiding it in the first trimester should be considered (see dexamethasone).

Cromolyn sodium (490)

Cromolyn was available as a nasal spray and oral solution, but it is no longer available in the United States. It is poorly absorbed into the systemic circulation. Neither the human nor the animal data suggest a risk of embryo-fetal harm.

Dexamethasone (392)

This is a corticosteroid with potency similar to betamethasone. Because large epidemiologic studies have found positive associations between systemic corticosteroids and nonsyndromic orofacial clefts, it is best to avoid this agent in the first trimester. However, when used for the treatment of asthma, other studies have not found a significantly increased risk of maternal or fetal complications. The difference in these outcomes may be related to the systemic concentrations of the drug.

Dyphylline (254) + guaifenesin (198) (Difil-G Forte) (Dilex-G 400) (Dy-G)

This is an OTC liquid drug taken orally. It has not been studied in pregnant animals, and there is no published human pregnancy data. However, these bronchodilator agents probably can be classified as low risk for the embryo and fetus. Dyphylline alone has been removed from the market.

Fluticasone (539) + vilanterol (Breo Ellipta) (775)

Fluticasone is a corticosteroid and vilanterol is a long acting beta2-adrenergic agonist that are given by inhalation. The molecular weights suggest that the two agents will cross the placenta throughout pregnancy. The drug did not cause fetal harm in animals. There is no published human pregnancy data for this fixed combination.

Fluticasone (539) + umeclidinium (509) + vilanterol (Trelegy Ellipta) (776)

The combination of fluticasone (glucocorticoid), umeclidinium, and vilanterol (long-acting beta2-adrenergic agonists) is given by inhalation. The molecular weights suggest that the three agents will cross the placenta throughout pregnancy. Although the three-drug combination has not been studied in pregnant rats and rabbits, the individual agents did not cause embryo-fetal harm in these species. There is no evidence that these agents, when given by inhalation, will harm the human embryo and/or fetus. No published human pregnancy reports for this fixed combination have been located.

Formoterol + mometasone (Dulera Aerosol) (841 / 521)

This combination is an aerosol product. Formoterol is a long-acting beta2-adrenergic agonist and mometasone is a topical corticosteroid. There is no published human pregnancy data for this fixed combination. The molecular weights suggest that both drugs will cross the placenta throughout pregnancy. In animals given high oral doses, both were teratogenic.

Ipratropium (Atrovent) (430)

Inhaled ipratropium, an anticholinergic bronchodilator, is recommended for asthma in patients not responding adequately to other therapy. It was not teratogenic mice, rats, and rabbits. Although the human pregnancy data is limited, there is no evidence that the drug is hazardous to the fetus. It produces fewer systemic effects then atropine and may have an additive bronchodilatory effect to beta2 agonists.

Isoproterenol (211)

Isoproterenol is a sympathomimetic (bronchodilator) with beta-adrenergic effects that is given intravenously. No reports linking this agent with congenital defects have been located. The drug was not teratogenic in rats and rabbits but was in hamsters.

Levalbuterol (Xopenex HFA) (240)

Levalbuterol is the (R)-enantiomer of racemic albuterol. It is given by inhalation. No reports of its use in human pregnancy have been located. However, racemic albuterol is considered compatible in pregnancy, and there is no apparent reason not to classify levalbuterol the same way. The drug, when given orally, is teratogenic in animals. If levalbuterol is used in pregnancy for the treatment of asthma, health care professionals are encouraged to call the toll-free number (1-877-311-8972) for information about patient enrollment in an Organization of Teratology Specialists study.

Mepolizumab (Nucala) (149,000)

Mepolizumab is given by subcutaneous injection. It is not indicated for status asthmaticus. There is no published human pregnancy data but the molecular weight suggests that it will not cross the placenta in the first half of pregnancy. The drug did not cause defects in monkeys and mice. There is a pregnancy exposure registry that monitors pregnancy outcomes in women with asthma exposed to Nucala during pregnancy. Health care providers can enroll patients or encourage patients to enroll themselves by calling 1-877-311-8972 or visiting www.mothertobaby.org/asthma.

Metaproterenol (521)

Metaproterenol, a selective beta2-adrenergic agonist, is a respiratory (bronchodilator) that is given orally. Use of this agent in pregnancy has not been linked with congenital defects. However, the drug is teratogenic in animals.

Methylprednisolone (Medrol) (374)

This is an oral glucocorticoid. The molecular weight suggests that it will cross the placenta throughout pregnancy. No reports relating to its use in human pregnancy or in pregnant animals have been located. However, teratogenicity is a potential problem (see below). If high doses of the drug are used in pregnancy, the newborn infants should be carefully observed for signs of hypoadrenalism. In addition, all corticosteroids increase calcium excretion.

Methylprednisolone acetate (Depo-Medrol) (417)

This is an injectable glucocorticoid. See below.

Methylprednisolone sodium succinate (Solu-Medrol) (497)

Methylprednisolone is a glucocorticoid given parenterally. The molecular weight suggests that it will cross the placenta throughout pregnancy. As with other corticosteroids, the drug was teratogenic, at doses equivalent to the human dose, in mice, rats, and rabbits. If the drug is used in pregnancy, the newborn infant should be carefully observed for signs of hypoadrenalism. In addition, all corticosteroids increase calcium excretion.

Mometasone + formoterol (Dulera) (321 + 841)

Dulera is a combination product of mometasone (corticosteroid) and formoterol (beta2-adrenergic agonist). There is no published human data for Dulera but the molecular weights suggest that the drugs will cross the placenta. Oral doses of formoterol were not teratogenic in animals but were with mometasone. The limited human pregnancy data with formoterol did not suggest a risk of embryo/fetal harm, but there is no human pregnancy data for mometasone.

Montelukast (Singulair) (608)

Montelukast is a leukotriene receptor antagonist that is given orally. Although the human data are limited, the drug does not appear to cause harm to the embryo and/or fetus. The drug was not teratogenic in rats and rabbits. The manufacturer maintains a pregnancy registry for women exposed to montelukast. Health care professionals are encouraged to report pregnancy exposures to the registry by calling the toll-free number 1-800-986-8999.

Omalizumab (Xolair) (149,000)

Omalizumab is a recombinant DNA–derived humanized immunoglobulin (IgG1k) monoclonal antibody that is administered subcutaneously for patients with moderate to severe persistent asthma. In monkeys, the drug did not cause embryotoxicity or teratogenicity. The human pregnancy data is very limited but does not suggest an increased embryo-fetal risk.

Prednisone (Rayos) (358)

The use of oral prednisone appears to represent a small risk to the developing fetus. One of these risks appears to be orofacial clefts. The drug causes birth defects in rats, mice, rabbits, and hamsters. However, the available evidence supports its use to control various maternal diseases, one of which is asthma.
 

Reslizumab (Cinqair) (147,000)

Reslizumab is given intravenously. Even though the molecular weight is high, the drug crosses the placenta during pregnancy. In placebo-controlled studies, anaphylaxis occurred in 0.3% of patients receiving the drug. No adverse effects were observed when the drug was given to pregnant mice and rabbits.

Salmeterol (Serevent Diskus) (416)

Salmeterol is a long-acting beta2-adrenergic agonist that is given as an aerosol or dry powder for oral inhalation. Because the drug acts locally in the lung, plasma levels are very low or undetectable and are a result of swallowed salmeterol. The limited human pregnancy data does not suggest risk of embryo-fetal harm. High oral doses in animals were not teratogenic.

Theophylline (180)

Oral theophylline is a methylxanthine that is indicated for the treatment of symptoms of chronic asthma and other chronic lung diseases. According to ACOG, theophylline is not a preferred asthma therapy but considered an alternative agent. No published reports linking the use of theophylline with congenital defects have been located. However, the drug is teratogenic in mice, rats, and rabbits at doses close to the human dose.

Tiotropium (Spiriva Respimat) (490)

Tiotropium, an anticholinergic bronchodilator, is given by oral inhalation only. No reports describing the use of tiotropium during human pregnancy have been located. The animal data suggest low risk. However, because of its long elimination half-life (about 25 hours), use of tiotropium immediately before the diagnosis of an inadvertent pregnancy would most likely result in the exposure of a portion of organogenesis.

Triamcinolone (Kenalog-40) (435)

Triamcinolone is an inhaled corticosteroid with potency slightly greater than prednisone. Although the systemic use of the drug has a small absolute risk of oral clefts and fetal growth restriction, inhaled triamcinolone does not appear to cause embryo-fetal harm. The drug is teratogenic when given orally to animals.

Breastfeeding

It is not known if the above drugs are excreted into breast milk. Agents with relatively low molecular weights will probably be in milk. However, if the maternal levels are low, the amount in milk will probably be very small, if at all. Nevertheless, it is doubtful if any of these agents, even if they are excreted into milk, will have a harmful effect on a nursing infant.

Mr. Briggs is clinical professor of pharmacy at the University of California, San Francisco, and adjunct professor of pharmacy at the University of Southern California, Los Angeles, as well as at Washington State University, Spokane. Mr. Briggs said he had no relevant financial disclosures. Email him at obnews@mdedge.com.

Primitive human habits have withstood the test of time but can pose health risks. Exploring a nasal cavity with a finger might have first occurred shortly after whichever species first developed a nasal opening and a digit able to reach it. Humans have been keen on continuing the long-standing yet taboo habit of nose-picking (rhinotillexis).

Even though nose-picking is stigmatized, anonymous surveys show that almost all adolescents and adults do it.¹ People are typically unaware of the risks of regular rhinotillexis. Studies exploring the intranasal human microbiome have elicited asymptomatic yet potential disease-causing microbes, including the notorious bacterium Staphylococcus aureus. As many as 30% of humans are asymptomatically permanently colonized with S aureus in their anterior nares.² These natural reservoirs can be the source of opportunistic infection that increases morbidity, mortality, and overall health care costs.

With the rise of antimicrobial resistance, especially methicillin-resistant S aureus (MRSA), a more direct approach might be necessary to curb nasally sourced cutaneous infection. Since dermatology patients deal with a wide array of skin barrier defects that put them at risk for S aureus–related infection, a medical provider’s understanding about the role of nasal colonization and transmission is important. Addressing the awkward question of “Do you pick your nose?” and providing education on the topic might be uncomfortable, but it might be necessary for dermatology patients at risk for S aureus–related cutaneous disease.

Staphylococcus aureus colonizes the anterior nares of 20% to 80% of humans; nasal colonization can begin during the first days of life.² The anterior nares are noted as the main reservoir of chronic carriage of S aureus, but carriage can occur at various body sites, including the rectum, vagina, gastrointestinal tract, and axilla, as well as other cutaneous sites. Hands are noted as the main vector of S aureus transmission from source to nose; a positive correlation between nose-picking habits and nasal carriage of S aureus has been noted.²

The percentage of S aureus–colonized humans who harbor MRSA is unknown, but it is a topic of concern with the rise of MRSA-related infection. Multisite MRSA carriage increases the risk for nasal MRSA colonization, and nasal MRSA has been noted to be more difficult to decolonize than nonresistant strains. Health care workers carrying S aureus can trigger a potential hospital outbreak of MRSA. Studies have shown that bacterial transmission is increased 40-fold when the nasal host is co-infected by rhinovirus.² Health care workers can be a source of MRSA during outbreaks, but they have not been shown to be more likely to carry MRSA than the general population.² Understanding which patients might be at risk for S aureus–associated disease in dermatology can lead clinicians to consider decolonization strategies.

Nasal colonization has been noted more frequently in patients with predisposing risk factors, including human immunodeficiency virus infection, obesity, diabetes mellitus, granulomatosis with polyangiitis, HLA-DR3 phenotype, skin and soft-tissue infections, atopic dermatitis, impetigo, and recurrent furunculosis.²Staphylococcus aureus is the most frequently noted pathogen in diabetic foot infection. A study found that 36% of sampled diabetic foot-infection patients also had S aureus isolated from both nares and the foot wound, with 65% of isolated strains being identical.² Although there are clear data on decolonization of patients prior to heart and orthopedic surgery, more data are needed to determine the benefit of screening and treating nasal carriers in populations with diabetic foot ulcers.

Staphylococcus aureus nasal colonization also has been shown in approximately 60% of patients with recurrent furunculosis and impetigo.² Although it is clear that there is a correlation between S aureus–related skin infection and nasal colonization, it is unclear what role nose-picking might have in perpetuating these complications.

There are multiple approaches to S aureus decolonization, including intranasal mupirocin, chlorhexidine body wipes, bleach baths, and even oral antibiotics (eg, trimethoprim-sulfamethoxazole, clindamycin). The Infectious Diseases Society of America has published guidelines for treating recurrent MRSA infection, including 5 to 10 days of intranasal mupirocin plus either body decolonization with a daily chlorhexidine wash for 5 to 14 days or a 15-minute dilute bleach bath twice weekly for 3 months.^3,4

There are ample meta-analyses and systematic reviews regarding S aureus decolonization and management in patients undergoing dialysis or surgery but limited data when it comes to this topic in dermatology. Those limited studies do show a benefit to decolonization in several diseases, including atopic dermatitis, hand dermatitis, recurrent skin and soft-tissue infections, cutaneous T-cell lymphoma, and surgical infection following Mohs micrographic surgery.⁴ Typically, it also is necessary to treat those who might come in contact with the patient or caregiver; in theory, treating contacts helps reduce the chance that the patient will become recolonized shortly afterward, but the data are limited regarding long-term colonization status following treatment. Contact surfaces, especially cell phones, are noted to be a contributing factor to nares colonization; therefore, it also may be necessary to educate patients on surface-cleaning techniques.⁵ Because there are multiple sources of S aureus that patients can come in contact with after decolonization attempts, a nose-picking habit might play a vital role in recolonization.

Due to rising bacterial resistance to mupirocin and chlorhexidine decolonization strategies, there is a growing need for more effective, long-term decolonization strategies.⁴ These strategies must address patients’ environmental exposure and nasal-touching habits. Overcoming the habit of nose-picking might aid S aureus decolonization strategies and thus aid in preventing future antimicrobial resistance.

But are at-risk patients receiving sufficient screening and education on the dangers of a nose-picking habit? Effective strategies to assess these practices and recommend the discontinuation of the habit could have positive effects in maintaining long-term decolonization. Potential euphemistic ways to approach this somewhat taboo topic include questions that elicit information on whether the patient ever touches the inside of his/her nose, washes his/her hands before and after touching the inside of the nose, knows about transfer of bacteria from hand to nose, or understands what decolonization is doing for them. The patient might be inclined to deny such activity, but education on nasal hygiene should be provided regardless, especially in pediatric patients.

Staphylococcus aureus might be a normal human nasal inhabitant, but it can cause a range of problems for dermatologic disease. Although pharmacotherapeutic decolonization strategies can have a positive effect on dermatologic disease, growing antibiotic resistance calls for health care providers to assess patients’ nose picking-habits and educate them on effective ways to prevent finger-to-nose practices.

Primitive human habits have withstood the test of time but can pose health risks. Exploring a nasal cavity with a finger might have first occurred shortly after whichever species first developed a nasal opening and a digit able to reach it. Humans have been keen on continuing the long-standing yet taboo habit of nose-picking (rhinotillexis).

Even though nose-picking is stigmatized, anonymous surveys show that almost all adolescents and adults do it.¹ People are typically unaware of the risks of regular rhinotillexis. Studies exploring the intranasal human microbiome have elicited asymptomatic yet potential disease-causing microbes, including the notorious bacterium Staphylococcus aureus. As many as 30% of humans are asymptomatically permanently colonized with S aureus in their anterior nares.² These natural reservoirs can be the source of opportunistic infection that increases morbidity, mortality, and overall health care costs.

With the rise of antimicrobial resistance, especially methicillin-resistant S aureus (MRSA), a more direct approach might be necessary to curb nasally sourced cutaneous infection. Since dermatology patients deal with a wide array of skin barrier defects that put them at risk for S aureus–related infection, a medical provider’s understanding about the role of nasal colonization and transmission is important. Addressing the awkward question of “Do you pick your nose?” and providing education on the topic might be uncomfortable, but it might be necessary for dermatology patients at risk for S aureus–related cutaneous disease.

Staphylococcus aureus colonizes the anterior nares of 20% to 80% of humans; nasal colonization can begin during the first days of life.² The anterior nares are noted as the main reservoir of chronic carriage of S aureus, but carriage can occur at various body sites, including the rectum, vagina, gastrointestinal tract, and axilla, as well as other cutaneous sites. Hands are noted as the main vector of S aureus transmission from source to nose; a positive correlation between nose-picking habits and nasal carriage of S aureus has been noted.²

The percentage of S aureus–colonized humans who harbor MRSA is unknown, but it is a topic of concern with the rise of MRSA-related infection. Multisite MRSA carriage increases the risk for nasal MRSA colonization, and nasal MRSA has been noted to be more difficult to decolonize than nonresistant strains. Health care workers carrying S aureus can trigger a potential hospital outbreak of MRSA. Studies have shown that bacterial transmission is increased 40-fold when the nasal host is co-infected by rhinovirus.² Health care workers can be a source of MRSA during outbreaks, but they have not been shown to be more likely to carry MRSA than the general population.² Understanding which patients might be at risk for S aureus–associated disease in dermatology can lead clinicians to consider decolonization strategies.

Nasal colonization has been noted more frequently in patients with predisposing risk factors, including human immunodeficiency virus infection, obesity, diabetes mellitus, granulomatosis with polyangiitis, HLA-DR3 phenotype, skin and soft-tissue infections, atopic dermatitis, impetigo, and recurrent furunculosis.²Staphylococcus aureus is the most frequently noted pathogen in diabetic foot infection. A study found that 36% of sampled diabetic foot-infection patients also had S aureus isolated from both nares and the foot wound, with 65% of isolated strains being identical.² Although there are clear data on decolonization of patients prior to heart and orthopedic surgery, more data are needed to determine the benefit of screening and treating nasal carriers in populations with diabetic foot ulcers.

Staphylococcus aureus nasal colonization also has been shown in approximately 60% of patients with recurrent furunculosis and impetigo.² Although it is clear that there is a correlation between S aureus–related skin infection and nasal colonization, it is unclear what role nose-picking might have in perpetuating these complications.

There are multiple approaches to S aureus decolonization, including intranasal mupirocin, chlorhexidine body wipes, bleach baths, and even oral antibiotics (eg, trimethoprim-sulfamethoxazole, clindamycin). The Infectious Diseases Society of America has published guidelines for treating recurrent MRSA infection, including 5 to 10 days of intranasal mupirocin plus either body decolonization with a daily chlorhexidine wash for 5 to 14 days or a 15-minute dilute bleach bath twice weekly for 3 months.^3,4

There are ample meta-analyses and systematic reviews regarding S aureus decolonization and management in patients undergoing dialysis or surgery but limited data when it comes to this topic in dermatology. Those limited studies do show a benefit to decolonization in several diseases, including atopic dermatitis, hand dermatitis, recurrent skin and soft-tissue infections, cutaneous T-cell lymphoma, and surgical infection following Mohs micrographic surgery.⁴ Typically, it also is necessary to treat those who might come in contact with the patient or caregiver; in theory, treating contacts helps reduce the chance that the patient will become recolonized shortly afterward, but the data are limited regarding long-term colonization status following treatment. Contact surfaces, especially cell phones, are noted to be a contributing factor to nares colonization; therefore, it also may be necessary to educate patients on surface-cleaning techniques.⁵ Because there are multiple sources of S aureus that patients can come in contact with after decolonization attempts, a nose-picking habit might play a vital role in recolonization.

Due to rising bacterial resistance to mupirocin and chlorhexidine decolonization strategies, there is a growing need for more effective, long-term decolonization strategies.⁴ These strategies must address patients’ environmental exposure and nasal-touching habits. Overcoming the habit of nose-picking might aid S aureus decolonization strategies and thus aid in preventing future antimicrobial resistance.

But are at-risk patients receiving sufficient screening and education on the dangers of a nose-picking habit? Effective strategies to assess these practices and recommend the discontinuation of the habit could have positive effects in maintaining long-term decolonization. Potential euphemistic ways to approach this somewhat taboo topic include questions that elicit information on whether the patient ever touches the inside of his/her nose, washes his/her hands before and after touching the inside of the nose, knows about transfer of bacteria from hand to nose, or understands what decolonization is doing for them. The patient might be inclined to deny such activity, but education on nasal hygiene should be provided regardless, especially in pediatric patients.

Staphylococcus aureus might be a normal human nasal inhabitant, but it can cause a range of problems for dermatologic disease. Although pharmacotherapeutic decolonization strategies can have a positive effect on dermatologic disease, growing antibiotic resistance calls for health care providers to assess patients’ nose picking-habits and educate them on effective ways to prevent finger-to-nose practices.

Primitive human habits have withstood the test of time but can pose health risks. Exploring a nasal cavity with a finger might have first occurred shortly after whichever species first developed a nasal opening and a digit able to reach it. Humans have been keen on continuing the long-standing yet taboo habit of nose-picking (rhinotillexis).

Even though nose-picking is stigmatized, anonymous surveys show that almost all adolescents and adults do it.¹ People are typically unaware of the risks of regular rhinotillexis. Studies exploring the intranasal human microbiome have elicited asymptomatic yet potential disease-causing microbes, including the notorious bacterium Staphylococcus aureus. As many as 30% of humans are asymptomatically permanently colonized with S aureus in their anterior nares.² These natural reservoirs can be the source of opportunistic infection that increases morbidity, mortality, and overall health care costs.

With the rise of antimicrobial resistance, especially methicillin-resistant S aureus (MRSA), a more direct approach might be necessary to curb nasally sourced cutaneous infection. Since dermatology patients deal with a wide array of skin barrier defects that put them at risk for S aureus–related infection, a medical provider’s understanding about the role of nasal colonization and transmission is important. Addressing the awkward question of “Do you pick your nose?” and providing education on the topic might be uncomfortable, but it might be necessary for dermatology patients at risk for S aureus–related cutaneous disease.

Staphylococcus aureus colonizes the anterior nares of 20% to 80% of humans; nasal colonization can begin during the first days of life.² The anterior nares are noted as the main reservoir of chronic carriage of S aureus, but carriage can occur at various body sites, including the rectum, vagina, gastrointestinal tract, and axilla, as well as other cutaneous sites. Hands are noted as the main vector of S aureus transmission from source to nose; a positive correlation between nose-picking habits and nasal carriage of S aureus has been noted.²

The percentage of S aureus–colonized humans who harbor MRSA is unknown, but it is a topic of concern with the rise of MRSA-related infection. Multisite MRSA carriage increases the risk for nasal MRSA colonization, and nasal MRSA has been noted to be more difficult to decolonize than nonresistant strains. Health care workers carrying S aureus can trigger a potential hospital outbreak of MRSA. Studies have shown that bacterial transmission is increased 40-fold when the nasal host is co-infected by rhinovirus.² Health care workers can be a source of MRSA during outbreaks, but they have not been shown to be more likely to carry MRSA than the general population.² Understanding which patients might be at risk for S aureus–associated disease in dermatology can lead clinicians to consider decolonization strategies.

Nasal colonization has been noted more frequently in patients with predisposing risk factors, including human immunodeficiency virus infection, obesity, diabetes mellitus, granulomatosis with polyangiitis, HLA-DR3 phenotype, skin and soft-tissue infections, atopic dermatitis, impetigo, and recurrent furunculosis.²Staphylococcus aureus is the most frequently noted pathogen in diabetic foot infection. A study found that 36% of sampled diabetic foot-infection patients also had S aureus isolated from both nares and the foot wound, with 65% of isolated strains being identical.² Although there are clear data on decolonization of patients prior to heart and orthopedic surgery, more data are needed to determine the benefit of screening and treating nasal carriers in populations with diabetic foot ulcers.

Staphylococcus aureus nasal colonization also has been shown in approximately 60% of patients with recurrent furunculosis and impetigo.² Although it is clear that there is a correlation between S aureus–related skin infection and nasal colonization, it is unclear what role nose-picking might have in perpetuating these complications.

There are multiple approaches to S aureus decolonization, including intranasal mupirocin, chlorhexidine body wipes, bleach baths, and even oral antibiotics (eg, trimethoprim-sulfamethoxazole, clindamycin). The Infectious Diseases Society of America has published guidelines for treating recurrent MRSA infection, including 5 to 10 days of intranasal mupirocin plus either body decolonization with a daily chlorhexidine wash for 5 to 14 days or a 15-minute dilute bleach bath twice weekly for 3 months.^3,4

There are ample meta-analyses and systematic reviews regarding S aureus decolonization and management in patients undergoing dialysis or surgery but limited data when it comes to this topic in dermatology. Those limited studies do show a benefit to decolonization in several diseases, including atopic dermatitis, hand dermatitis, recurrent skin and soft-tissue infections, cutaneous T-cell lymphoma, and surgical infection following Mohs micrographic surgery.⁴ Typically, it also is necessary to treat those who might come in contact with the patient or caregiver; in theory, treating contacts helps reduce the chance that the patient will become recolonized shortly afterward, but the data are limited regarding long-term colonization status following treatment. Contact surfaces, especially cell phones, are noted to be a contributing factor to nares colonization; therefore, it also may be necessary to educate patients on surface-cleaning techniques.⁵ Because there are multiple sources of S aureus that patients can come in contact with after decolonization attempts, a nose-picking habit might play a vital role in recolonization.

Due to rising bacterial resistance to mupirocin and chlorhexidine decolonization strategies, there is a growing need for more effective, long-term decolonization strategies.⁴ These strategies must address patients’ environmental exposure and nasal-touching habits. Overcoming the habit of nose-picking might aid S aureus decolonization strategies and thus aid in preventing future antimicrobial resistance.

But are at-risk patients receiving sufficient screening and education on the dangers of a nose-picking habit? Effective strategies to assess these practices and recommend the discontinuation of the habit could have positive effects in maintaining long-term decolonization. Potential euphemistic ways to approach this somewhat taboo topic include questions that elicit information on whether the patient ever touches the inside of his/her nose, washes his/her hands before and after touching the inside of the nose, knows about transfer of bacteria from hand to nose, or understands what decolonization is doing for them. The patient might be inclined to deny such activity, but education on nasal hygiene should be provided regardless, especially in pediatric patients.

Staphylococcus aureus might be a normal human nasal inhabitant, but it can cause a range of problems for dermatologic disease. Although pharmacotherapeutic decolonization strategies can have a positive effect on dermatologic disease, growing antibiotic resistance calls for health care providers to assess patients’ nose picking-habits and educate them on effective ways to prevent finger-to-nose practices.

The ongoing COVID-19 pandemic poses clear threats to mental well-being, but an increase in suicide is not inevitable if appropriate action is taken, one expert says.

“Increases in suicide rates should not be a foregone conclusion, even with the negative effects of the pandemic. If the lessons of suicide prevention research are heeded during and after the pandemic, this potential for increased risk could be substantially mitigated,” writes Christine Moutier, MD, chief medical officer of the American Foundation for Suicide Prevention, in an invited communication in JAMA Psychiatry.

“This is a moment in history when suicide prevention must be prioritized as a serious public health concern,” she writes.

Mitigating suicide risk

Although evidence from the first 6 months of the pandemic reveal specific effects on suicide risk, real-time data on suicide deaths are not available in most regions of the world. From emerging data from several countries, there is no evidence of increased suicide rates during the pandemic thus far, Moutier notes.

Still, a number of pandemic-related risk factors could increase individual and population suicide risk.

They include deterioration or recurrence of serious mental illness; increased isolation, loneliness, and bereavement; increased use of drugs and alcohol; job loss and other financial stressors; and increases in domestic violence.

There are mitigating strategies for each of these “threats to suicide risk.” The science is “very clear,” Moutier told Medscape Medical News.

“Suicide risk is never a situation of inevitability. It’s dynamic, with multiple forces at play in each individual and in the population. Lives can be saved simply by making people feel more connected to each other, that they are part of a larger community,” she added.

The political will

Moutier notes that prior to the pandemic, four countries ― Finland, Norway, Sweden, and Australia ― had fully implemented national suicide prevention plans and had achieved reductions in their national suicide rates. However, in the United States, the suicide rate has been steadily increasing since 1999.

A Centers for Disease Control and Prevention survey released in August 2020 found that 40% of US adults reported symptoms of depression, anxiety, or increased substance use during COVID-19 and that about 11% reported suicidal ideation in the past month, all increases from prior surveys.

COVID-19 presents a “new and urgent opportunity” to focus political will, federal investments, and the global community on suicide prevention, Moutier writes.

“The political will to address suicide has actually moved in the right direction during COVID, as evidenced by a number of pieces of legislation that have suddenly found their way to passing that we’ve been working on for years,” she said in an interview.

One example, she said, is the National Suicide Hotline Designation Act, signed into law earlier this month by President Donald Trump.

As previously reported, under the law, beginning in July 2022, Americans experiencing a mental health crisis will be able to dial 9-8-8 and be connected to the services and counselors at the National Suicide Prevention Lifeline.

Moutier reports no relevant financial relationships.

This article first appeared on Medscape.com.

The ongoing COVID-19 pandemic poses clear threats to mental well-being, but an increase in suicide is not inevitable if appropriate action is taken, one expert says.

“Increases in suicide rates should not be a foregone conclusion, even with the negative effects of the pandemic. If the lessons of suicide prevention research are heeded during and after the pandemic, this potential for increased risk could be substantially mitigated,” writes Christine Moutier, MD, chief medical officer of the American Foundation for Suicide Prevention, in an invited communication in JAMA Psychiatry.

“This is a moment in history when suicide prevention must be prioritized as a serious public health concern,” she writes.

Mitigating suicide risk

Although evidence from the first 6 months of the pandemic reveal specific effects on suicide risk, real-time data on suicide deaths are not available in most regions of the world. From emerging data from several countries, there is no evidence of increased suicide rates during the pandemic thus far, Moutier notes.

Still, a number of pandemic-related risk factors could increase individual and population suicide risk.

They include deterioration or recurrence of serious mental illness; increased isolation, loneliness, and bereavement; increased use of drugs and alcohol; job loss and other financial stressors; and increases in domestic violence.

There are mitigating strategies for each of these “threats to suicide risk.” The science is “very clear,” Moutier told Medscape Medical News.

“Suicide risk is never a situation of inevitability. It’s dynamic, with multiple forces at play in each individual and in the population. Lives can be saved simply by making people feel more connected to each other, that they are part of a larger community,” she added.

The political will

Moutier notes that prior to the pandemic, four countries ― Finland, Norway, Sweden, and Australia ― had fully implemented national suicide prevention plans and had achieved reductions in their national suicide rates. However, in the United States, the suicide rate has been steadily increasing since 1999.

A Centers for Disease Control and Prevention survey released in August 2020 found that 40% of US adults reported symptoms of depression, anxiety, or increased substance use during COVID-19 and that about 11% reported suicidal ideation in the past month, all increases from prior surveys.

COVID-19 presents a “new and urgent opportunity” to focus political will, federal investments, and the global community on suicide prevention, Moutier writes.

“The political will to address suicide has actually moved in the right direction during COVID, as evidenced by a number of pieces of legislation that have suddenly found their way to passing that we’ve been working on for years,” she said in an interview.

One example, she said, is the National Suicide Hotline Designation Act, signed into law earlier this month by President Donald Trump.

As previously reported, under the law, beginning in July 2022, Americans experiencing a mental health crisis will be able to dial 9-8-8 and be connected to the services and counselors at the National Suicide Prevention Lifeline.

Moutier reports no relevant financial relationships.

This article first appeared on Medscape.com.

The ongoing COVID-19 pandemic poses clear threats to mental well-being, but an increase in suicide is not inevitable if appropriate action is taken, one expert says.

“Increases in suicide rates should not be a foregone conclusion, even with the negative effects of the pandemic. If the lessons of suicide prevention research are heeded during and after the pandemic, this potential for increased risk could be substantially mitigated,” writes Christine Moutier, MD, chief medical officer of the American Foundation for Suicide Prevention, in an invited communication in JAMA Psychiatry.

“This is a moment in history when suicide prevention must be prioritized as a serious public health concern,” she writes.

Mitigating suicide risk

Although evidence from the first 6 months of the pandemic reveal specific effects on suicide risk, real-time data on suicide deaths are not available in most regions of the world. From emerging data from several countries, there is no evidence of increased suicide rates during the pandemic thus far, Moutier notes.

Still, a number of pandemic-related risk factors could increase individual and population suicide risk.

They include deterioration or recurrence of serious mental illness; increased isolation, loneliness, and bereavement; increased use of drugs and alcohol; job loss and other financial stressors; and increases in domestic violence.

There are mitigating strategies for each of these “threats to suicide risk.” The science is “very clear,” Moutier told Medscape Medical News.

“Suicide risk is never a situation of inevitability. It’s dynamic, with multiple forces at play in each individual and in the population. Lives can be saved simply by making people feel more connected to each other, that they are part of a larger community,” she added.

The political will

Moutier notes that prior to the pandemic, four countries ― Finland, Norway, Sweden, and Australia ― had fully implemented national suicide prevention plans and had achieved reductions in their national suicide rates. However, in the United States, the suicide rate has been steadily increasing since 1999.

A Centers for Disease Control and Prevention survey released in August 2020 found that 40% of US adults reported symptoms of depression, anxiety, or increased substance use during COVID-19 and that about 11% reported suicidal ideation in the past month, all increases from prior surveys.

COVID-19 presents a “new and urgent opportunity” to focus political will, federal investments, and the global community on suicide prevention, Moutier writes.

“The political will to address suicide has actually moved in the right direction during COVID, as evidenced by a number of pieces of legislation that have suddenly found their way to passing that we’ve been working on for years,” she said in an interview.

One example, she said, is the National Suicide Hotline Designation Act, signed into law earlier this month by President Donald Trump.

As previously reported, under the law, beginning in July 2022, Americans experiencing a mental health crisis will be able to dial 9-8-8 and be connected to the services and counselors at the National Suicide Prevention Lifeline.

Moutier reports no relevant financial relationships.

This article first appeared on Medscape.com.

Between 23,000 and 46,000 U.S. children live with chronic hepatitis C virus with a prevalence of 0.17% anti–hepatitis C virus (HCV) antibody positivity in those aged 6-11 years and 0.39% among children aged 12-19 years. In the United States, genotype 1 is most frequent, followed by genotypes 2 and 3. About 99% of cases result from vertical transmission; transfusion-related cases have not been observed in recent decades.Only viremic mothers are at risk of transmission as those who have spontaneously cleared HCV viremia or have been treated successfully do not risk transmission. Maternal HCV viral load appears to be a risk factor for HCV transmission, however transmission is reported at all levels of viremia.

In conjunction with the opioid epidemics, the prevalence of HCV infection has increased over the last decade. The Centers for Disease Control and Prevention reported that, between 2009 and 2014, the prevalence of HCV infection increased from 1.8 to 3.4 per 1,000 live births. They identified substantial state-to-state variation with the highest rate in West Virginia (22.6 per 1,000 live births), and the lowest in Hawaii (0.7 per 1,000 live births). The implications are clear that increasing numbers of newborns are exposed to HCV and, if transmission rates are between 1% and 5%, 80-400 U.S. infants each year acquire HCV infection.
 

HCV in children

HCV in children is almost always associated with persistent transaminitis. Chronic infection is defined as the persistence of HCV RNA for at least 6 months, and clearance of HCV infection is determined by the persistent disappearance of HCV RNA. Regardless of infection status, an infant may have detectable maternal anti-HCV antibody in serum until 18 months of age, resulting from passive transfer. In addition, prolonged infection can lead to cirrhosis, hepatocellular carcinoma, or decompensated liver disease. Potential extrahepatic manifestations including reduced physical and psychosocial health also are linked to chronic HCV. Autoimmune disease also has been reported in children with HCV. As well, the stigma of HCV elicits fear in school and child care settings that is a result of public misunderstanding regarding routes of hepatitis C transmission. No restriction of regular childhood activities is required in the daily life of HCV-infected children.

Taken together, increasing rates of HCV infection in pregnant women, increasing numbers of exposed and infected infants annually, potential for both short- and long-term morbidity, and curative nontoxic treatment, the paradigm for early identification and treatment at age 3 years is changing.
 

Screening for HCV

There is considerable discussion about which strategy for screening of at-risk infants is more appropriate. Some groups advocate for HCV-RNA testing within the first year of life. Proponents argue the use of a highly sensitive RNA assay early in life has potential to increase detection of infected infants while a negative result allows the conclusion the infant is not infected. Advocates hypothesize that early identification has potential to improve continued follow-up.

Opponents argue that early testing does not change the need for repeat testing after 18 months to confirm diagnosis. They also argue that HCV RNA is more expensive than an antibody-based testing; and treatment will not begin prior to age 3 as there is still opportunity for viremia to spontaneously clear.
 

Direct acting agents licensed

Ledipasvir/sofosbuvir (Harvoni) was initially demonstrated as curative for genotype 1, 4, 5, or 6 infection in a phase 2, multicenter, open-label study of 100 adolescents with genotype 1 treated for 12 weeks. Sustained virologic response (SVR) was documented in 98% of participants.The regimen was safe and well tolerated in this population, and the adult dosage formulation resulted in pharmacokinetic characteristics similar to those observed in adults. Two clinical trials supported the efficacy of ledipasvir/sofosbuvir in the pediatric population aged 3-11 years. This regimen also is recommended for interferon-experienced (± ribavirin, with or without an HCV protease inhibitor) children and adolescents aged 3 years or older with genotype 1 or 4. A 12-week course is recommended for patients without cirrhosis; 24 weeks is recommended for those with compensated cirrhosis. The combination of ledipasvir/sofosbuvir is the only treatment option for children aged 3-6 years with genotype 1, 4, 5, or 6 infection.

The efficacy of sofosbuvir/velpatasvir (Epclusa) once daily for 12 weeks was first evaluated in an open-label trial among children aged 6 years and older with genotype 1, 2, 3, 4, or 6 infection, without cirrhosis or with compensated cirrhosis. Subsequently, the “cocktail” was evaluated in children aged 6-12 years, with 76% genotype 1, 3% genotype 2, 15% genotype 3, and 6% genotype 4. SVR12 rates were 93% (50/54) in children with genotype 1, 91% (10/11) in those with genotype 3, and 100% in participants with genotype 2 (2/2) or genotype 4 (4/4). Sofosbuvir/velpatasvir was approved in March 2020 by the Food and Drug Administration for pediatric patients aged 6 years and older. Given its pangenotypic activity, safety, and efficacy, sofosbuvir/velpatasvir is currently recommended as a first choice for HCV treatment in children and adolescents aged at least 6 years.

The daily fixed-dose combination of glecaprevir/pibrentasvir (Mavyret) was approved in April 2019 for adolescents aged 12-17 years, and weighing at least 45 kg.Treatment is for 8 weeks, and includes treatment-naive patients without cirrhosis or those with compensated cirrhosis. SVR12 rates for Mavyret have ranged from 91% to 100 % across clinic trials. FDA approval and HCV guideline treatment recommendations for direct-acting antiviral (DAA)–experienced adolescents are based on clinical trial data from adults. Given its pangenotypic activity, safety, and efficacy record in adult patients, glecaprevir/pibrentasvir is recommended as a first choice for adolescent HCV treatment. Glecaprevir/pibrentasvir once approved for children less than 3 years of age will be safe and efficacious as a pangenotypic treatment option in children with chronic HCV infection.
 

Current recommendations

Tools for identifying HCV infected infants as early as a few months of age are available, yet studies demonstrate that a minority of at-risk children are tested for HCV using either an HCV polymerase chain reaction strategy early in life or an anti-HCV antibody strategy after 18 months of age.

Therapy with direct-acting agents is now licensed to those aged 3 years and offers the potential for cure, eliminating concern for possible progression after prolonged infection. Such therapy offers the potential to eliminate the stigma faced by many children as well as the hepatic and extrahepatic manifestations observed in children. Medication formulation and the child’s abilities to take the medication needs to be considered when prescribing DAAs. It is important to assess if the child can successfully swallow pills. Currently, Harvoni is the only medication that comes in both pellet and pill formulations. The dose is based on weight. The pellets need to be given in a small amount of nonacidic food; they cannot be chewed.

All children with chronic HCV infection are candidates for treatment. When significant fibrosis and/or cirrhosis is present treatment should not be delayed once the child is age 3 years; when only transaminitis is present, treatment can be delayed. In our experience, parents are eager to complete treatment before starting kindergarten.

Liver biopsy for obtaining liver tissue for histopathologic examination is not routinely indicated in children with chronic HCV infection but should be evaluated case by case. Noninvasive tests of hepatic fibrosis have been used in children, these include serologic markers (i.e., FibroSure) and radiologic tests such as ultrasound-based transient elastography (i.e., Fibroscan). Validation for pediatric patients is variable for the different serologic tests. Studies have shown that Fibroscan using the M probe is feasible for a wide range of ages, but poor patient cooperation may make measurement difficult.

Further details regarding dosing and choice of formulation is available at https://www.hcvguidelines.org/unique-populations/children.

Dr. Sabharwal is assistant professor of pediatrics at Boston University and attending physician in pediatric infectious diseases at Boston Medical Center. Ms. Moloney is an instructor in pediatrics at Boston University and a pediatric nurse practitioner in pediatric infectious diseases at Boston Medicine Center. Dr. Pelton is professor of pediatrics and epidemiology at Boston University and public health and senior attending physician at Boston Medical Center. Boston Medical Center received funding from AbbVie for study of Harvoni in Children 3 years of age and older. Email them at pdnews@mdedge.com.

References

MMWR Morb Mortal Wkly Rep. 2017 May 12;66(18):470-3. Hepatol Commun. 2017 March 23. doi: 10.1002/hep4.1028. Hepatology. 2020 Feb;71(2):422-30. Lancet Gastroenterol Hepatol. 2019 Apr 11. doi: 10.1016/S2468-1253(19)30046-9. Arch Dis Child. 2006 Sep;91(9):781-5. J Pediatr Gastroenterol Nutr. 2010 Feb;50(2):123-31.

Between 23,000 and 46,000 U.S. children live with chronic hepatitis C virus with a prevalence of 0.17% anti–hepatitis C virus (HCV) antibody positivity in those aged 6-11 years and 0.39% among children aged 12-19 years. In the United States, genotype 1 is most frequent, followed by genotypes 2 and 3. About 99% of cases result from vertical transmission; transfusion-related cases have not been observed in recent decades.Only viremic mothers are at risk of transmission as those who have spontaneously cleared HCV viremia or have been treated successfully do not risk transmission. Maternal HCV viral load appears to be a risk factor for HCV transmission, however transmission is reported at all levels of viremia.

In conjunction with the opioid epidemics, the prevalence of HCV infection has increased over the last decade. The Centers for Disease Control and Prevention reported that, between 2009 and 2014, the prevalence of HCV infection increased from 1.8 to 3.4 per 1,000 live births. They identified substantial state-to-state variation with the highest rate in West Virginia (22.6 per 1,000 live births), and the lowest in Hawaii (0.7 per 1,000 live births). The implications are clear that increasing numbers of newborns are exposed to HCV and, if transmission rates are between 1% and 5%, 80-400 U.S. infants each year acquire HCV infection.
 

HCV in children

HCV in children is almost always associated with persistent transaminitis. Chronic infection is defined as the persistence of HCV RNA for at least 6 months, and clearance of HCV infection is determined by the persistent disappearance of HCV RNA. Regardless of infection status, an infant may have detectable maternal anti-HCV antibody in serum until 18 months of age, resulting from passive transfer. In addition, prolonged infection can lead to cirrhosis, hepatocellular carcinoma, or decompensated liver disease. Potential extrahepatic manifestations including reduced physical and psychosocial health also are linked to chronic HCV. Autoimmune disease also has been reported in children with HCV. As well, the stigma of HCV elicits fear in school and child care settings that is a result of public misunderstanding regarding routes of hepatitis C transmission. No restriction of regular childhood activities is required in the daily life of HCV-infected children.

Taken together, increasing rates of HCV infection in pregnant women, increasing numbers of exposed and infected infants annually, potential for both short- and long-term morbidity, and curative nontoxic treatment, the paradigm for early identification and treatment at age 3 years is changing.
 

Screening for HCV

There is considerable discussion about which strategy for screening of at-risk infants is more appropriate. Some groups advocate for HCV-RNA testing within the first year of life. Proponents argue the use of a highly sensitive RNA assay early in life has potential to increase detection of infected infants while a negative result allows the conclusion the infant is not infected. Advocates hypothesize that early identification has potential to improve continued follow-up.

Opponents argue that early testing does not change the need for repeat testing after 18 months to confirm diagnosis. They also argue that HCV RNA is more expensive than an antibody-based testing; and treatment will not begin prior to age 3 as there is still opportunity for viremia to spontaneously clear.
 

Direct acting agents licensed

Ledipasvir/sofosbuvir (Harvoni) was initially demonstrated as curative for genotype 1, 4, 5, or 6 infection in a phase 2, multicenter, open-label study of 100 adolescents with genotype 1 treated for 12 weeks. Sustained virologic response (SVR) was documented in 98% of participants.The regimen was safe and well tolerated in this population, and the adult dosage formulation resulted in pharmacokinetic characteristics similar to those observed in adults. Two clinical trials supported the efficacy of ledipasvir/sofosbuvir in the pediatric population aged 3-11 years. This regimen also is recommended for interferon-experienced (± ribavirin, with or without an HCV protease inhibitor) children and adolescents aged 3 years or older with genotype 1 or 4. A 12-week course is recommended for patients without cirrhosis; 24 weeks is recommended for those with compensated cirrhosis. The combination of ledipasvir/sofosbuvir is the only treatment option for children aged 3-6 years with genotype 1, 4, 5, or 6 infection.

The efficacy of sofosbuvir/velpatasvir (Epclusa) once daily for 12 weeks was first evaluated in an open-label trial among children aged 6 years and older with genotype 1, 2, 3, 4, or 6 infection, without cirrhosis or with compensated cirrhosis. Subsequently, the “cocktail” was evaluated in children aged 6-12 years, with 76% genotype 1, 3% genotype 2, 15% genotype 3, and 6% genotype 4. SVR12 rates were 93% (50/54) in children with genotype 1, 91% (10/11) in those with genotype 3, and 100% in participants with genotype 2 (2/2) or genotype 4 (4/4). Sofosbuvir/velpatasvir was approved in March 2020 by the Food and Drug Administration for pediatric patients aged 6 years and older. Given its pangenotypic activity, safety, and efficacy, sofosbuvir/velpatasvir is currently recommended as a first choice for HCV treatment in children and adolescents aged at least 6 years.

The daily fixed-dose combination of glecaprevir/pibrentasvir (Mavyret) was approved in April 2019 for adolescents aged 12-17 years, and weighing at least 45 kg.Treatment is for 8 weeks, and includes treatment-naive patients without cirrhosis or those with compensated cirrhosis. SVR12 rates for Mavyret have ranged from 91% to 100 % across clinic trials. FDA approval and HCV guideline treatment recommendations for direct-acting antiviral (DAA)–experienced adolescents are based on clinical trial data from adults. Given its pangenotypic activity, safety, and efficacy record in adult patients, glecaprevir/pibrentasvir is recommended as a first choice for adolescent HCV treatment. Glecaprevir/pibrentasvir once approved for children less than 3 years of age will be safe and efficacious as a pangenotypic treatment option in children with chronic HCV infection.
 

Current recommendations

Tools for identifying HCV infected infants as early as a few months of age are available, yet studies demonstrate that a minority of at-risk children are tested for HCV using either an HCV polymerase chain reaction strategy early in life or an anti-HCV antibody strategy after 18 months of age.

Therapy with direct-acting agents is now licensed to those aged 3 years and offers the potential for cure, eliminating concern for possible progression after prolonged infection. Such therapy offers the potential to eliminate the stigma faced by many children as well as the hepatic and extrahepatic manifestations observed in children. Medication formulation and the child’s abilities to take the medication needs to be considered when prescribing DAAs. It is important to assess if the child can successfully swallow pills. Currently, Harvoni is the only medication that comes in both pellet and pill formulations. The dose is based on weight. The pellets need to be given in a small amount of nonacidic food; they cannot be chewed.

All children with chronic HCV infection are candidates for treatment. When significant fibrosis and/or cirrhosis is present treatment should not be delayed once the child is age 3 years; when only transaminitis is present, treatment can be delayed. In our experience, parents are eager to complete treatment before starting kindergarten.

Liver biopsy for obtaining liver tissue for histopathologic examination is not routinely indicated in children with chronic HCV infection but should be evaluated case by case. Noninvasive tests of hepatic fibrosis have been used in children, these include serologic markers (i.e., FibroSure) and radiologic tests such as ultrasound-based transient elastography (i.e., Fibroscan). Validation for pediatric patients is variable for the different serologic tests. Studies have shown that Fibroscan using the M probe is feasible for a wide range of ages, but poor patient cooperation may make measurement difficult.

Further details regarding dosing and choice of formulation is available at https://www.hcvguidelines.org/unique-populations/children.

Dr. Sabharwal is assistant professor of pediatrics at Boston University and attending physician in pediatric infectious diseases at Boston Medical Center. Ms. Moloney is an instructor in pediatrics at Boston University and a pediatric nurse practitioner in pediatric infectious diseases at Boston Medicine Center. Dr. Pelton is professor of pediatrics and epidemiology at Boston University and public health and senior attending physician at Boston Medical Center. Boston Medical Center received funding from AbbVie for study of Harvoni in Children 3 years of age and older. Email them at pdnews@mdedge.com.

References

MMWR Morb Mortal Wkly Rep. 2017 May 12;66(18):470-3. Hepatol Commun. 2017 March 23. doi: 10.1002/hep4.1028. Hepatology. 2020 Feb;71(2):422-30. Lancet Gastroenterol Hepatol. 2019 Apr 11. doi: 10.1016/S2468-1253(19)30046-9. Arch Dis Child. 2006 Sep;91(9):781-5. J Pediatr Gastroenterol Nutr. 2010 Feb;50(2):123-31.

Between 23,000 and 46,000 U.S. children live with chronic hepatitis C virus with a prevalence of 0.17% anti–hepatitis C virus (HCV) antibody positivity in those aged 6-11 years and 0.39% among children aged 12-19 years. In the United States, genotype 1 is most frequent, followed by genotypes 2 and 3. About 99% of cases result from vertical transmission; transfusion-related cases have not been observed in recent decades.Only viremic mothers are at risk of transmission as those who have spontaneously cleared HCV viremia or have been treated successfully do not risk transmission. Maternal HCV viral load appears to be a risk factor for HCV transmission, however transmission is reported at all levels of viremia.

In conjunction with the opioid epidemics, the prevalence of HCV infection has increased over the last decade. The Centers for Disease Control and Prevention reported that, between 2009 and 2014, the prevalence of HCV infection increased from 1.8 to 3.4 per 1,000 live births. They identified substantial state-to-state variation with the highest rate in West Virginia (22.6 per 1,000 live births), and the lowest in Hawaii (0.7 per 1,000 live births). The implications are clear that increasing numbers of newborns are exposed to HCV and, if transmission rates are between 1% and 5%, 80-400 U.S. infants each year acquire HCV infection.
 

HCV in children

HCV in children is almost always associated with persistent transaminitis. Chronic infection is defined as the persistence of HCV RNA for at least 6 months, and clearance of HCV infection is determined by the persistent disappearance of HCV RNA. Regardless of infection status, an infant may have detectable maternal anti-HCV antibody in serum until 18 months of age, resulting from passive transfer. In addition, prolonged infection can lead to cirrhosis, hepatocellular carcinoma, or decompensated liver disease. Potential extrahepatic manifestations including reduced physical and psychosocial health also are linked to chronic HCV. Autoimmune disease also has been reported in children with HCV. As well, the stigma of HCV elicits fear in school and child care settings that is a result of public misunderstanding regarding routes of hepatitis C transmission. No restriction of regular childhood activities is required in the daily life of HCV-infected children.

Taken together, increasing rates of HCV infection in pregnant women, increasing numbers of exposed and infected infants annually, potential for both short- and long-term morbidity, and curative nontoxic treatment, the paradigm for early identification and treatment at age 3 years is changing.
 

Screening for HCV

There is considerable discussion about which strategy for screening of at-risk infants is more appropriate. Some groups advocate for HCV-RNA testing within the first year of life. Proponents argue the use of a highly sensitive RNA assay early in life has potential to increase detection of infected infants while a negative result allows the conclusion the infant is not infected. Advocates hypothesize that early identification has potential to improve continued follow-up.

Opponents argue that early testing does not change the need for repeat testing after 18 months to confirm diagnosis. They also argue that HCV RNA is more expensive than an antibody-based testing; and treatment will not begin prior to age 3 as there is still opportunity for viremia to spontaneously clear.
 

Direct acting agents licensed

Ledipasvir/sofosbuvir (Harvoni) was initially demonstrated as curative for genotype 1, 4, 5, or 6 infection in a phase 2, multicenter, open-label study of 100 adolescents with genotype 1 treated for 12 weeks. Sustained virologic response (SVR) was documented in 98% of participants.The regimen was safe and well tolerated in this population, and the adult dosage formulation resulted in pharmacokinetic characteristics similar to those observed in adults. Two clinical trials supported the efficacy of ledipasvir/sofosbuvir in the pediatric population aged 3-11 years. This regimen also is recommended for interferon-experienced (± ribavirin, with or without an HCV protease inhibitor) children and adolescents aged 3 years or older with genotype 1 or 4. A 12-week course is recommended for patients without cirrhosis; 24 weeks is recommended for those with compensated cirrhosis. The combination of ledipasvir/sofosbuvir is the only treatment option for children aged 3-6 years with genotype 1, 4, 5, or 6 infection.

The efficacy of sofosbuvir/velpatasvir (Epclusa) once daily for 12 weeks was first evaluated in an open-label trial among children aged 6 years and older with genotype 1, 2, 3, 4, or 6 infection, without cirrhosis or with compensated cirrhosis. Subsequently, the “cocktail” was evaluated in children aged 6-12 years, with 76% genotype 1, 3% genotype 2, 15% genotype 3, and 6% genotype 4. SVR12 rates were 93% (50/54) in children with genotype 1, 91% (10/11) in those with genotype 3, and 100% in participants with genotype 2 (2/2) or genotype 4 (4/4). Sofosbuvir/velpatasvir was approved in March 2020 by the Food and Drug Administration for pediatric patients aged 6 years and older. Given its pangenotypic activity, safety, and efficacy, sofosbuvir/velpatasvir is currently recommended as a first choice for HCV treatment in children and adolescents aged at least 6 years.

The daily fixed-dose combination of glecaprevir/pibrentasvir (Mavyret) was approved in April 2019 for adolescents aged 12-17 years, and weighing at least 45 kg.Treatment is for 8 weeks, and includes treatment-naive patients without cirrhosis or those with compensated cirrhosis. SVR12 rates for Mavyret have ranged from 91% to 100 % across clinic trials. FDA approval and HCV guideline treatment recommendations for direct-acting antiviral (DAA)–experienced adolescents are based on clinical trial data from adults. Given its pangenotypic activity, safety, and efficacy record in adult patients, glecaprevir/pibrentasvir is recommended as a first choice for adolescent HCV treatment. Glecaprevir/pibrentasvir once approved for children less than 3 years of age will be safe and efficacious as a pangenotypic treatment option in children with chronic HCV infection.
 

Current recommendations

Tools for identifying HCV infected infants as early as a few months of age are available, yet studies demonstrate that a minority of at-risk children are tested for HCV using either an HCV polymerase chain reaction strategy early in life or an anti-HCV antibody strategy after 18 months of age.

Therapy with direct-acting agents is now licensed to those aged 3 years and offers the potential for cure, eliminating concern for possible progression after prolonged infection. Such therapy offers the potential to eliminate the stigma faced by many children as well as the hepatic and extrahepatic manifestations observed in children. Medication formulation and the child’s abilities to take the medication needs to be considered when prescribing DAAs. It is important to assess if the child can successfully swallow pills. Currently, Harvoni is the only medication that comes in both pellet and pill formulations. The dose is based on weight. The pellets need to be given in a small amount of nonacidic food; they cannot be chewed.

All children with chronic HCV infection are candidates for treatment. When significant fibrosis and/or cirrhosis is present treatment should not be delayed once the child is age 3 years; when only transaminitis is present, treatment can be delayed. In our experience, parents are eager to complete treatment before starting kindergarten.

Liver biopsy for obtaining liver tissue for histopathologic examination is not routinely indicated in children with chronic HCV infection but should be evaluated case by case. Noninvasive tests of hepatic fibrosis have been used in children, these include serologic markers (i.e., FibroSure) and radiologic tests such as ultrasound-based transient elastography (i.e., Fibroscan). Validation for pediatric patients is variable for the different serologic tests. Studies have shown that Fibroscan using the M probe is feasible for a wide range of ages, but poor patient cooperation may make measurement difficult.

Further details regarding dosing and choice of formulation is available at https://www.hcvguidelines.org/unique-populations/children.

Dr. Sabharwal is assistant professor of pediatrics at Boston University and attending physician in pediatric infectious diseases at Boston Medical Center. Ms. Moloney is an instructor in pediatrics at Boston University and a pediatric nurse practitioner in pediatric infectious diseases at Boston Medicine Center. Dr. Pelton is professor of pediatrics and epidemiology at Boston University and public health and senior attending physician at Boston Medical Center. Boston Medical Center received funding from AbbVie for study of Harvoni in Children 3 years of age and older. Email them at pdnews@mdedge.com.

References

MMWR Morb Mortal Wkly Rep. 2017 May 12;66(18):470-3. Hepatol Commun. 2017 March 23. doi: 10.1002/hep4.1028. Hepatology. 2020 Feb;71(2):422-30. Lancet Gastroenterol Hepatol. 2019 Apr 11. doi: 10.1016/S2468-1253(19)30046-9. Arch Dis Child. 2006 Sep;91(9):781-5. J Pediatr Gastroenterol Nutr. 2010 Feb;50(2):123-31.

This is the third in a series of columns discussing the important roles that dermatologists have played in the skin care industry. This section will discuss those dermatologists who worked behind the scenes with the cosmetic industry, rather than developing their own skin care lines.
 

Norman Orentreich, MD

Dr. Orentreich was a successful New York City dermatologist and the first to perform hair transplants. This new technique brought him fame and notoriety and arguably made him the first “celebrity dermatologist.” (He was also a member of the original advisory board of Dermatology News, at that time Skin & Allergy News, in January 1970.) Dr. Orentreich was a seminal figure in the trend to link the cosmetic industry and dermatology. In August 1967, Vogue magazine¹ published an article on him, titled “Can Great Skin be Created?” This popular article caught the attention of Leonard Lauder, of Estée Lauder, who recruited Dr. Orentreich to help create the skin care line Clinique. Clinique was intended to be a brand with a medical look that promoted its products as “allergy tested,” with packaging that has an antiseptic look and beauty counter salespeople wearing white coats.

Dr. Orentreich’s input into the development of a skin type–based skin care line was fundamental to the development of this brand. The four-question questionnaire with an iconic plastic lever that customers slide left or right instantly provided them with an assessment of their skin type at the beauty counter, with one of four skin types: Very Dry to Dry Skin (Skin Type 1), Dry Combination (Skin Type 2), Combination Oily (Skin Type 3), and Oily (Skin Type 4).

Although this skin-typing system was not scientifically accurate (there is no scientific definition of combination skin), it was reminiscent of the system developed by cosmetic company tycoon Helena Rubinstein in the 1940s that classified people into four skin types: oily, dry, combination, and sensitive. Clinique became a blockbuster skin care brand and was one of the first developed by a dermatologist – although Dr. Orentreich did not put his name on it.

In 1972, Dr. Orentreich filed a patent² for an exfoliating pad for the skin that later became known as the “Buf-Puf.” I heard years ago that he got the idea from the machines used to buff the floors in the hospital. The buffing pad had a hole in the center where the machine attached. Dr. Orentreich purportedly thought “I wonder what they do with the cut-out centers?” He looked into this, and subsequently used the centers to create the Buf-Puf. I cannot find a reference for this, but I love this story and hope it’s true. If any readers have any knowledge of this, please let me know, so I can amend my story if it is incorrect.
 

Almay

Almay, an amalgamation of the founders’ names, Alfred and Fanny May Woititz, was the first hypoallergenic brand, established in 1931, and the first to provide hypoallergenic cosmetics, long before Clinique. In addition, the company was the first skin care brand to become available by prescription only (as it was initially), fully disclose all individual ingredients in its products (well before this became mandatory in 1976), provide totally fragrance-free products, develop a hypoallergenic fragrance – and provide patch tests and other materials to physicians to identify contact allergens.

Over 90 years, the company was also the first among skin care brands to do the following:

• Provide custom formulations to individuals proven to be allergic to a specific ingredient, through their physicians.
• Perform a full range of premarket safety testing on all products for allergy and irritation, and test all its products for comedogenicity.
• Formulate cosmetics for use around the eye area (eye shadows and eyeliners) specifically for contact lens wearers.
• Formulate hypoallergenic regimens for specific skin types in the mass market.
• Provide a specific cosmetic regimen for acne-prone women, including a silicone-based makeup and active ingredients for treatment in cosmetics and skin care.

I recently interviewed Stanley Levy, MD, who was one of the consultants to Almay, and practices in Chapel Hill, N.C., where he has an academic niche related to skin care formulation and safety. He told me how Almay provided patch test materials to dermatologists to help identify contact dermatitis to cosmetic ingredients, and described Almay’s relationship with the dermatology field as follows: “From the outset, Almay was linked to dermatology. In 1930, a chemist and pharmacist in New York City, Al Woititz, was looking to compound cosmetics for his wife suffering from cosmetic allergies, Fannie May. He enlisted the counsel of the preeminent dermatologic expert in contact dermatitis at the time, Dr. Marion Sulzberger, to suggest ingredients to avoid. [Dr. Sulzberger was also a member of the original Dermatology News editorial advisory board.] Soon, dermatologists around New York City were recommending these formulations. This led to a product line free of the known allergens and a fledgling company trademarked as Almay. For the past 90 years, [the company] has kept a close relationship with dermatologists, well before that was the norm.”

The Almay research overseen by Dr. Levy and others contributed greatly to our understanding of the allergenicity of skin care.
 

Albert Kligman, MD

The turning point for the interface of dermatology with the cosmetic industry was the shift from a safety-based approach (hypoallergenic and noncomedogenic) to an emphasis on efficacy claims in the 1980s. Part of the impetus for this was the Dr. Kligman’s observation that retinoids could improve photoaging.

Dr. Kligman, a well-known dermatologist at the University of Pennsylvania, Philadelphia, showed that retinoids were an effective treatment for acne. For more about this, listen to my interview on the Dermatology Weekly podcast, with James Leyden, MD, about his work at the University of Pennsylvania with Dr. Kligman on the development of oral and topical retinoids. During Dr. Kligman’s research on acne, he noticed that wrinkles improved after treatment with tretinoin, and in 1986, he and Dr. Leyden (and several other authors) published the first article about tretinoin’s use for photoaged skin.³ This led to a double-blind study⁴ conducted by John J. Voorhees, MD, University of Michigan, Ann Arbor, and coauthors that showed statistically significant improvement of photoaged skin when treated with topical tretinoin. Dr. Voorhees and his group did many more studies on retinoids^5,6 and photoaging⁷ – so many that, at one time, he was (and maybe still is) the most widely published dermatologist in the United States. These studies showed that, not only did prescription tretinoin improve the appearance of wrinkles, but so did over-the-counter retinol.⁸ Retinoids remain the most efficacious prescription and cosmeceutical ingredients to treat wrinkled skin.

When studies conducted by Dr. Kligman, Dr. Voorhees, and by Barbara Gilcrest, MD, ^9,10 showed that retinoids improved wrinkles, a major change in the focus in the skin care industry occurred.

During the same time period, the studies on alpha hydroxy acids by Chérie Ditre, MD, Eugene Van Scott, MD, and colleages^11,12; and studies by Sheldon Pinnell, MD, on Vitamin C (see part 1 of this series) all demonstrated the efficacy of cosmetic ingredients on photoaged skin. This triggered a major change in how skin care products were marketed, with an efficacy approach rather than a safety approach.

With the shift from safety (hypoallergenic and noncomedogenic issues) to efficacy claims in the 1980s, and as nondrug active ingredients like retinol were shown to have biologic effects, the lines between the Food and Drug Administration’s definition of a drug versus a cosmetic became blurred. In 1984, Dr. Kligman suggested a new classification for the ingredients that fell in the middle, proposing the term “cosmeceutical” and thus, the concept of a cosmeceutical was introduced. To this day, cosmeceutical is not an official definition and the FDA has yet to deal with it as a quasi-drug category. FDA regulations as to what constitutes a drug versus a cosmetic date back to the 1938 Food, Drug and Cosmetic Act.

Once marketing focused on efficacy, many companies made outrageous claims. During the second half of the 1980s, the FDA issued some warning letters to some companies in an effort to control these claims.

Now efficacy claims abound and we, as dermatologists, should be the experts who back up these claims with scientific data. As the cosmeceutical market has evolved and grown, consumers are bewildered by the myriad of active ingredients being promoted and the number of products in the marketplace. As dermatologic innovation has led to more efficacious active ingredients, our patients look to us as knowledgeable and credible sources of information and for recommendations about the best skin care routines for their skin issues. This is all reflected in the fact that physician-dispensed skin care is becoming the fastest growing segment in this market. It is incumbent upon dermatologists to be knowledgeable and conversant about skin care products and skin care routines, and is particularly true for those of us who sell skin care products in our offices.

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann has written two textbooks and a New York Times Best Sellers book for consumers. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Burt’s Bees, Evolus, Galderma, and Revance. She is the CEO of Skin Type Solutions, a company that independently tests skin care products and makes recommendations to physicians on which skin care technologies are best. Write to her at dermnews@mdedge.com.

References

1. Vogue Magazine, 1967 Aug 15. “Can Great Skin be Created?”

2. https://patents.google.com/patent/US3910284.

3. Kligman AM et al. J Am Acad Dermatol. 1986 Oct;15(4 Pt 2):836-59.

4. Weiss JS et al. JAMA. 1988 Jan 22-29;259(4):527-32.

5. Goldfarb MT et al. J Am Acad Dermatol. 1989 Sep;21(3 Pt 2):645-50.

6. Ellis CN et al. J Am Acad Dermatol. 1990 Oct;23(4 Pt 1):629-37.

7. Kang S; Voorhees JJ. J Am Acad Dermatol. 1998 Aug;39(2 Pt 3):S55-61.

8. Kafi R et al. Arch Dermatol. 2007 May;143(5):606-12.

9. Gilchrest BA. J Am Acad Dermatol. 1989 Sep;21(3 Pt 2):610-3.

10. Bhawan J et al. Arch Dermatol. 1991 May;127(5):666-72.

11. Griffin TD et al. J Am Acad Dermatol. 1996 Feb;34(2 Pt 1):196-203.

12. Ditre CM et al. J Am Acad Dermatol. 1996 Feb;34(2 Pt 1):187-95.
 

This is the third in a series of columns discussing the important roles that dermatologists have played in the skin care industry. This section will discuss those dermatologists who worked behind the scenes with the cosmetic industry, rather than developing their own skin care lines.
 

Norman Orentreich, MD

Dr. Orentreich was a successful New York City dermatologist and the first to perform hair transplants. This new technique brought him fame and notoriety and arguably made him the first “celebrity dermatologist.” (He was also a member of the original advisory board of Dermatology News, at that time Skin & Allergy News, in January 1970.) Dr. Orentreich was a seminal figure in the trend to link the cosmetic industry and dermatology. In August 1967, Vogue magazine¹ published an article on him, titled “Can Great Skin be Created?” This popular article caught the attention of Leonard Lauder, of Estée Lauder, who recruited Dr. Orentreich to help create the skin care line Clinique. Clinique was intended to be a brand with a medical look that promoted its products as “allergy tested,” with packaging that has an antiseptic look and beauty counter salespeople wearing white coats.

Dr. Orentreich’s input into the development of a skin type–based skin care line was fundamental to the development of this brand. The four-question questionnaire with an iconic plastic lever that customers slide left or right instantly provided them with an assessment of their skin type at the beauty counter, with one of four skin types: Very Dry to Dry Skin (Skin Type 1), Dry Combination (Skin Type 2), Combination Oily (Skin Type 3), and Oily (Skin Type 4).

Although this skin-typing system was not scientifically accurate (there is no scientific definition of combination skin), it was reminiscent of the system developed by cosmetic company tycoon Helena Rubinstein in the 1940s that classified people into four skin types: oily, dry, combination, and sensitive. Clinique became a blockbuster skin care brand and was one of the first developed by a dermatologist – although Dr. Orentreich did not put his name on it.

In 1972, Dr. Orentreich filed a patent² for an exfoliating pad for the skin that later became known as the “Buf-Puf.” I heard years ago that he got the idea from the machines used to buff the floors in the hospital. The buffing pad had a hole in the center where the machine attached. Dr. Orentreich purportedly thought “I wonder what they do with the cut-out centers?” He looked into this, and subsequently used the centers to create the Buf-Puf. I cannot find a reference for this, but I love this story and hope it’s true. If any readers have any knowledge of this, please let me know, so I can amend my story if it is incorrect.
 

Almay

Almay, an amalgamation of the founders’ names, Alfred and Fanny May Woititz, was the first hypoallergenic brand, established in 1931, and the first to provide hypoallergenic cosmetics, long before Clinique. In addition, the company was the first skin care brand to become available by prescription only (as it was initially), fully disclose all individual ingredients in its products (well before this became mandatory in 1976), provide totally fragrance-free products, develop a hypoallergenic fragrance – and provide patch tests and other materials to physicians to identify contact allergens.

Over 90 years, the company was also the first among skin care brands to do the following:

• Provide custom formulations to individuals proven to be allergic to a specific ingredient, through their physicians.
• Perform a full range of premarket safety testing on all products for allergy and irritation, and test all its products for comedogenicity.
• Formulate cosmetics for use around the eye area (eye shadows and eyeliners) specifically for contact lens wearers.
• Formulate hypoallergenic regimens for specific skin types in the mass market.
• Provide a specific cosmetic regimen for acne-prone women, including a silicone-based makeup and active ingredients for treatment in cosmetics and skin care.

I recently interviewed Stanley Levy, MD, who was one of the consultants to Almay, and practices in Chapel Hill, N.C., where he has an academic niche related to skin care formulation and safety. He told me how Almay provided patch test materials to dermatologists to help identify contact dermatitis to cosmetic ingredients, and described Almay’s relationship with the dermatology field as follows: “From the outset, Almay was linked to dermatology. In 1930, a chemist and pharmacist in New York City, Al Woititz, was looking to compound cosmetics for his wife suffering from cosmetic allergies, Fannie May. He enlisted the counsel of the preeminent dermatologic expert in contact dermatitis at the time, Dr. Marion Sulzberger, to suggest ingredients to avoid. [Dr. Sulzberger was also a member of the original Dermatology News editorial advisory board.] Soon, dermatologists around New York City were recommending these formulations. This led to a product line free of the known allergens and a fledgling company trademarked as Almay. For the past 90 years, [the company] has kept a close relationship with dermatologists, well before that was the norm.”

The Almay research overseen by Dr. Levy and others contributed greatly to our understanding of the allergenicity of skin care.
 

Albert Kligman, MD

The turning point for the interface of dermatology with the cosmetic industry was the shift from a safety-based approach (hypoallergenic and noncomedogenic) to an emphasis on efficacy claims in the 1980s. Part of the impetus for this was the Dr. Kligman’s observation that retinoids could improve photoaging.

Dr. Kligman, a well-known dermatologist at the University of Pennsylvania, Philadelphia, showed that retinoids were an effective treatment for acne. For more about this, listen to my interview on the Dermatology Weekly podcast, with James Leyden, MD, about his work at the University of Pennsylvania with Dr. Kligman on the development of oral and topical retinoids. During Dr. Kligman’s research on acne, he noticed that wrinkles improved after treatment with tretinoin, and in 1986, he and Dr. Leyden (and several other authors) published the first article about tretinoin’s use for photoaged skin.³ This led to a double-blind study⁴ conducted by John J. Voorhees, MD, University of Michigan, Ann Arbor, and coauthors that showed statistically significant improvement of photoaged skin when treated with topical tretinoin. Dr. Voorhees and his group did many more studies on retinoids^5,6 and photoaging⁷ – so many that, at one time, he was (and maybe still is) the most widely published dermatologist in the United States. These studies showed that, not only did prescription tretinoin improve the appearance of wrinkles, but so did over-the-counter retinol.⁸ Retinoids remain the most efficacious prescription and cosmeceutical ingredients to treat wrinkled skin.

When studies conducted by Dr. Kligman, Dr. Voorhees, and by Barbara Gilcrest, MD, ^9,10 showed that retinoids improved wrinkles, a major change in the focus in the skin care industry occurred.

During the same time period, the studies on alpha hydroxy acids by Chérie Ditre, MD, Eugene Van Scott, MD, and colleages^11,12; and studies by Sheldon Pinnell, MD, on Vitamin C (see part 1 of this series) all demonstrated the efficacy of cosmetic ingredients on photoaged skin. This triggered a major change in how skin care products were marketed, with an efficacy approach rather than a safety approach.

With the shift from safety (hypoallergenic and noncomedogenic issues) to efficacy claims in the 1980s, and as nondrug active ingredients like retinol were shown to have biologic effects, the lines between the Food and Drug Administration’s definition of a drug versus a cosmetic became blurred. In 1984, Dr. Kligman suggested a new classification for the ingredients that fell in the middle, proposing the term “cosmeceutical” and thus, the concept of a cosmeceutical was introduced. To this day, cosmeceutical is not an official definition and the FDA has yet to deal with it as a quasi-drug category. FDA regulations as to what constitutes a drug versus a cosmetic date back to the 1938 Food, Drug and Cosmetic Act.

Once marketing focused on efficacy, many companies made outrageous claims. During the second half of the 1980s, the FDA issued some warning letters to some companies in an effort to control these claims.

Now efficacy claims abound and we, as dermatologists, should be the experts who back up these claims with scientific data. As the cosmeceutical market has evolved and grown, consumers are bewildered by the myriad of active ingredients being promoted and the number of products in the marketplace. As dermatologic innovation has led to more efficacious active ingredients, our patients look to us as knowledgeable and credible sources of information and for recommendations about the best skin care routines for their skin issues. This is all reflected in the fact that physician-dispensed skin care is becoming the fastest growing segment in this market. It is incumbent upon dermatologists to be knowledgeable and conversant about skin care products and skin care routines, and is particularly true for those of us who sell skin care products in our offices.

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann has written two textbooks and a New York Times Best Sellers book for consumers. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Burt’s Bees, Evolus, Galderma, and Revance. She is the CEO of Skin Type Solutions, a company that independently tests skin care products and makes recommendations to physicians on which skin care technologies are best. Write to her at dermnews@mdedge.com.

References

1. Vogue Magazine, 1967 Aug 15. “Can Great Skin be Created?”

2. https://patents.google.com/patent/US3910284.

3. Kligman AM et al. J Am Acad Dermatol. 1986 Oct;15(4 Pt 2):836-59.

4. Weiss JS et al. JAMA. 1988 Jan 22-29;259(4):527-32.

5. Goldfarb MT et al. J Am Acad Dermatol. 1989 Sep;21(3 Pt 2):645-50.

6. Ellis CN et al. J Am Acad Dermatol. 1990 Oct;23(4 Pt 1):629-37.

7. Kang S; Voorhees JJ. J Am Acad Dermatol. 1998 Aug;39(2 Pt 3):S55-61.

8. Kafi R et al. Arch Dermatol. 2007 May;143(5):606-12.

9. Gilchrest BA. J Am Acad Dermatol. 1989 Sep;21(3 Pt 2):610-3.

10. Bhawan J et al. Arch Dermatol. 1991 May;127(5):666-72.

11. Griffin TD et al. J Am Acad Dermatol. 1996 Feb;34(2 Pt 1):196-203.

12. Ditre CM et al. J Am Acad Dermatol. 1996 Feb;34(2 Pt 1):187-95.
 

This is the third in a series of columns discussing the important roles that dermatologists have played in the skin care industry. This section will discuss those dermatologists who worked behind the scenes with the cosmetic industry, rather than developing their own skin care lines.
 

Norman Orentreich, MD

Dr. Orentreich was a successful New York City dermatologist and the first to perform hair transplants. This new technique brought him fame and notoriety and arguably made him the first “celebrity dermatologist.” (He was also a member of the original advisory board of Dermatology News, at that time Skin & Allergy News, in January 1970.) Dr. Orentreich was a seminal figure in the trend to link the cosmetic industry and dermatology. In August 1967, Vogue magazine¹ published an article on him, titled “Can Great Skin be Created?” This popular article caught the attention of Leonard Lauder, of Estée Lauder, who recruited Dr. Orentreich to help create the skin care line Clinique. Clinique was intended to be a brand with a medical look that promoted its products as “allergy tested,” with packaging that has an antiseptic look and beauty counter salespeople wearing white coats.

Dr. Orentreich’s input into the development of a skin type–based skin care line was fundamental to the development of this brand. The four-question questionnaire with an iconic plastic lever that customers slide left or right instantly provided them with an assessment of their skin type at the beauty counter, with one of four skin types: Very Dry to Dry Skin (Skin Type 1), Dry Combination (Skin Type 2), Combination Oily (Skin Type 3), and Oily (Skin Type 4).

Although this skin-typing system was not scientifically accurate (there is no scientific definition of combination skin), it was reminiscent of the system developed by cosmetic company tycoon Helena Rubinstein in the 1940s that classified people into four skin types: oily, dry, combination, and sensitive. Clinique became a blockbuster skin care brand and was one of the first developed by a dermatologist – although Dr. Orentreich did not put his name on it.

In 1972, Dr. Orentreich filed a patent² for an exfoliating pad for the skin that later became known as the “Buf-Puf.” I heard years ago that he got the idea from the machines used to buff the floors in the hospital. The buffing pad had a hole in the center where the machine attached. Dr. Orentreich purportedly thought “I wonder what they do with the cut-out centers?” He looked into this, and subsequently used the centers to create the Buf-Puf. I cannot find a reference for this, but I love this story and hope it’s true. If any readers have any knowledge of this, please let me know, so I can amend my story if it is incorrect.
 

Almay

Almay, an amalgamation of the founders’ names, Alfred and Fanny May Woititz, was the first hypoallergenic brand, established in 1931, and the first to provide hypoallergenic cosmetics, long before Clinique. In addition, the company was the first skin care brand to become available by prescription only (as it was initially), fully disclose all individual ingredients in its products (well before this became mandatory in 1976), provide totally fragrance-free products, develop a hypoallergenic fragrance – and provide patch tests and other materials to physicians to identify contact allergens.

Over 90 years, the company was also the first among skin care brands to do the following:

• Provide custom formulations to individuals proven to be allergic to a specific ingredient, through their physicians.
• Perform a full range of premarket safety testing on all products for allergy and irritation, and test all its products for comedogenicity.
• Formulate cosmetics for use around the eye area (eye shadows and eyeliners) specifically for contact lens wearers.
• Formulate hypoallergenic regimens for specific skin types in the mass market.
• Provide a specific cosmetic regimen for acne-prone women, including a silicone-based makeup and active ingredients for treatment in cosmetics and skin care.

I recently interviewed Stanley Levy, MD, who was one of the consultants to Almay, and practices in Chapel Hill, N.C., where he has an academic niche related to skin care formulation and safety. He told me how Almay provided patch test materials to dermatologists to help identify contact dermatitis to cosmetic ingredients, and described Almay’s relationship with the dermatology field as follows: “From the outset, Almay was linked to dermatology. In 1930, a chemist and pharmacist in New York City, Al Woititz, was looking to compound cosmetics for his wife suffering from cosmetic allergies, Fannie May. He enlisted the counsel of the preeminent dermatologic expert in contact dermatitis at the time, Dr. Marion Sulzberger, to suggest ingredients to avoid. [Dr. Sulzberger was also a member of the original Dermatology News editorial advisory board.] Soon, dermatologists around New York City were recommending these formulations. This led to a product line free of the known allergens and a fledgling company trademarked as Almay. For the past 90 years, [the company] has kept a close relationship with dermatologists, well before that was the norm.”

The Almay research overseen by Dr. Levy and others contributed greatly to our understanding of the allergenicity of skin care.
 

Albert Kligman, MD

The turning point for the interface of dermatology with the cosmetic industry was the shift from a safety-based approach (hypoallergenic and noncomedogenic) to an emphasis on efficacy claims in the 1980s. Part of the impetus for this was the Dr. Kligman’s observation that retinoids could improve photoaging.

Dr. Kligman, a well-known dermatologist at the University of Pennsylvania, Philadelphia, showed that retinoids were an effective treatment for acne. For more about this, listen to my interview on the Dermatology Weekly podcast, with James Leyden, MD, about his work at the University of Pennsylvania with Dr. Kligman on the development of oral and topical retinoids. During Dr. Kligman’s research on acne, he noticed that wrinkles improved after treatment with tretinoin, and in 1986, he and Dr. Leyden (and several other authors) published the first article about tretinoin’s use for photoaged skin.³ This led to a double-blind study⁴ conducted by John J. Voorhees, MD, University of Michigan, Ann Arbor, and coauthors that showed statistically significant improvement of photoaged skin when treated with topical tretinoin. Dr. Voorhees and his group did many more studies on retinoids^5,6 and photoaging⁷ – so many that, at one time, he was (and maybe still is) the most widely published dermatologist in the United States. These studies showed that, not only did prescription tretinoin improve the appearance of wrinkles, but so did over-the-counter retinol.⁸ Retinoids remain the most efficacious prescription and cosmeceutical ingredients to treat wrinkled skin.

When studies conducted by Dr. Kligman, Dr. Voorhees, and by Barbara Gilcrest, MD, ^9,10 showed that retinoids improved wrinkles, a major change in the focus in the skin care industry occurred.

During the same time period, the studies on alpha hydroxy acids by Chérie Ditre, MD, Eugene Van Scott, MD, and colleages^11,12; and studies by Sheldon Pinnell, MD, on Vitamin C (see part 1 of this series) all demonstrated the efficacy of cosmetic ingredients on photoaged skin. This triggered a major change in how skin care products were marketed, with an efficacy approach rather than a safety approach.

With the shift from safety (hypoallergenic and noncomedogenic issues) to efficacy claims in the 1980s, and as nondrug active ingredients like retinol were shown to have biologic effects, the lines between the Food and Drug Administration’s definition of a drug versus a cosmetic became blurred. In 1984, Dr. Kligman suggested a new classification for the ingredients that fell in the middle, proposing the term “cosmeceutical” and thus, the concept of a cosmeceutical was introduced. To this day, cosmeceutical is not an official definition and the FDA has yet to deal with it as a quasi-drug category. FDA regulations as to what constitutes a drug versus a cosmetic date back to the 1938 Food, Drug and Cosmetic Act.

Once marketing focused on efficacy, many companies made outrageous claims. During the second half of the 1980s, the FDA issued some warning letters to some companies in an effort to control these claims.

Now efficacy claims abound and we, as dermatologists, should be the experts who back up these claims with scientific data. As the cosmeceutical market has evolved and grown, consumers are bewildered by the myriad of active ingredients being promoted and the number of products in the marketplace. As dermatologic innovation has led to more efficacious active ingredients, our patients look to us as knowledgeable and credible sources of information and for recommendations about the best skin care routines for their skin issues. This is all reflected in the fact that physician-dispensed skin care is becoming the fastest growing segment in this market. It is incumbent upon dermatologists to be knowledgeable and conversant about skin care products and skin care routines, and is particularly true for those of us who sell skin care products in our offices.

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann has written two textbooks and a New York Times Best Sellers book for consumers. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Burt’s Bees, Evolus, Galderma, and Revance. She is the CEO of Skin Type Solutions, a company that independently tests skin care products and makes recommendations to physicians on which skin care technologies are best. Write to her at dermnews@mdedge.com.

References

1. Vogue Magazine, 1967 Aug 15. “Can Great Skin be Created?”

2. https://patents.google.com/patent/US3910284.

3. Kligman AM et al. J Am Acad Dermatol. 1986 Oct;15(4 Pt 2):836-59.

4. Weiss JS et al. JAMA. 1988 Jan 22-29;259(4):527-32.

5. Goldfarb MT et al. J Am Acad Dermatol. 1989 Sep;21(3 Pt 2):645-50.

6. Ellis CN et al. J Am Acad Dermatol. 1990 Oct;23(4 Pt 1):629-37.

7. Kang S; Voorhees JJ. J Am Acad Dermatol. 1998 Aug;39(2 Pt 3):S55-61.

8. Kafi R et al. Arch Dermatol. 2007 May;143(5):606-12.

9. Gilchrest BA. J Am Acad Dermatol. 1989 Sep;21(3 Pt 2):610-3.

10. Bhawan J et al. Arch Dermatol. 1991 May;127(5):666-72.

11. Griffin TD et al. J Am Acad Dermatol. 1996 Feb;34(2 Pt 1):196-203.

12. Ditre CM et al. J Am Acad Dermatol. 1996 Feb;34(2 Pt 1):187-95.
 

Although medical education is constantly evolving, unique and rapid developments in recent years have sparked controversy. The next generation of physicians is learning much differently from how established doctors once did. Training has shifted from an acute focus on disease to a wider approach that considers patients within the larger context of their community and society. Although many, like myself, see this as progress, others have expressed doubts about this and many other changes.

Amid the madness that is the year 2020, I’m grateful to have a moment to reflect on this subject. Five years ago, in celebration of Medscape’s 20th anniversary, I spoke with various leaders in medical education to learn how med ed had evolved since they were in school. Since then, I’ve gone from student to faculty. This year, for Medscape’s 25th anniversary, I reached out to current medical trainees to reflect on how much things have changed in such a short time.

From adjustments forced on us by COVID-19 to trends that predated the pandemic – including an increased emphasis on social justice and a decreased emphasis on other material – becoming a doctor no longer looks like it did just a half-decade ago.
 

Social justice is now in the curricula

More than ever, medical training has shifted toward humanism, population health, and social justice. Students are now being shown not only how to treat the patient in front of them but how to “treat” the larger communities they serve. Research skills around social drivers of health, such as structural racism, are increasingly becoming status quo.

In reflecting on her current experience, Emily Kahoud, a third-year medical student at New Jersey Medical School, Newark, told me about a course she took that was devoted to health equity. She applauded how her professors have incorporated this education into their courses. “It’s so nice and refreshing to be in a community that appreciates that.”

I, too, have seen this change firsthand. In addition to caring for patients and teaching at the University of North Carolina at Chapel Hill, I work with a team that develops curricula around social justice. We strive to integrate this material into existing courses and rotations. I believe that this is not only the right thing to teach trainees in order to help their future patients, but that it also reduces harm that many students experience. The “hidden curriculum” of medical school has long marginalized anyone who isn’t White and/or male.

Children, women, and the elderly were often referred to as “special populations” during my training. Even now, content about social and structural drivers of health is still most often relegated to separate courses rather than integrated into existing material. I hope to help improve this at my institution and that others are doing the same elsewhere.

If the current students I spoke with are any indication, further integration will be a welcomed change. Travis Benson, a third-year medical student at Harvard Medical School, Boston, appreciates where medical training is headed. Specifically, he is interested in inequities in the care of transgender patients. He says he has loved what his school has done with education on issues not previously considered part of med ed. “In the first week of school, we go on tours and spend time in community health centers and learn about the ‘Family Van,’ a mobile health care clinic that offers free care. I even had an opportunity to have a longitudinal clinic experience at a jail.”

While some critics argue that this learning goes too far, others argue that it has not gone far enough fast enough. In general, I consider the progress made in this area since my time in med school to be a very good thing. Medical students are now being taught to think about the science of medicine in the context of the larger human condition.
 

More technology, less preclinical time and cost

Beyond evolution in curricular content, technical and logistical changes have dramatically reshaped med ed. Since I started my training in 2012, most medical schools now no longer formally require students to attend lectures. Instead, they make them available online for students to view on demand. This undoubtedly makes schedules more flexible, allows students to learn at their own pace, and helps accommodate students with different needs.

Another big change: Preclinical years may now be as short as 1.5 years or less. This is a big draw for some students. Most choose to go to medical school to take care of patients. Shortening the preclinical years means students have more time immersed in patient care and less time dealing with medical minutiae.

That also means that they can spend more time thinking about professional development. Ramie Fathy, a fourth-year student, told me, “I came to Penn [University of Pennsylvania in Philadelphia] because of the shortened preclinical curriculum. That allowed more time on the back end to explore different specialties.” Although some established doctors worry about what scientific details may be left out, providing more hands-on experience sure seems like a good thing to me. Learning from textbooks can only take you so far in this profession.

Another, and more expected, development is the use of ever-advancing technology. Some schools now offer 3D virtual modeling for the study of anatomy, as well as a myriad of electronic visual aids for subjects like pathology and microbiology. Adapting to technological changes can be challenging, however, especially because more nontraditional students are being admitted to medical school each year.

Kahoud is one such nontraditional – older – student. She had some concerns about reliance on newer resources going in. “It [medical school] has become increasingly dependent on technology, even before COVID,” she said. “When you are not well versed in these tools it can definitely be a struggle.”

Thanks to the pandemic, remote learning is now the name of the game for many. As a result, instructors have had to amend their teaching styles to suit distance education, various untested applications and programs have been integrated into the curriculum, and students and administrators alike have had to find alternative ways to build a sense of community.

Is this a glimpse at the future for med ed? And if so, what may be lost or gained from this transition? Tino Delamerced, a third-year student at the Brown University, Providence, R.I., shared a likely very widely held hope: “If the preclinical years can be totally remote permanently, then can tuition be cheaper?”

Med ed debt keeps growing and remains a huge deterrent for potential students, especially those who are the first in their family to pursue medicine, come from a disadvantaged background, or have other people for whom they are financially responsible. Is it possible that the restrictions of COVID-19 could finally lead to cost cutting?

A bigger solution – free medical school – predated the pandemic. Institutions such as New York University have completely eliminated tuition, whereas others such as the Icahn School of Medicine at Mount Sinai (my alma mater) have limited the amount of debt with which a student graduates. You can imagine my frustration that the debt limit policy was enacted after I graduated.

Still, as optimistic as some have been at this movement that developed in the past 5 years, many think this specific evolution is little more than a “pipe dream.”
 

Current students score big with USMLE change

Beyond med school cost, another universally despised part of medical training that has seen a dramatic change is the licensing examination. My dedicated study period for the United States Medical Licensing Examination (USMLE) Step 1 was my worst time of medical school. Well, it was second to holding a retractor in the operating room for hours at a time.

Like everyone, I suspected that Step 1 would not be an accurate indicator of my ability to actually care for patients. As a practicing physician, I can now tell you for sure that this is the case. How lucky for the next generation, then, that the test is going to a pass/fail grading system.

Step 1 has always been important, as residency programs rely on the score to weed out applicants. Even if that screening emphasis simply gets shifted to scores on other examinations, this change still feels like progress. As Fathy told me, “There will likely be more emphasis on USMLE Step 2. But I think, based on practice questions I’ve done, that is more relevant to clinical abilities.” From my new vantage point, I can confirm that.

Not everyone is excited, though. Delamerced told me that he fears that the pass/fail Step 1 score may disparately affect students outside of allopathic medical schools. He said that the new scoring system “does not allow students to distinguish themselves via a standardized test score. That may hurt IMGs or DO students.”

Even then, Delamerced conceded that the change has some clear benefits. “For med students’ mental health, it’s probably a good thing.” From a population-based perspective, a medical student’s mental health often declines throughout school. Standardized exams are not the only cause, but we all know that it is a big contributor. The Step 1 switch can only help with that.
 

Finish faster or learn more?

In addition to evolution in the content and methods used to teach and assess current med students, the duration of med ed has also changed. Today’s students can choose to complete medical school in less than 4 years.

At the school where I work, the Fully Integrated Readiness for Service Training (FIRST) program allows certain students to complete their education in just 3 years. This program is for students who already know early on that they want to pursue a specialty included on our curated list. The goal of the program is to ultimately train physicians in family medicine, psychiatry, pediatrics, or general surgery in order to provide crucial care to those who need it most in our state.

Other medical schools offer accelerated MD programs for students based on various admissions criteria and specialty interest. The benefit of these programs is that shortening training time cuts down on debt for students.

Accelerated MD programs also aim to quickly increase the number of practicing physicians. This is especially important for primary care, which expects to see a growing gap in the years to come. That aim has come under some criticism, as some believe that the 4-year program was the standard for a reason. But when I reflect on it, I often wonder whether my fourth year was really worth $60,000. I spent a lot of that year traveling for residency interviews and watching Netflix between clinic electives.

Instead of finishing medical school faster, some students now have an opportunity to integrate additional training and education. Benson told me that, at Harvard, many students take a year off to pursue other opportunities. He said, “About 40% of students end up taking a fifth year to do either a master’s degree, global health, or research.” Benson said the additional learning opportunities are broad. “Some classmates even go to other schools altogether to get additional education.” Widened areas of learning are likely to produce better doctors, in my opinion.

This chance to look back on medical education has shown me that the ways in which it has changed rapidly in just the past few years are largely positive. Although COVID-19 has been an unwanted bane, it has also forced schools to integrate new technology and has placed an even brighter spotlight on health inequities and other areas in which education further improved. I hope that, when I look back on med ed in another 5 years, it has grown even more flexible and nimble in meeting the ever-changing needs of students and patients alike.

Alexa Mieses Malchuk, MD, MPH, was born and raised in Queens, New York. Social justice is what drew her to family medicine. As an academic physician at the University of North Carolina, she practices inpatient and outpatient medicine and serves as a medical educator for students and residents.
 

This article first appeared on Medscape.com.

Although medical education is constantly evolving, unique and rapid developments in recent years have sparked controversy. The next generation of physicians is learning much differently from how established doctors once did. Training has shifted from an acute focus on disease to a wider approach that considers patients within the larger context of their community and society. Although many, like myself, see this as progress, others have expressed doubts about this and many other changes.

Amid the madness that is the year 2020, I’m grateful to have a moment to reflect on this subject. Five years ago, in celebration of Medscape’s 20th anniversary, I spoke with various leaders in medical education to learn how med ed had evolved since they were in school. Since then, I’ve gone from student to faculty. This year, for Medscape’s 25th anniversary, I reached out to current medical trainees to reflect on how much things have changed in such a short time.

From adjustments forced on us by COVID-19 to trends that predated the pandemic – including an increased emphasis on social justice and a decreased emphasis on other material – becoming a doctor no longer looks like it did just a half-decade ago.
 

Social justice is now in the curricula

More than ever, medical training has shifted toward humanism, population health, and social justice. Students are now being shown not only how to treat the patient in front of them but how to “treat” the larger communities they serve. Research skills around social drivers of health, such as structural racism, are increasingly becoming status quo.

In reflecting on her current experience, Emily Kahoud, a third-year medical student at New Jersey Medical School, Newark, told me about a course she took that was devoted to health equity. She applauded how her professors have incorporated this education into their courses. “It’s so nice and refreshing to be in a community that appreciates that.”

I, too, have seen this change firsthand. In addition to caring for patients and teaching at the University of North Carolina at Chapel Hill, I work with a team that develops curricula around social justice. We strive to integrate this material into existing courses and rotations. I believe that this is not only the right thing to teach trainees in order to help their future patients, but that it also reduces harm that many students experience. The “hidden curriculum” of medical school has long marginalized anyone who isn’t White and/or male.

Children, women, and the elderly were often referred to as “special populations” during my training. Even now, content about social and structural drivers of health is still most often relegated to separate courses rather than integrated into existing material. I hope to help improve this at my institution and that others are doing the same elsewhere.

If the current students I spoke with are any indication, further integration will be a welcomed change. Travis Benson, a third-year medical student at Harvard Medical School, Boston, appreciates where medical training is headed. Specifically, he is interested in inequities in the care of transgender patients. He says he has loved what his school has done with education on issues not previously considered part of med ed. “In the first week of school, we go on tours and spend time in community health centers and learn about the ‘Family Van,’ a mobile health care clinic that offers free care. I even had an opportunity to have a longitudinal clinic experience at a jail.”

While some critics argue that this learning goes too far, others argue that it has not gone far enough fast enough. In general, I consider the progress made in this area since my time in med school to be a very good thing. Medical students are now being taught to think about the science of medicine in the context of the larger human condition.
 

More technology, less preclinical time and cost

Beyond evolution in curricular content, technical and logistical changes have dramatically reshaped med ed. Since I started my training in 2012, most medical schools now no longer formally require students to attend lectures. Instead, they make them available online for students to view on demand. This undoubtedly makes schedules more flexible, allows students to learn at their own pace, and helps accommodate students with different needs.

Another big change: Preclinical years may now be as short as 1.5 years or less. This is a big draw for some students. Most choose to go to medical school to take care of patients. Shortening the preclinical years means students have more time immersed in patient care and less time dealing with medical minutiae.

That also means that they can spend more time thinking about professional development. Ramie Fathy, a fourth-year student, told me, “I came to Penn [University of Pennsylvania in Philadelphia] because of the shortened preclinical curriculum. That allowed more time on the back end to explore different specialties.” Although some established doctors worry about what scientific details may be left out, providing more hands-on experience sure seems like a good thing to me. Learning from textbooks can only take you so far in this profession.

Another, and more expected, development is the use of ever-advancing technology. Some schools now offer 3D virtual modeling for the study of anatomy, as well as a myriad of electronic visual aids for subjects like pathology and microbiology. Adapting to technological changes can be challenging, however, especially because more nontraditional students are being admitted to medical school each year.

Kahoud is one such nontraditional – older – student. She had some concerns about reliance on newer resources going in. “It [medical school] has become increasingly dependent on technology, even before COVID,” she said. “When you are not well versed in these tools it can definitely be a struggle.”

Thanks to the pandemic, remote learning is now the name of the game for many. As a result, instructors have had to amend their teaching styles to suit distance education, various untested applications and programs have been integrated into the curriculum, and students and administrators alike have had to find alternative ways to build a sense of community.

Is this a glimpse at the future for med ed? And if so, what may be lost or gained from this transition? Tino Delamerced, a third-year student at the Brown University, Providence, R.I., shared a likely very widely held hope: “If the preclinical years can be totally remote permanently, then can tuition be cheaper?”

Med ed debt keeps growing and remains a huge deterrent for potential students, especially those who are the first in their family to pursue medicine, come from a disadvantaged background, or have other people for whom they are financially responsible. Is it possible that the restrictions of COVID-19 could finally lead to cost cutting?

A bigger solution – free medical school – predated the pandemic. Institutions such as New York University have completely eliminated tuition, whereas others such as the Icahn School of Medicine at Mount Sinai (my alma mater) have limited the amount of debt with which a student graduates. You can imagine my frustration that the debt limit policy was enacted after I graduated.

Still, as optimistic as some have been at this movement that developed in the past 5 years, many think this specific evolution is little more than a “pipe dream.”
 

Current students score big with USMLE change

Beyond med school cost, another universally despised part of medical training that has seen a dramatic change is the licensing examination. My dedicated study period for the United States Medical Licensing Examination (USMLE) Step 1 was my worst time of medical school. Well, it was second to holding a retractor in the operating room for hours at a time.

Like everyone, I suspected that Step 1 would not be an accurate indicator of my ability to actually care for patients. As a practicing physician, I can now tell you for sure that this is the case. How lucky for the next generation, then, that the test is going to a pass/fail grading system.

Step 1 has always been important, as residency programs rely on the score to weed out applicants. Even if that screening emphasis simply gets shifted to scores on other examinations, this change still feels like progress. As Fathy told me, “There will likely be more emphasis on USMLE Step 2. But I think, based on practice questions I’ve done, that is more relevant to clinical abilities.” From my new vantage point, I can confirm that.

Not everyone is excited, though. Delamerced told me that he fears that the pass/fail Step 1 score may disparately affect students outside of allopathic medical schools. He said that the new scoring system “does not allow students to distinguish themselves via a standardized test score. That may hurt IMGs or DO students.”

Even then, Delamerced conceded that the change has some clear benefits. “For med students’ mental health, it’s probably a good thing.” From a population-based perspective, a medical student’s mental health often declines throughout school. Standardized exams are not the only cause, but we all know that it is a big contributor. The Step 1 switch can only help with that.
 

Finish faster or learn more?

In addition to evolution in the content and methods used to teach and assess current med students, the duration of med ed has also changed. Today’s students can choose to complete medical school in less than 4 years.

At the school where I work, the Fully Integrated Readiness for Service Training (FIRST) program allows certain students to complete their education in just 3 years. This program is for students who already know early on that they want to pursue a specialty included on our curated list. The goal of the program is to ultimately train physicians in family medicine, psychiatry, pediatrics, or general surgery in order to provide crucial care to those who need it most in our state.

Other medical schools offer accelerated MD programs for students based on various admissions criteria and specialty interest. The benefit of these programs is that shortening training time cuts down on debt for students.

Accelerated MD programs also aim to quickly increase the number of practicing physicians. This is especially important for primary care, which expects to see a growing gap in the years to come. That aim has come under some criticism, as some believe that the 4-year program was the standard for a reason. But when I reflect on it, I often wonder whether my fourth year was really worth $60,000. I spent a lot of that year traveling for residency interviews and watching Netflix between clinic electives.

Instead of finishing medical school faster, some students now have an opportunity to integrate additional training and education. Benson told me that, at Harvard, many students take a year off to pursue other opportunities. He said, “About 40% of students end up taking a fifth year to do either a master’s degree, global health, or research.” Benson said the additional learning opportunities are broad. “Some classmates even go to other schools altogether to get additional education.” Widened areas of learning are likely to produce better doctors, in my opinion.

This chance to look back on medical education has shown me that the ways in which it has changed rapidly in just the past few years are largely positive. Although COVID-19 has been an unwanted bane, it has also forced schools to integrate new technology and has placed an even brighter spotlight on health inequities and other areas in which education further improved. I hope that, when I look back on med ed in another 5 years, it has grown even more flexible and nimble in meeting the ever-changing needs of students and patients alike.

Alexa Mieses Malchuk, MD, MPH, was born and raised in Queens, New York. Social justice is what drew her to family medicine. As an academic physician at the University of North Carolina, she practices inpatient and outpatient medicine and serves as a medical educator for students and residents.
 

This article first appeared on Medscape.com.

Although medical education is constantly evolving, unique and rapid developments in recent years have sparked controversy. The next generation of physicians is learning much differently from how established doctors once did. Training has shifted from an acute focus on disease to a wider approach that considers patients within the larger context of their community and society. Although many, like myself, see this as progress, others have expressed doubts about this and many other changes.

Amid the madness that is the year 2020, I’m grateful to have a moment to reflect on this subject. Five years ago, in celebration of Medscape’s 20th anniversary, I spoke with various leaders in medical education to learn how med ed had evolved since they were in school. Since then, I’ve gone from student to faculty. This year, for Medscape’s 25th anniversary, I reached out to current medical trainees to reflect on how much things have changed in such a short time.

From adjustments forced on us by COVID-19 to trends that predated the pandemic – including an increased emphasis on social justice and a decreased emphasis on other material – becoming a doctor no longer looks like it did just a half-decade ago.
 

Social justice is now in the curricula

More than ever, medical training has shifted toward humanism, population health, and social justice. Students are now being shown not only how to treat the patient in front of them but how to “treat” the larger communities they serve. Research skills around social drivers of health, such as structural racism, are increasingly becoming status quo.

In reflecting on her current experience, Emily Kahoud, a third-year medical student at New Jersey Medical School, Newark, told me about a course she took that was devoted to health equity. She applauded how her professors have incorporated this education into their courses. “It’s so nice and refreshing to be in a community that appreciates that.”

I, too, have seen this change firsthand. In addition to caring for patients and teaching at the University of North Carolina at Chapel Hill, I work with a team that develops curricula around social justice. We strive to integrate this material into existing courses and rotations. I believe that this is not only the right thing to teach trainees in order to help their future patients, but that it also reduces harm that many students experience. The “hidden curriculum” of medical school has long marginalized anyone who isn’t White and/or male.

Children, women, and the elderly were often referred to as “special populations” during my training. Even now, content about social and structural drivers of health is still most often relegated to separate courses rather than integrated into existing material. I hope to help improve this at my institution and that others are doing the same elsewhere.

If the current students I spoke with are any indication, further integration will be a welcomed change. Travis Benson, a third-year medical student at Harvard Medical School, Boston, appreciates where medical training is headed. Specifically, he is interested in inequities in the care of transgender patients. He says he has loved what his school has done with education on issues not previously considered part of med ed. “In the first week of school, we go on tours and spend time in community health centers and learn about the ‘Family Van,’ a mobile health care clinic that offers free care. I even had an opportunity to have a longitudinal clinic experience at a jail.”

While some critics argue that this learning goes too far, others argue that it has not gone far enough fast enough. In general, I consider the progress made in this area since my time in med school to be a very good thing. Medical students are now being taught to think about the science of medicine in the context of the larger human condition.
 

More technology, less preclinical time and cost

Beyond evolution in curricular content, technical and logistical changes have dramatically reshaped med ed. Since I started my training in 2012, most medical schools now no longer formally require students to attend lectures. Instead, they make them available online for students to view on demand. This undoubtedly makes schedules more flexible, allows students to learn at their own pace, and helps accommodate students with different needs.

Another big change: Preclinical years may now be as short as 1.5 years or less. This is a big draw for some students. Most choose to go to medical school to take care of patients. Shortening the preclinical years means students have more time immersed in patient care and less time dealing with medical minutiae.

That also means that they can spend more time thinking about professional development. Ramie Fathy, a fourth-year student, told me, “I came to Penn [University of Pennsylvania in Philadelphia] because of the shortened preclinical curriculum. That allowed more time on the back end to explore different specialties.” Although some established doctors worry about what scientific details may be left out, providing more hands-on experience sure seems like a good thing to me. Learning from textbooks can only take you so far in this profession.

Another, and more expected, development is the use of ever-advancing technology. Some schools now offer 3D virtual modeling for the study of anatomy, as well as a myriad of electronic visual aids for subjects like pathology and microbiology. Adapting to technological changes can be challenging, however, especially because more nontraditional students are being admitted to medical school each year.

Kahoud is one such nontraditional – older – student. She had some concerns about reliance on newer resources going in. “It [medical school] has become increasingly dependent on technology, even before COVID,” she said. “When you are not well versed in these tools it can definitely be a struggle.”

Thanks to the pandemic, remote learning is now the name of the game for many. As a result, instructors have had to amend their teaching styles to suit distance education, various untested applications and programs have been integrated into the curriculum, and students and administrators alike have had to find alternative ways to build a sense of community.

Is this a glimpse at the future for med ed? And if so, what may be lost or gained from this transition? Tino Delamerced, a third-year student at the Brown University, Providence, R.I., shared a likely very widely held hope: “If the preclinical years can be totally remote permanently, then can tuition be cheaper?”

Med ed debt keeps growing and remains a huge deterrent for potential students, especially those who are the first in their family to pursue medicine, come from a disadvantaged background, or have other people for whom they are financially responsible. Is it possible that the restrictions of COVID-19 could finally lead to cost cutting?

A bigger solution – free medical school – predated the pandemic. Institutions such as New York University have completely eliminated tuition, whereas others such as the Icahn School of Medicine at Mount Sinai (my alma mater) have limited the amount of debt with which a student graduates. You can imagine my frustration that the debt limit policy was enacted after I graduated.

Still, as optimistic as some have been at this movement that developed in the past 5 years, many think this specific evolution is little more than a “pipe dream.”
 

Current students score big with USMLE change

Beyond med school cost, another universally despised part of medical training that has seen a dramatic change is the licensing examination. My dedicated study period for the United States Medical Licensing Examination (USMLE) Step 1 was my worst time of medical school. Well, it was second to holding a retractor in the operating room for hours at a time.

Like everyone, I suspected that Step 1 would not be an accurate indicator of my ability to actually care for patients. As a practicing physician, I can now tell you for sure that this is the case. How lucky for the next generation, then, that the test is going to a pass/fail grading system.

Step 1 has always been important, as residency programs rely on the score to weed out applicants. Even if that screening emphasis simply gets shifted to scores on other examinations, this change still feels like progress. As Fathy told me, “There will likely be more emphasis on USMLE Step 2. But I think, based on practice questions I’ve done, that is more relevant to clinical abilities.” From my new vantage point, I can confirm that.

Not everyone is excited, though. Delamerced told me that he fears that the pass/fail Step 1 score may disparately affect students outside of allopathic medical schools. He said that the new scoring system “does not allow students to distinguish themselves via a standardized test score. That may hurt IMGs or DO students.”

Even then, Delamerced conceded that the change has some clear benefits. “For med students’ mental health, it’s probably a good thing.” From a population-based perspective, a medical student’s mental health often declines throughout school. Standardized exams are not the only cause, but we all know that it is a big contributor. The Step 1 switch can only help with that.
 

Finish faster or learn more?

In addition to evolution in the content and methods used to teach and assess current med students, the duration of med ed has also changed. Today’s students can choose to complete medical school in less than 4 years.

At the school where I work, the Fully Integrated Readiness for Service Training (FIRST) program allows certain students to complete their education in just 3 years. This program is for students who already know early on that they want to pursue a specialty included on our curated list. The goal of the program is to ultimately train physicians in family medicine, psychiatry, pediatrics, or general surgery in order to provide crucial care to those who need it most in our state.

Other medical schools offer accelerated MD programs for students based on various admissions criteria and specialty interest. The benefit of these programs is that shortening training time cuts down on debt for students.

Accelerated MD programs also aim to quickly increase the number of practicing physicians. This is especially important for primary care, which expects to see a growing gap in the years to come. That aim has come under some criticism, as some believe that the 4-year program was the standard for a reason. But when I reflect on it, I often wonder whether my fourth year was really worth $60,000. I spent a lot of that year traveling for residency interviews and watching Netflix between clinic electives.

Instead of finishing medical school faster, some students now have an opportunity to integrate additional training and education. Benson told me that, at Harvard, many students take a year off to pursue other opportunities. He said, “About 40% of students end up taking a fifth year to do either a master’s degree, global health, or research.” Benson said the additional learning opportunities are broad. “Some classmates even go to other schools altogether to get additional education.” Widened areas of learning are likely to produce better doctors, in my opinion.

This chance to look back on medical education has shown me that the ways in which it has changed rapidly in just the past few years are largely positive. Although COVID-19 has been an unwanted bane, it has also forced schools to integrate new technology and has placed an even brighter spotlight on health inequities and other areas in which education further improved. I hope that, when I look back on med ed in another 5 years, it has grown even more flexible and nimble in meeting the ever-changing needs of students and patients alike.

Alexa Mieses Malchuk, MD, MPH, was born and raised in Queens, New York. Social justice is what drew her to family medicine. As an academic physician at the University of North Carolina, she practices inpatient and outpatient medicine and serves as a medical educator for students and residents.
 

This article first appeared on Medscape.com.

The recent death of “Black Panther” star Chadwick Boseman has resulted in colorectal cancer (CRC) screening guidelines receiving more attention. Mr. Boseman was diagnosed with Stage 3 CRC in 2016 and underwent treatment. He passed away 4 years later at the young age of 44.

Mr. Boseman’s death has highlighted two important concerns about current screening guidelines for CRC. These include racial disparities in patients with colon cancer and the fact that more younger patients are getting this disease.

There are at least three different sets of CRC screening recommendations from different trusted professional organizations that primary care physicians must decide how to follow. These organizations each published their guidelines indicating review of the best available evidence. On first glance there is discrepancy between these guidelines, but a closer look at them reveals they have a lot of similarities.

The U.S. Multi-Society Task Force of Colorectal Cancer (MSTF), which represents the American College of Gastroenterology, the American Gatroenterological Association, and the American Society for Gastrointestinal Endoscopy, is one of the organizations that offers guidelines. The MSTF recommends CRC screening for non-African American average risked persons at the age of 50 years (strong recommendation; moderate quality evidence). The first-tier options for this recommendation are to have a colonoscopy every 10 years or annual fecal immunochemial test. Additionally, the MSTF recommends beginning screening of African Americans at age 45 years (weak recommendation; very-low-quality evidence). This recommendation cites higher incidence rates, earlier mean age at onset, higher proportion of cancers before age 50 years and late-stage presentation. The MSTF indicates that the increased rate of CRC at an earlier age in African Americans is caused by a combination of biologic and societal factors, but do not point to what those are. This earlier screening is not backed by evidence that it in fact improves morbidity or mortality outcomes. The MSTF also address screening among high-risk individuals. Those with first degree relatives with CRC or advanced adenomas diagnosed before the age of 60 years should be screened beginning at age 40 years or 10 years younger than the age the relative was diagnosed, whichever comes first, according to the MSTF recommendations. These individuals should have a colonoscopy every 5 years, the MSTF says. Those with first degree relatives with CRC or advanced adenomas diagnosed at older than 60 years should have CRC beginning at 40 years, though with the same testing intervals as average-risk individuals.¹

The American College of Physicians (ACP) and the American Academy of Family Physicians (AAFP), however, endorse the guidelines set forth by the United States Preventive Services Task Force (USPSTF). These guidelines were published in 2016 in the JAMA and notably are currently under review. These guidelines recommend routine screening for those at average risk at the age of 50 years. In the publication of these guidelines, the increasing incidence of CRC in those under 50 was acknowledged. It is however stated that the modest benefit of earlier diagnosis made via screening is not better than the increased risk of increased lifetime colonoscopy.²

The publication specifically addresses the disparity among Black adults who have the highest incidence and mortality rates in comparison with other racial/ethnic groups. These guidelines specifically state that there are higher rates of colon cancer among black adults. They however clarify that they think it is because of decreased screening and treatment in this group. When compared with other groups and the screening and treatment is controlled for, there is no longer a difference. Lowering the age for starting screening, therefore, won’t help resolve the disparity because the higher cases in Black adults has resulted from not enough Black adults being screened at the recommended age of 50, according to the USPSTF recommendation statement. As such, rather than changing the age of screening for Black adults, this publication recommends efforts to ensure that screening, follow-up, and treatment are received.

The USPSTF specifically did not include adults with known disorders that have a genetic predisposition to CRC or those with a first degree relative with CRC. They instead refer to other professional organizations for these recommendations.²

The American Cancer Society (ACS) also had a separate guideline published in CA: A Cancer Journal for Clinicians. It provides a qualified recommendation that CRC screening begin at age 45 years for those with average risk. The guideline also includes a strong recommendation for CRC screening beginning at age 50 years. The qualified recommendation for the younger age group is based on the incidence of colorectal cancer being similar between those aged 45-49 and those aged 50-54 years. The ACS also hypothesized that screening at an earlier age will decrease the disparity among population groups with a higher burden. Importantly, this updated guideline prioritized incidence reduction rather than mortality reduction. The ACS also stressed the need for a multipronged approach to mitigate barriers to CRC screening at the individual, provider, organizational, and policy levels. Similar to the USPSTF, the ACS did not address the screening of those with known disorders that have a genetic predisposition to CRC or those with a first degree relative with CRC.³

In all of the publications discussing CRC screening guidelines, it is stressed that there is not sufficient uptake of any of these recommendations. Rather than conduct earlier screening, in my opinion, we should focus on programmatic ways to ensure that the existing screening recommendations are followed. This is a space in which we can help affect the disparity seen among population groups.

The most important screening test is the one that patients are willing to use. Primary care physicians can use any of these guidelines to have conversations with patients about risk and when to start screening. Although these guidelines may seem to be different from each other, each one includes strong recommendations with the same information.

Additional studies should be done to determine the benefits and harms of screening in patients with known risk factors such as obesity, cigarette smoking, diabetes, high consumption of alcohol, high consumption of red meat and processed food, inactivity, and low intake of dietary fiber, fruits, and vegetables. It is possible that the higher burden of disease among Black adults is related to societal factors leading to increased obesity and dietary habits that increase rates of CRC.

Primary care physicians would be better served by a tool that allows for risk stratification to help guide early screening for all patients. For certain patients, such a tool might result in them qualifying for screening that begins at a later age than the current guidelines recommend. Finally, primary care physicians must remember that these are just the guidelines for screening for CRC. They all specifically exclude patients experiencing any symptoms. As such, patients with unexplained bleeding, anemia, weight loss, and other symptoms should be evaluated fully, including being considered for colonoscopy to diagnose CRC. Primary care physicians should use these guidelines to screen their asymptomatic patients and should ensure that they provide evaluation of any of the symptoms of CRC.
 

Dr. Wheat is a family physician at Erie Family Health Center in Chicago. She is also program director of Northwestern’s McGaw Family Medicine residency program at Humboldt Park, Chicago. Dr. Wheat serves on editorial advisory board of Family Practice News.

References

1. Rex DK et al. Gastrointest Endosc. 2017;86(1):18-33.

2. US Preventive Services Task Force. JAMA. 2016;315(23):2564-2575.

3. Wolf AMD et al. CA Cancer J Clin. 2018 Jul;68(4):250-281.

fpnews@mdedge.com

The recent death of “Black Panther” star Chadwick Boseman has resulted in colorectal cancer (CRC) screening guidelines receiving more attention. Mr. Boseman was diagnosed with Stage 3 CRC in 2016 and underwent treatment. He passed away 4 years later at the young age of 44.

Mr. Boseman’s death has highlighted two important concerns about current screening guidelines for CRC. These include racial disparities in patients with colon cancer and the fact that more younger patients are getting this disease.

There are at least three different sets of CRC screening recommendations from different trusted professional organizations that primary care physicians must decide how to follow. These organizations each published their guidelines indicating review of the best available evidence. On first glance there is discrepancy between these guidelines, but a closer look at them reveals they have a lot of similarities.

The U.S. Multi-Society Task Force of Colorectal Cancer (MSTF), which represents the American College of Gastroenterology, the American Gatroenterological Association, and the American Society for Gastrointestinal Endoscopy, is one of the organizations that offers guidelines. The MSTF recommends CRC screening for non-African American average risked persons at the age of 50 years (strong recommendation; moderate quality evidence). The first-tier options for this recommendation are to have a colonoscopy every 10 years or annual fecal immunochemial test. Additionally, the MSTF recommends beginning screening of African Americans at age 45 years (weak recommendation; very-low-quality evidence). This recommendation cites higher incidence rates, earlier mean age at onset, higher proportion of cancers before age 50 years and late-stage presentation. The MSTF indicates that the increased rate of CRC at an earlier age in African Americans is caused by a combination of biologic and societal factors, but do not point to what those are. This earlier screening is not backed by evidence that it in fact improves morbidity or mortality outcomes. The MSTF also address screening among high-risk individuals. Those with first degree relatives with CRC or advanced adenomas diagnosed before the age of 60 years should be screened beginning at age 40 years or 10 years younger than the age the relative was diagnosed, whichever comes first, according to the MSTF recommendations. These individuals should have a colonoscopy every 5 years, the MSTF says. Those with first degree relatives with CRC or advanced adenomas diagnosed at older than 60 years should have CRC beginning at 40 years, though with the same testing intervals as average-risk individuals.¹

The American College of Physicians (ACP) and the American Academy of Family Physicians (AAFP), however, endorse the guidelines set forth by the United States Preventive Services Task Force (USPSTF). These guidelines were published in 2016 in the JAMA and notably are currently under review. These guidelines recommend routine screening for those at average risk at the age of 50 years. In the publication of these guidelines, the increasing incidence of CRC in those under 50 was acknowledged. It is however stated that the modest benefit of earlier diagnosis made via screening is not better than the increased risk of increased lifetime colonoscopy.²

The publication specifically addresses the disparity among Black adults who have the highest incidence and mortality rates in comparison with other racial/ethnic groups. These guidelines specifically state that there are higher rates of colon cancer among black adults. They however clarify that they think it is because of decreased screening and treatment in this group. When compared with other groups and the screening and treatment is controlled for, there is no longer a difference. Lowering the age for starting screening, therefore, won’t help resolve the disparity because the higher cases in Black adults has resulted from not enough Black adults being screened at the recommended age of 50, according to the USPSTF recommendation statement. As such, rather than changing the age of screening for Black adults, this publication recommends efforts to ensure that screening, follow-up, and treatment are received.

The USPSTF specifically did not include adults with known disorders that have a genetic predisposition to CRC or those with a first degree relative with CRC. They instead refer to other professional organizations for these recommendations.²

The American Cancer Society (ACS) also had a separate guideline published in CA: A Cancer Journal for Clinicians. It provides a qualified recommendation that CRC screening begin at age 45 years for those with average risk. The guideline also includes a strong recommendation for CRC screening beginning at age 50 years. The qualified recommendation for the younger age group is based on the incidence of colorectal cancer being similar between those aged 45-49 and those aged 50-54 years. The ACS also hypothesized that screening at an earlier age will decrease the disparity among population groups with a higher burden. Importantly, this updated guideline prioritized incidence reduction rather than mortality reduction. The ACS also stressed the need for a multipronged approach to mitigate barriers to CRC screening at the individual, provider, organizational, and policy levels. Similar to the USPSTF, the ACS did not address the screening of those with known disorders that have a genetic predisposition to CRC or those with a first degree relative with CRC.³

In all of the publications discussing CRC screening guidelines, it is stressed that there is not sufficient uptake of any of these recommendations. Rather than conduct earlier screening, in my opinion, we should focus on programmatic ways to ensure that the existing screening recommendations are followed. This is a space in which we can help affect the disparity seen among population groups.

The most important screening test is the one that patients are willing to use. Primary care physicians can use any of these guidelines to have conversations with patients about risk and when to start screening. Although these guidelines may seem to be different from each other, each one includes strong recommendations with the same information.

Additional studies should be done to determine the benefits and harms of screening in patients with known risk factors such as obesity, cigarette smoking, diabetes, high consumption of alcohol, high consumption of red meat and processed food, inactivity, and low intake of dietary fiber, fruits, and vegetables. It is possible that the higher burden of disease among Black adults is related to societal factors leading to increased obesity and dietary habits that increase rates of CRC.

Primary care physicians would be better served by a tool that allows for risk stratification to help guide early screening for all patients. For certain patients, such a tool might result in them qualifying for screening that begins at a later age than the current guidelines recommend. Finally, primary care physicians must remember that these are just the guidelines for screening for CRC. They all specifically exclude patients experiencing any symptoms. As such, patients with unexplained bleeding, anemia, weight loss, and other symptoms should be evaluated fully, including being considered for colonoscopy to diagnose CRC. Primary care physicians should use these guidelines to screen their asymptomatic patients and should ensure that they provide evaluation of any of the symptoms of CRC.
 

Dr. Wheat is a family physician at Erie Family Health Center in Chicago. She is also program director of Northwestern’s McGaw Family Medicine residency program at Humboldt Park, Chicago. Dr. Wheat serves on editorial advisory board of Family Practice News.

References

1. Rex DK et al. Gastrointest Endosc. 2017;86(1):18-33.

2. US Preventive Services Task Force. JAMA. 2016;315(23):2564-2575.

3. Wolf AMD et al. CA Cancer J Clin. 2018 Jul;68(4):250-281.

fpnews@mdedge.com

The recent death of “Black Panther” star Chadwick Boseman has resulted in colorectal cancer (CRC) screening guidelines receiving more attention. Mr. Boseman was diagnosed with Stage 3 CRC in 2016 and underwent treatment. He passed away 4 years later at the young age of 44.

Mr. Boseman’s death has highlighted two important concerns about current screening guidelines for CRC. These include racial disparities in patients with colon cancer and the fact that more younger patients are getting this disease.

There are at least three different sets of CRC screening recommendations from different trusted professional organizations that primary care physicians must decide how to follow. These organizations each published their guidelines indicating review of the best available evidence. On first glance there is discrepancy between these guidelines, but a closer look at them reveals they have a lot of similarities.

The U.S. Multi-Society Task Force of Colorectal Cancer (MSTF), which represents the American College of Gastroenterology, the American Gatroenterological Association, and the American Society for Gastrointestinal Endoscopy, is one of the organizations that offers guidelines. The MSTF recommends CRC screening for non-African American average risked persons at the age of 50 years (strong recommendation; moderate quality evidence). The first-tier options for this recommendation are to have a colonoscopy every 10 years or annual fecal immunochemial test. Additionally, the MSTF recommends beginning screening of African Americans at age 45 years (weak recommendation; very-low-quality evidence). This recommendation cites higher incidence rates, earlier mean age at onset, higher proportion of cancers before age 50 years and late-stage presentation. The MSTF indicates that the increased rate of CRC at an earlier age in African Americans is caused by a combination of biologic and societal factors, but do not point to what those are. This earlier screening is not backed by evidence that it in fact improves morbidity or mortality outcomes. The MSTF also address screening among high-risk individuals. Those with first degree relatives with CRC or advanced adenomas diagnosed before the age of 60 years should be screened beginning at age 40 years or 10 years younger than the age the relative was diagnosed, whichever comes first, according to the MSTF recommendations. These individuals should have a colonoscopy every 5 years, the MSTF says. Those with first degree relatives with CRC or advanced adenomas diagnosed at older than 60 years should have CRC beginning at 40 years, though with the same testing intervals as average-risk individuals.¹

The American College of Physicians (ACP) and the American Academy of Family Physicians (AAFP), however, endorse the guidelines set forth by the United States Preventive Services Task Force (USPSTF). These guidelines were published in 2016 in the JAMA and notably are currently under review. These guidelines recommend routine screening for those at average risk at the age of 50 years. In the publication of these guidelines, the increasing incidence of CRC in those under 50 was acknowledged. It is however stated that the modest benefit of earlier diagnosis made via screening is not better than the increased risk of increased lifetime colonoscopy.²

The publication specifically addresses the disparity among Black adults who have the highest incidence and mortality rates in comparison with other racial/ethnic groups. These guidelines specifically state that there are higher rates of colon cancer among black adults. They however clarify that they think it is because of decreased screening and treatment in this group. When compared with other groups and the screening and treatment is controlled for, there is no longer a difference. Lowering the age for starting screening, therefore, won’t help resolve the disparity because the higher cases in Black adults has resulted from not enough Black adults being screened at the recommended age of 50, according to the USPSTF recommendation statement. As such, rather than changing the age of screening for Black adults, this publication recommends efforts to ensure that screening, follow-up, and treatment are received.

The USPSTF specifically did not include adults with known disorders that have a genetic predisposition to CRC or those with a first degree relative with CRC. They instead refer to other professional organizations for these recommendations.²

The American Cancer Society (ACS) also had a separate guideline published in CA: A Cancer Journal for Clinicians. It provides a qualified recommendation that CRC screening begin at age 45 years for those with average risk. The guideline also includes a strong recommendation for CRC screening beginning at age 50 years. The qualified recommendation for the younger age group is based on the incidence of colorectal cancer being similar between those aged 45-49 and those aged 50-54 years. The ACS also hypothesized that screening at an earlier age will decrease the disparity among population groups with a higher burden. Importantly, this updated guideline prioritized incidence reduction rather than mortality reduction. The ACS also stressed the need for a multipronged approach to mitigate barriers to CRC screening at the individual, provider, organizational, and policy levels. Similar to the USPSTF, the ACS did not address the screening of those with known disorders that have a genetic predisposition to CRC or those with a first degree relative with CRC.³

In all of the publications discussing CRC screening guidelines, it is stressed that there is not sufficient uptake of any of these recommendations. Rather than conduct earlier screening, in my opinion, we should focus on programmatic ways to ensure that the existing screening recommendations are followed. This is a space in which we can help affect the disparity seen among population groups.

The most important screening test is the one that patients are willing to use. Primary care physicians can use any of these guidelines to have conversations with patients about risk and when to start screening. Although these guidelines may seem to be different from each other, each one includes strong recommendations with the same information.

Additional studies should be done to determine the benefits and harms of screening in patients with known risk factors such as obesity, cigarette smoking, diabetes, high consumption of alcohol, high consumption of red meat and processed food, inactivity, and low intake of dietary fiber, fruits, and vegetables. It is possible that the higher burden of disease among Black adults is related to societal factors leading to increased obesity and dietary habits that increase rates of CRC.

Primary care physicians would be better served by a tool that allows for risk stratification to help guide early screening for all patients. For certain patients, such a tool might result in them qualifying for screening that begins at a later age than the current guidelines recommend. Finally, primary care physicians must remember that these are just the guidelines for screening for CRC. They all specifically exclude patients experiencing any symptoms. As such, patients with unexplained bleeding, anemia, weight loss, and other symptoms should be evaluated fully, including being considered for colonoscopy to diagnose CRC. Primary care physicians should use these guidelines to screen their asymptomatic patients and should ensure that they provide evaluation of any of the symptoms of CRC.
 

Dr. Wheat is a family physician at Erie Family Health Center in Chicago. She is also program director of Northwestern’s McGaw Family Medicine residency program at Humboldt Park, Chicago. Dr. Wheat serves on editorial advisory board of Family Practice News.

References

1. Rex DK et al. Gastrointest Endosc. 2017;86(1):18-33.

2. US Preventive Services Task Force. JAMA. 2016;315(23):2564-2575.

3. Wolf AMD et al. CA Cancer J Clin. 2018 Jul;68(4):250-281.

fpnews@mdedge.com

Among the many tolls inflicted on health care workers by COVID-19 is one that is not as easily measured as rates of death or disease, but is no less tangible: moral injury. This is the term by which we describe the psychological, social, and spiritual impact of high-stakes situations that lead to the betrayal or transgression of our own deeply held moral beliefs and values.

The current pandemic has provided innumerable such situations that can increase the risk for moral injury, whether we deal directly with patients infected by the coronavirus or not. Telling family members they cannot visit critically ill loved ones. Delaying code activities, even momentarily, to get fully protected with personal protective equipment. Seeing patients who have delayed their necessary or preventive care. Using video rather than touch to reassure people.

Knowing that we are following guidelines from the Centers for Disease Control and Prevention does not stop our feelings of guilt. The longer this pandemic goes on, the more likely it is that these situations will begin to take a toll on us.

For most of us, being exposed to moral injuries is new; they have historically been most associated with severe traumatic wartime experiences. Soldiers, philosophers, and writers have described the ethical dilemmas inherent in war for as long as recorded history. But the use of this term is a more recent development, which the Moral Injury Project at Syracuse (N.Y.) University describes as probably originating in the Vietnam War–era writings of veteran and peace activist Camillo “Mac” Bica and psychiatrist Jonathan Shay. Examples of wartime events that have been thought to lead to moral injury include: causing the harm or death of civilians, knowingly but without alternatives, or accidentally; failing to provide medical aid to an injured civilian or service member; and following orders that were illegal, immoral, and/or against the rules of engagement or the Geneva Conventions.

However, the occurrence of moral injuries in modern health care is increasingly being reported, primarily as an adverse effect of health care inefficiencies that can contribute to burnout. COVID-19 has now provided an array of additional stressors that can cause moral injuries among health care workers. A recent guidance document on moral injury published by the American Psychiatric Association noted that, in the context of a public health disaster, such as COVID-19, it is sometimes necessary to transition from ordinary standards of care to those more appropriate in a crisis, as in wartime. This forces us all to confront challenging questions for which there may be no clear answers, and to make “lose-lose” choices in which no one involved – patients, family, or clinicians – ends up feeling satisfied or even comfortable.

Moral injuries affect most of us as physicians, as well as our colleagues and families, during this unusual, painful, traumatic, and potentially lethal time. Our lives have been altered significantly, and for many, completely turned upside down by enormous sacrifices and tragic losses. Globally, physicians account for over half of healthcare worker deaths. In the United States alone, over 900 health care workers have died of COVID-19.

Most of us have felt the symptoms of moral injury: frustration, anger, disgust, guilt. A recent report describes three levels of stressors in health care occurring during the pandemic, which are not dissimilar to those wartime events described previously.

• Severe moral stressors, such as the denial of treatment to a COVID-19 patient owing to lack of resources, the inability to provide optimal care to non–COVID-19 patients for many reasons, and concern about passing COVID to loved ones.
• Moderate moral stressors, such as preventing visitors, especially to dying patients, triaging patients for healthcare services with inadequate information, and trying to solve the tension between the need for self-preservation and the need to treat.
• Lower-level but common moral challenges, especially in the community – for example, seeing others not protecting the community by hoarding food, gathering for large parties, and not social distancing or wearing masks. Such stressors lead to frustration and contempt, especially from healthcare workers making personal sacrifices and who may be at risk for infection caused by these behaviors.

Every one of us is affected by these stressors. I certainly am.

What are the outcomes? We know that moral injuries are a risk factor for the development of mental health problems and burnout, and not surprisingly we are seeing that mental health problems, suicidality, and substance use disorders have increased markedly during COVID-19, as recently detailed by the CDC.

• Acknowledge that you, like me, are affected by these stressors. This is not a secret, and you should not be ashamed of your feelings.
• Talk with your colleagues, loved ones, and friends about how you and they are affected. You are not alone. Encourage others to share their thoughts, stories, and feelings.
• Put this topic on your meeting and departmental agendas and discuss these moral issues openly with your colleagues. Allow sufficient time to engage in open dialogue.
• Work out ways of assisting those who are in high-risk situations, especially for moderate to severe injuries. Be supportive toward those affected.
• Modify policies and change rosters and rotate staff between high- and low-stress roles. Protect and support at-risk colleagues.
• Think about difficult ethical decisions in advance so they can be made by groups, not individuals, and certainly not “on the fly.”
• Keep everyone in your workplace constantly informed, especially of impending staff or equipment shortages.
• Maintain your inherent self-care and resilience with rest, good nutrition, sleep, exercise, love, caring, socialization, and work-life balance.
• Be prepared to access the many professional support services available in our community if you are intensely distressed or if the above suggestions are not enough.

Remember, we are in this together and will find strength in each other. This too will pass.

This article first appeared on Medscape.com.

Among the many tolls inflicted on health care workers by COVID-19 is one that is not as easily measured as rates of death or disease, but is no less tangible: moral injury. This is the term by which we describe the psychological, social, and spiritual impact of high-stakes situations that lead to the betrayal or transgression of our own deeply held moral beliefs and values.

The current pandemic has provided innumerable such situations that can increase the risk for moral injury, whether we deal directly with patients infected by the coronavirus or not. Telling family members they cannot visit critically ill loved ones. Delaying code activities, even momentarily, to get fully protected with personal protective equipment. Seeing patients who have delayed their necessary or preventive care. Using video rather than touch to reassure people.

Knowing that we are following guidelines from the Centers for Disease Control and Prevention does not stop our feelings of guilt. The longer this pandemic goes on, the more likely it is that these situations will begin to take a toll on us.

For most of us, being exposed to moral injuries is new; they have historically been most associated with severe traumatic wartime experiences. Soldiers, philosophers, and writers have described the ethical dilemmas inherent in war for as long as recorded history. But the use of this term is a more recent development, which the Moral Injury Project at Syracuse (N.Y.) University describes as probably originating in the Vietnam War–era writings of veteran and peace activist Camillo “Mac” Bica and psychiatrist Jonathan Shay. Examples of wartime events that have been thought to lead to moral injury include: causing the harm or death of civilians, knowingly but without alternatives, or accidentally; failing to provide medical aid to an injured civilian or service member; and following orders that were illegal, immoral, and/or against the rules of engagement or the Geneva Conventions.

However, the occurrence of moral injuries in modern health care is increasingly being reported, primarily as an adverse effect of health care inefficiencies that can contribute to burnout. COVID-19 has now provided an array of additional stressors that can cause moral injuries among health care workers. A recent guidance document on moral injury published by the American Psychiatric Association noted that, in the context of a public health disaster, such as COVID-19, it is sometimes necessary to transition from ordinary standards of care to those more appropriate in a crisis, as in wartime. This forces us all to confront challenging questions for which there may be no clear answers, and to make “lose-lose” choices in which no one involved – patients, family, or clinicians – ends up feeling satisfied or even comfortable.

Moral injuries affect most of us as physicians, as well as our colleagues and families, during this unusual, painful, traumatic, and potentially lethal time. Our lives have been altered significantly, and for many, completely turned upside down by enormous sacrifices and tragic losses. Globally, physicians account for over half of healthcare worker deaths. In the United States alone, over 900 health care workers have died of COVID-19.

Most of us have felt the symptoms of moral injury: frustration, anger, disgust, guilt. A recent report describes three levels of stressors in health care occurring during the pandemic, which are not dissimilar to those wartime events described previously.

• Severe moral stressors, such as the denial of treatment to a COVID-19 patient owing to lack of resources, the inability to provide optimal care to non–COVID-19 patients for many reasons, and concern about passing COVID to loved ones.
• Moderate moral stressors, such as preventing visitors, especially to dying patients, triaging patients for healthcare services with inadequate information, and trying to solve the tension between the need for self-preservation and the need to treat.
• Lower-level but common moral challenges, especially in the community – for example, seeing others not protecting the community by hoarding food, gathering for large parties, and not social distancing or wearing masks. Such stressors lead to frustration and contempt, especially from healthcare workers making personal sacrifices and who may be at risk for infection caused by these behaviors.

Every one of us is affected by these stressors. I certainly am.

What are the outcomes? We know that moral injuries are a risk factor for the development of mental health problems and burnout, and not surprisingly we are seeing that mental health problems, suicidality, and substance use disorders have increased markedly during COVID-19, as recently detailed by the CDC.

• Acknowledge that you, like me, are affected by these stressors. This is not a secret, and you should not be ashamed of your feelings.
• Talk with your colleagues, loved ones, and friends about how you and they are affected. You are not alone. Encourage others to share their thoughts, stories, and feelings.
• Put this topic on your meeting and departmental agendas and discuss these moral issues openly with your colleagues. Allow sufficient time to engage in open dialogue.
• Work out ways of assisting those who are in high-risk situations, especially for moderate to severe injuries. Be supportive toward those affected.
• Modify policies and change rosters and rotate staff between high- and low-stress roles. Protect and support at-risk colleagues.
• Think about difficult ethical decisions in advance so they can be made by groups, not individuals, and certainly not “on the fly.”
• Keep everyone in your workplace constantly informed, especially of impending staff or equipment shortages.
• Maintain your inherent self-care and resilience with rest, good nutrition, sleep, exercise, love, caring, socialization, and work-life balance.
• Be prepared to access the many professional support services available in our community if you are intensely distressed or if the above suggestions are not enough.

Remember, we are in this together and will find strength in each other. This too will pass.

This article first appeared on Medscape.com.

Among the many tolls inflicted on health care workers by COVID-19 is one that is not as easily measured as rates of death or disease, but is no less tangible: moral injury. This is the term by which we describe the psychological, social, and spiritual impact of high-stakes situations that lead to the betrayal or transgression of our own deeply held moral beliefs and values.

The current pandemic has provided innumerable such situations that can increase the risk for moral injury, whether we deal directly with patients infected by the coronavirus or not. Telling family members they cannot visit critically ill loved ones. Delaying code activities, even momentarily, to get fully protected with personal protective equipment. Seeing patients who have delayed their necessary or preventive care. Using video rather than touch to reassure people.

Knowing that we are following guidelines from the Centers for Disease Control and Prevention does not stop our feelings of guilt. The longer this pandemic goes on, the more likely it is that these situations will begin to take a toll on us.

For most of us, being exposed to moral injuries is new; they have historically been most associated with severe traumatic wartime experiences. Soldiers, philosophers, and writers have described the ethical dilemmas inherent in war for as long as recorded history. But the use of this term is a more recent development, which the Moral Injury Project at Syracuse (N.Y.) University describes as probably originating in the Vietnam War–era writings of veteran and peace activist Camillo “Mac” Bica and psychiatrist Jonathan Shay. Examples of wartime events that have been thought to lead to moral injury include: causing the harm or death of civilians, knowingly but without alternatives, or accidentally; failing to provide medical aid to an injured civilian or service member; and following orders that were illegal, immoral, and/or against the rules of engagement or the Geneva Conventions.

However, the occurrence of moral injuries in modern health care is increasingly being reported, primarily as an adverse effect of health care inefficiencies that can contribute to burnout. COVID-19 has now provided an array of additional stressors that can cause moral injuries among health care workers. A recent guidance document on moral injury published by the American Psychiatric Association noted that, in the context of a public health disaster, such as COVID-19, it is sometimes necessary to transition from ordinary standards of care to those more appropriate in a crisis, as in wartime. This forces us all to confront challenging questions for which there may be no clear answers, and to make “lose-lose” choices in which no one involved – patients, family, or clinicians – ends up feeling satisfied or even comfortable.

Moral injuries affect most of us as physicians, as well as our colleagues and families, during this unusual, painful, traumatic, and potentially lethal time. Our lives have been altered significantly, and for many, completely turned upside down by enormous sacrifices and tragic losses. Globally, physicians account for over half of healthcare worker deaths. In the United States alone, over 900 health care workers have died of COVID-19.

Most of us have felt the symptoms of moral injury: frustration, anger, disgust, guilt. A recent report describes three levels of stressors in health care occurring during the pandemic, which are not dissimilar to those wartime events described previously.

• Severe moral stressors, such as the denial of treatment to a COVID-19 patient owing to lack of resources, the inability to provide optimal care to non–COVID-19 patients for many reasons, and concern about passing COVID to loved ones.
• Moderate moral stressors, such as preventing visitors, especially to dying patients, triaging patients for healthcare services with inadequate information, and trying to solve the tension between the need for self-preservation and the need to treat.
• Lower-level but common moral challenges, especially in the community – for example, seeing others not protecting the community by hoarding food, gathering for large parties, and not social distancing or wearing masks. Such stressors lead to frustration and contempt, especially from healthcare workers making personal sacrifices and who may be at risk for infection caused by these behaviors.

Every one of us is affected by these stressors. I certainly am.

What are the outcomes? We know that moral injuries are a risk factor for the development of mental health problems and burnout, and not surprisingly we are seeing that mental health problems, suicidality, and substance use disorders have increased markedly during COVID-19, as recently detailed by the CDC.

• Acknowledge that you, like me, are affected by these stressors. This is not a secret, and you should not be ashamed of your feelings.
• Talk with your colleagues, loved ones, and friends about how you and they are affected. You are not alone. Encourage others to share their thoughts, stories, and feelings.
• Put this topic on your meeting and departmental agendas and discuss these moral issues openly with your colleagues. Allow sufficient time to engage in open dialogue.
• Work out ways of assisting those who are in high-risk situations, especially for moderate to severe injuries. Be supportive toward those affected.
• Modify policies and change rosters and rotate staff between high- and low-stress roles. Protect and support at-risk colleagues.
• Think about difficult ethical decisions in advance so they can be made by groups, not individuals, and certainly not “on the fly.”
• Keep everyone in your workplace constantly informed, especially of impending staff or equipment shortages.
• Maintain your inherent self-care and resilience with rest, good nutrition, sleep, exercise, love, caring, socialization, and work-life balance.
• Be prepared to access the many professional support services available in our community if you are intensely distressed or if the above suggestions are not enough.

Remember, we are in this together and will find strength in each other. This too will pass.

This article first appeared on Medscape.com.