Douglas S. Paauw, MD

A 25-year-old woman presents to discuss treatment of her headaches. They occur two or three times a month and last for 4-6 hours. The headaches are disabling, have a pounding quality behind the patient’s right eye, and worsen with exercise. The patient’s neurologic exam is normal.

She has tried oral sumatriptan and naproxen, but neither drug provided her with any relief from the headaches. What treatment would you recommend?
 

A. Topiramate

B. Beta-blocker

C. Lasmiditan

D. Metoclopramide plus sumatriptan

E. Ubrogepant

It is common to see patients with migraine headaches and to see patients with migraines who have not responded to previous migraine therapies. This column will focus on some migraine therapy pearls.

DKart/iStockphoto

For this patient, I would try choice D first, giving metoclopramide with oral sumatriptan to see if it can improve response to sumatriptan. The two new classes of drugs for acute migraine therapy, the gepants and ditans, certainly have a role in patients unresponsive or intolerant of triptans/NSAIDS, but I would try several tricks with these less expensive medications first before entering into prior authorization hell trying to get a gepant or ditan.

When a patient has already used a triptan but experienced no benefit from it, often the next medication a patient tries is a different triptan. Dahlof reviewed four trials that looked at the efficacy of switching sumatriptan nonresponders to a different triptan and found that lack of response to sumatriptan did not predict lack of response to an alternative triptan.¹ Unfortunately, acquiring insurance coverage for an alternate triptan can be difficult.

Other treatment options are nasal or injectable formulations of sumatriptan. Both of these are more costly than oral sumatriptan, and injectable sumatriptan has more side effects than oral triptans.

Combining treatment with metoclopramide can be helpful. In a study by Schulman and Dermott looking at patients who had previously been triptan nonresponders, 63% of those who took metoclopramide with sumatriptan had meaningful pain relief, compared with 31% of those who received sumatriptan and placebo.²

In a different study, Tfelt-Hansen et al. compared treatment with the combination of lysine acetylsalicylate plus metoclopramide versus treatment with 100 mg of sumatriptan.³ There was no difference in outcomes between the two treatment groups, with the lysine acetylsalicylate plus metoclopramide patients having a 57% success rate for first treated migraine compared with 53% of the sumatriptan-treated patients.

Treating with the combination of naproxen plus sumatriptan is superior to treating with either medication alone. Brandes et al. reported on two studies involving the use of the sumatriptan/naproxen combination, compared with using sumatriptan, naproxen, or placebo.⁴ In both, taking the sumatriptan/naproxen combination was superior to taking sumatriptan, naproxen, or placebo (P < .001).

In a study of patients with poor prior response to triptans, Mathew et al. found that the sumatriptan/naproxen combination was superior to placebo for both 2- and 24-hour headache relief (P < .001).⁵
 

Pearl

Try several options before abandoning triptans in previous triptan nonresponders, including trying a different triptan, adding metoclopramide, orcombining with an NSAID.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he 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 [email protected].

References

1. Dahlöf CG. Infrequent or nonresponse to oral sumatriptan does not predict response to other triptans – review of four trials. Cephalalgia. 2006 Feb;26(2):98-106.

2. Schulman EA, Dermott KF. Sumatriptan plus metoclopramide in triptan-nonresponsive migraineurs. Headache. 2003 Jul-Aug;43(7):729-33.

3. Tfelt-Hansen P et al. The effectiveness of combined oral lysine acetylsalicylate and metoclopramide compared with oral sumatriptan for migraine. Lancet. 1995 Oct 7;346(8980):923-6.

4. Brandes JL et al. Sumatriptan‐naproxen for acute treatment of migraine: A randomized trial. JAMA. 2007;297:1443‐54.

5. Mathew NT, Landy S, Stark S, et al. Fixed‐dose sumatriptan and naproxen in poor responders to triptans with a short half‐life. Headache. 2009;49:971‐82.

A 25-year-old woman presents to discuss treatment of her headaches. They occur two or three times a month and last for 4-6 hours. The headaches are disabling, have a pounding quality behind the patient’s right eye, and worsen with exercise. The patient’s neurologic exam is normal.

She has tried oral sumatriptan and naproxen, but neither drug provided her with any relief from the headaches. What treatment would you recommend?
 

A. Topiramate

B. Beta-blocker

C. Lasmiditan

D. Metoclopramide plus sumatriptan

E. Ubrogepant

It is common to see patients with migraine headaches and to see patients with migraines who have not responded to previous migraine therapies. This column will focus on some migraine therapy pearls.

DKart/iStockphoto

For this patient, I would try choice D first, giving metoclopramide with oral sumatriptan to see if it can improve response to sumatriptan. The two new classes of drugs for acute migraine therapy, the gepants and ditans, certainly have a role in patients unresponsive or intolerant of triptans/NSAIDS, but I would try several tricks with these less expensive medications first before entering into prior authorization hell trying to get a gepant or ditan.

When a patient has already used a triptan but experienced no benefit from it, often the next medication a patient tries is a different triptan. Dahlof reviewed four trials that looked at the efficacy of switching sumatriptan nonresponders to a different triptan and found that lack of response to sumatriptan did not predict lack of response to an alternative triptan.¹ Unfortunately, acquiring insurance coverage for an alternate triptan can be difficult.

Other treatment options are nasal or injectable formulations of sumatriptan. Both of these are more costly than oral sumatriptan, and injectable sumatriptan has more side effects than oral triptans.

Combining treatment with metoclopramide can be helpful. In a study by Schulman and Dermott looking at patients who had previously been triptan nonresponders, 63% of those who took metoclopramide with sumatriptan had meaningful pain relief, compared with 31% of those who received sumatriptan and placebo.²

In a different study, Tfelt-Hansen et al. compared treatment with the combination of lysine acetylsalicylate plus metoclopramide versus treatment with 100 mg of sumatriptan.³ There was no difference in outcomes between the two treatment groups, with the lysine acetylsalicylate plus metoclopramide patients having a 57% success rate for first treated migraine compared with 53% of the sumatriptan-treated patients.

Treating with the combination of naproxen plus sumatriptan is superior to treating with either medication alone. Brandes et al. reported on two studies involving the use of the sumatriptan/naproxen combination, compared with using sumatriptan, naproxen, or placebo.⁴ In both, taking the sumatriptan/naproxen combination was superior to taking sumatriptan, naproxen, or placebo (P < .001).

In a study of patients with poor prior response to triptans, Mathew et al. found that the sumatriptan/naproxen combination was superior to placebo for both 2- and 24-hour headache relief (P < .001).⁵
 

Pearl

Try several options before abandoning triptans in previous triptan nonresponders, including trying a different triptan, adding metoclopramide, orcombining with an NSAID.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he 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 [email protected].

References

1. Dahlöf CG. Infrequent or nonresponse to oral sumatriptan does not predict response to other triptans – review of four trials. Cephalalgia. 2006 Feb;26(2):98-106.

2. Schulman EA, Dermott KF. Sumatriptan plus metoclopramide in triptan-nonresponsive migraineurs. Headache. 2003 Jul-Aug;43(7):729-33.

3. Tfelt-Hansen P et al. The effectiveness of combined oral lysine acetylsalicylate and metoclopramide compared with oral sumatriptan for migraine. Lancet. 1995 Oct 7;346(8980):923-6.

4. Brandes JL et al. Sumatriptan‐naproxen for acute treatment of migraine: A randomized trial. JAMA. 2007;297:1443‐54.

5. Mathew NT, Landy S, Stark S, et al. Fixed‐dose sumatriptan and naproxen in poor responders to triptans with a short half‐life. Headache. 2009;49:971‐82.

A 25-year-old woman presents to discuss treatment of her headaches. They occur two or three times a month and last for 4-6 hours. The headaches are disabling, have a pounding quality behind the patient’s right eye, and worsen with exercise. The patient’s neurologic exam is normal.

She has tried oral sumatriptan and naproxen, but neither drug provided her with any relief from the headaches. What treatment would you recommend?
 

A. Topiramate

B. Beta-blocker

C. Lasmiditan

D. Metoclopramide plus sumatriptan

E. Ubrogepant

It is common to see patients with migraine headaches and to see patients with migraines who have not responded to previous migraine therapies. This column will focus on some migraine therapy pearls.

DKart/iStockphoto

For this patient, I would try choice D first, giving metoclopramide with oral sumatriptan to see if it can improve response to sumatriptan. The two new classes of drugs for acute migraine therapy, the gepants and ditans, certainly have a role in patients unresponsive or intolerant of triptans/NSAIDS, but I would try several tricks with these less expensive medications first before entering into prior authorization hell trying to get a gepant or ditan.

When a patient has already used a triptan but experienced no benefit from it, often the next medication a patient tries is a different triptan. Dahlof reviewed four trials that looked at the efficacy of switching sumatriptan nonresponders to a different triptan and found that lack of response to sumatriptan did not predict lack of response to an alternative triptan.¹ Unfortunately, acquiring insurance coverage for an alternate triptan can be difficult.

Other treatment options are nasal or injectable formulations of sumatriptan. Both of these are more costly than oral sumatriptan, and injectable sumatriptan has more side effects than oral triptans.

Combining treatment with metoclopramide can be helpful. In a study by Schulman and Dermott looking at patients who had previously been triptan nonresponders, 63% of those who took metoclopramide with sumatriptan had meaningful pain relief, compared with 31% of those who received sumatriptan and placebo.²

In a different study, Tfelt-Hansen et al. compared treatment with the combination of lysine acetylsalicylate plus metoclopramide versus treatment with 100 mg of sumatriptan.³ There was no difference in outcomes between the two treatment groups, with the lysine acetylsalicylate plus metoclopramide patients having a 57% success rate for first treated migraine compared with 53% of the sumatriptan-treated patients.

Treating with the combination of naproxen plus sumatriptan is superior to treating with either medication alone. Brandes et al. reported on two studies involving the use of the sumatriptan/naproxen combination, compared with using sumatriptan, naproxen, or placebo.⁴ In both, taking the sumatriptan/naproxen combination was superior to taking sumatriptan, naproxen, or placebo (P < .001).

In a study of patients with poor prior response to triptans, Mathew et al. found that the sumatriptan/naproxen combination was superior to placebo for both 2- and 24-hour headache relief (P < .001).⁵
 

Pearl

Try several options before abandoning triptans in previous triptan nonresponders, including trying a different triptan, adding metoclopramide, orcombining with an NSAID.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he 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 [email protected].

References

1. Dahlöf CG. Infrequent or nonresponse to oral sumatriptan does not predict response to other triptans – review of four trials. Cephalalgia. 2006 Feb;26(2):98-106.

2. Schulman EA, Dermott KF. Sumatriptan plus metoclopramide in triptan-nonresponsive migraineurs. Headache. 2003 Jul-Aug;43(7):729-33.

3. Tfelt-Hansen P et al. The effectiveness of combined oral lysine acetylsalicylate and metoclopramide compared with oral sumatriptan for migraine. Lancet. 1995 Oct 7;346(8980):923-6.

4. Brandes JL et al. Sumatriptan‐naproxen for acute treatment of migraine: A randomized trial. JAMA. 2007;297:1443‐54.

5. Mathew NT, Landy S, Stark S, et al. Fixed‐dose sumatriptan and naproxen in poor responders to triptans with a short half‐life. Headache. 2009;49:971‐82.

A 46-year-old man who lives in Tacoma, Wash., is seen for fatigue. He has a no significant past medical history. He is not taking any medications. His physical exam is unremarkable. His hemoglobin is 12 gm/dL, hematocrit is 37 gm/dL, mean corpuscular volume (MCV) is 103 fL, and thyroid-stimulating hormone level is 1.2 mU/L.

What workup do you recommend?

A) B₁₂, folate testing

B) Alcohol history, B₁₂, folate testing

C) Alcohol history, B₁₂ testing

I would choose doing a careful alcohol history and vitamin B₁₂ testing.

Dr. Seppä and colleagues looked at all outpatients who had a blood count done over an 8-month period.¹ A total of 9,527 blood counts were ordered, and 287 (3%) had macrocytosis.¹ Further workup was done for 113 of the patients. The most common cause found for macrocytosis was alcohol abuse, in 74 (65%) of the patients (80% of the men and 36% of the women). In several studies, vitamin B₁₂ deficiency was the cause of macrocytosis in 5%-7% of patients.^2,3

In 1978, a study by Davidson and Hamilton looked at 200 consecutive patients with MCVs over 100, and were able to find a cause in 80%.⁴ Sixteen of these patients had a low B₁₂ level and 10 had a low folate level.

In recent years, folate has become an extremely unlikely cause of macrocytic anemias. In 1998, the Food and Drug Administration required folic acid fortification of enriched grain products in the United States to help decrease the risk of neural tube defects. Similar fortification efforts were undertaken in Canada. Since 1998, anemia due to folate deficiency has essentially disappeared in individuals who have access to fortified grain products.

Joelson and colleagues looked at data on folate testing from the year prior to fortification of the grain supply (1997) and after (2004).⁵ They found that, in 1997, 4.8% of tests had a folate level less than 160 ng/mL compared with only 0.6% of tests in 2004.

When a more stringent cutoff for deficiency was used (94 ng/mL) 0.98% of tests were below that level in 1997, and 0.09% in 2004. The mean RBC folate level in 1997 was 420 ng/mL and rose to 697 ng/mL in 2004. Of the patients who did have low folate levels, only a minority had elevated MCVs.

Shojania et al. looked at folate testing in Canada after widespread fortification had started.⁶ They found that 0.5% of 2,154 serum folate levels were low and 0.7% of 560 red blood cell folate levels were low. Folate deficiency was not the cause of anemia in any of the patients with low folate levels.

Theisen-Toupal and colleagues did a retrospective study looking at folate testing over an 11-year period after fortification.⁷ The researchers examined the results of 84,187 assessments of folate levels. Forty-seven (0.056%) of the tests found patients with folate deficiency, 166 (0.197%), found patients with low-normal folate levels, 57,411 (68.195%) of tests yielded normal results, and 26,563 (31.552%) of tests found high folate levels. The opinion of the authors was that folate testing should be severely reduced or eliminated. Furthermore, the American Society for Clinical Pathology, as part of the Choosing Wisely campaign, states: “Do not order red blood cell folate levels at all.”⁸

So what does this all mean? We have been taught to have a reflex response to the evaluation of macrocytosis to test for B₁₂ and folate. Neither of these are particularly common causes of macrocytosis, and in countries where there is grain fortification, folate deficiency is exceedingly uncommon, and should not be tested for early in any diagnostic process.
 

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he 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 [email protected].

References

1. Seppä K et al. Evaluation of macrocytosis by general practitioners. J Stud Alcohol. 1996 Jan;57(1):97-100.

2. Seppä K et al. Blood count and hematologic morphology in nonanemic macrocytosis: Differences between alcohol abuse and pernicious anemia. Alcohol. 1993 Sep-Oct;10(5):343-7.

3. Wymer A, Becker DM. Recognition and evaluation of red blood cell macrocytosis in the primary care setting. J Gen Intern Med. 1990 May-Jun;5(3):192-7.

4. Davidson RJ, Hamilton PJ. High mean red cell volume: Its incidence and significance in routine haematology. J Clin Pathol. 1978 May;31[5]:493-8.

5. Joelson DW, Fiebig EW. Diminished need for folate measurements among indigent populations in the post folic acid supplementation era. Arch Pathol Lab Med. 2007 Mar;131(3):477-80.

6. Shojania AM, von Kuster K. Ordering folate assays is no longer justified for investigation of anemias, in folic acid fortified countries. BMC Res Notes. 2010 Jan 25;3:22. doi: 10.1186/1756-0500-3-22.

7. Theisen-Toupal et al. Low yield of outpatient serum folate testing. JAMA Intern Med. 2014 Oct. doi: 10.1001/jamainternmed.2014.3593.

8. Choosing Wisely: American Society for Clinical Pathology, Oct. 19, 2017. Recommendation.

A 46-year-old man who lives in Tacoma, Wash., is seen for fatigue. He has a no significant past medical history. He is not taking any medications. His physical exam is unremarkable. His hemoglobin is 12 gm/dL, hematocrit is 37 gm/dL, mean corpuscular volume (MCV) is 103 fL, and thyroid-stimulating hormone level is 1.2 mU/L.

What workup do you recommend?

A) B₁₂, folate testing

B) Alcohol history, B₁₂, folate testing

C) Alcohol history, B₁₂ testing

I would choose doing a careful alcohol history and vitamin B₁₂ testing.

Dr. Seppä and colleagues looked at all outpatients who had a blood count done over an 8-month period.¹ A total of 9,527 blood counts were ordered, and 287 (3%) had macrocytosis.¹ Further workup was done for 113 of the patients. The most common cause found for macrocytosis was alcohol abuse, in 74 (65%) of the patients (80% of the men and 36% of the women). In several studies, vitamin B₁₂ deficiency was the cause of macrocytosis in 5%-7% of patients.^2,3

In 1978, a study by Davidson and Hamilton looked at 200 consecutive patients with MCVs over 100, and were able to find a cause in 80%.⁴ Sixteen of these patients had a low B₁₂ level and 10 had a low folate level.

In recent years, folate has become an extremely unlikely cause of macrocytic anemias. In 1998, the Food and Drug Administration required folic acid fortification of enriched grain products in the United States to help decrease the risk of neural tube defects. Similar fortification efforts were undertaken in Canada. Since 1998, anemia due to folate deficiency has essentially disappeared in individuals who have access to fortified grain products.

Joelson and colleagues looked at data on folate testing from the year prior to fortification of the grain supply (1997) and after (2004).⁵ They found that, in 1997, 4.8% of tests had a folate level less than 160 ng/mL compared with only 0.6% of tests in 2004.

When a more stringent cutoff for deficiency was used (94 ng/mL) 0.98% of tests were below that level in 1997, and 0.09% in 2004. The mean RBC folate level in 1997 was 420 ng/mL and rose to 697 ng/mL in 2004. Of the patients who did have low folate levels, only a minority had elevated MCVs.

Shojania et al. looked at folate testing in Canada after widespread fortification had started.⁶ They found that 0.5% of 2,154 serum folate levels were low and 0.7% of 560 red blood cell folate levels were low. Folate deficiency was not the cause of anemia in any of the patients with low folate levels.

Theisen-Toupal and colleagues did a retrospective study looking at folate testing over an 11-year period after fortification.⁷ The researchers examined the results of 84,187 assessments of folate levels. Forty-seven (0.056%) of the tests found patients with folate deficiency, 166 (0.197%), found patients with low-normal folate levels, 57,411 (68.195%) of tests yielded normal results, and 26,563 (31.552%) of tests found high folate levels. The opinion of the authors was that folate testing should be severely reduced or eliminated. Furthermore, the American Society for Clinical Pathology, as part of the Choosing Wisely campaign, states: “Do not order red blood cell folate levels at all.”⁸

So what does this all mean? We have been taught to have a reflex response to the evaluation of macrocytosis to test for B₁₂ and folate. Neither of these are particularly common causes of macrocytosis, and in countries where there is grain fortification, folate deficiency is exceedingly uncommon, and should not be tested for early in any diagnostic process.
 

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he 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 [email protected].

References

1. Seppä K et al. Evaluation of macrocytosis by general practitioners. J Stud Alcohol. 1996 Jan;57(1):97-100.

2. Seppä K et al. Blood count and hematologic morphology in nonanemic macrocytosis: Differences between alcohol abuse and pernicious anemia. Alcohol. 1993 Sep-Oct;10(5):343-7.

3. Wymer A, Becker DM. Recognition and evaluation of red blood cell macrocytosis in the primary care setting. J Gen Intern Med. 1990 May-Jun;5(3):192-7.

4. Davidson RJ, Hamilton PJ. High mean red cell volume: Its incidence and significance in routine haematology. J Clin Pathol. 1978 May;31[5]:493-8.

5. Joelson DW, Fiebig EW. Diminished need for folate measurements among indigent populations in the post folic acid supplementation era. Arch Pathol Lab Med. 2007 Mar;131(3):477-80.

6. Shojania AM, von Kuster K. Ordering folate assays is no longer justified for investigation of anemias, in folic acid fortified countries. BMC Res Notes. 2010 Jan 25;3:22. doi: 10.1186/1756-0500-3-22.

7. Theisen-Toupal et al. Low yield of outpatient serum folate testing. JAMA Intern Med. 2014 Oct. doi: 10.1001/jamainternmed.2014.3593.

8. Choosing Wisely: American Society for Clinical Pathology, Oct. 19, 2017. Recommendation.

A 46-year-old man who lives in Tacoma, Wash., is seen for fatigue. He has a no significant past medical history. He is not taking any medications. His physical exam is unremarkable. His hemoglobin is 12 gm/dL, hematocrit is 37 gm/dL, mean corpuscular volume (MCV) is 103 fL, and thyroid-stimulating hormone level is 1.2 mU/L.

What workup do you recommend?

A) B₁₂, folate testing

B) Alcohol history, B₁₂, folate testing

C) Alcohol history, B₁₂ testing

I would choose doing a careful alcohol history and vitamin B₁₂ testing.

Dr. Seppä and colleagues looked at all outpatients who had a blood count done over an 8-month period.¹ A total of 9,527 blood counts were ordered, and 287 (3%) had macrocytosis.¹ Further workup was done for 113 of the patients. The most common cause found for macrocytosis was alcohol abuse, in 74 (65%) of the patients (80% of the men and 36% of the women). In several studies, vitamin B₁₂ deficiency was the cause of macrocytosis in 5%-7% of patients.^2,3

In 1978, a study by Davidson and Hamilton looked at 200 consecutive patients with MCVs over 100, and were able to find a cause in 80%.⁴ Sixteen of these patients had a low B₁₂ level and 10 had a low folate level.

In recent years, folate has become an extremely unlikely cause of macrocytic anemias. In 1998, the Food and Drug Administration required folic acid fortification of enriched grain products in the United States to help decrease the risk of neural tube defects. Similar fortification efforts were undertaken in Canada. Since 1998, anemia due to folate deficiency has essentially disappeared in individuals who have access to fortified grain products.

Joelson and colleagues looked at data on folate testing from the year prior to fortification of the grain supply (1997) and after (2004).⁵ They found that, in 1997, 4.8% of tests had a folate level less than 160 ng/mL compared with only 0.6% of tests in 2004.

When a more stringent cutoff for deficiency was used (94 ng/mL) 0.98% of tests were below that level in 1997, and 0.09% in 2004. The mean RBC folate level in 1997 was 420 ng/mL and rose to 697 ng/mL in 2004. Of the patients who did have low folate levels, only a minority had elevated MCVs.

Shojania et al. looked at folate testing in Canada after widespread fortification had started.⁶ They found that 0.5% of 2,154 serum folate levels were low and 0.7% of 560 red blood cell folate levels were low. Folate deficiency was not the cause of anemia in any of the patients with low folate levels.

Theisen-Toupal and colleagues did a retrospective study looking at folate testing over an 11-year period after fortification.⁷ The researchers examined the results of 84,187 assessments of folate levels. Forty-seven (0.056%) of the tests found patients with folate deficiency, 166 (0.197%), found patients with low-normal folate levels, 57,411 (68.195%) of tests yielded normal results, and 26,563 (31.552%) of tests found high folate levels. The opinion of the authors was that folate testing should be severely reduced or eliminated. Furthermore, the American Society for Clinical Pathology, as part of the Choosing Wisely campaign, states: “Do not order red blood cell folate levels at all.”⁸

So what does this all mean? We have been taught to have a reflex response to the evaluation of macrocytosis to test for B₁₂ and folate. Neither of these are particularly common causes of macrocytosis, and in countries where there is grain fortification, folate deficiency is exceedingly uncommon, and should not be tested for early in any diagnostic process.
 

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he 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 [email protected].

References

1. Seppä K et al. Evaluation of macrocytosis by general practitioners. J Stud Alcohol. 1996 Jan;57(1):97-100.

2. Seppä K et al. Blood count and hematologic morphology in nonanemic macrocytosis: Differences between alcohol abuse and pernicious anemia. Alcohol. 1993 Sep-Oct;10(5):343-7.

3. Wymer A, Becker DM. Recognition and evaluation of red blood cell macrocytosis in the primary care setting. J Gen Intern Med. 1990 May-Jun;5(3):192-7.

4. Davidson RJ, Hamilton PJ. High mean red cell volume: Its incidence and significance in routine haematology. J Clin Pathol. 1978 May;31[5]:493-8.

5. Joelson DW, Fiebig EW. Diminished need for folate measurements among indigent populations in the post folic acid supplementation era. Arch Pathol Lab Med. 2007 Mar;131(3):477-80.

6. Shojania AM, von Kuster K. Ordering folate assays is no longer justified for investigation of anemias, in folic acid fortified countries. BMC Res Notes. 2010 Jan 25;3:22. doi: 10.1186/1756-0500-3-22.

7. Theisen-Toupal et al. Low yield of outpatient serum folate testing. JAMA Intern Med. 2014 Oct. doi: 10.1001/jamainternmed.2014.3593.

8. Choosing Wisely: American Society for Clinical Pathology, Oct. 19, 2017. Recommendation.

This month, I would like to touch on a few COVID-19 topics that have received much publicity, with some messages about them having been confusing.

Let’s start with a case:

A 37-year-old woman is seen in clinic for a 5-day history of cough, fever, chest tightness, and onset of dyspnea on the day of her office visit.

An exam reveals her blood pressure is 100/60 mm Hg, her pulse is 100 beats per minute, her temperature is 38.7° C, her oxygen saturation is 93%, and her respiratory rate is 20 breaths per minute.

Auscultation of the chest revealed bilateral wheezing and rhonchi. A nasopharyngeal swab is sent for COVID-19 and is negative; she also tests negative for influenza.

Her hemoglobin level is 13 g/dL, hematocrit was 39%, platelet count was 155,000 per mcL of blood, and D-dimer level was 8.4 mcg/mL (normal is less than 0.4 mcg/mL.) Her white blood cell count was 6,000 per mcL of blood (neutrophils, 4,900; lymphocytes, 800; basophils, 200). Her chest x-ray showed bilateral lower lobe infiltrates.
 

What do you recommend?

A. Begin azithromycin plus ceftriaxone

B. Begin azithromycin

C. Begin oseltamivir

D. Obtain chest CT

E. Repeat COVID-19 test

With the massive amount of information coming out every day on COVID-19, it is hard to keep up with all of it, and sort out accurate, reviewed studies. We are in a position where we need to take in what we can and assess the best data available.

In the case above, I think choices D or E would make sense. This patient very likely has COVID-19 based on clinical symptoms and lab parameters. The negative COVID-19 test gives us pause, but several studies show that false negative tests are not uncommon.

Long et al. reported on 36 patients who had received both chest CT and real-time reverse transcription polymerase chain reaction (rRT-PCR) for COVID-19.¹ All were eventually diagnosed with COVID-19 pneumonia. The CT scan had a very high sensitivity (35/36) of 97.2%, whereas the rRT-PCR had a lower sensitivity (30/36) of 83%. All six of the patients with a negative COVID-19 test initially were positive on repeat testing (three on the second test, three on the third test).

There are concerns about what the sensitivity of the rRT-PCR tests being run in the United States are. At this point, I think that, when the pretest probability of COVID-19 infection is very high based on local epidemiology and clinical symptoms, a negative COVID rRT-PCR does not eliminate the diagnosis. In many cases, COVID-19 may still be the most likely diagnosis.

Early in the pandemic, the symptoms that were emphasized were fever, cough, and dyspnea. Those were all crucial symptoms for a disease that causes pneumonia. GI symptoms were initially deemphasized. In an early study released from Wuhan, China, only about 5% of COVID-19 patients had nausea or diarrhea.² In a study of 305 patients focused on gastrointestinal symptoms, half of the patients had diarrhea, half had anorexia and 30% had nausea.³ In a small series of nine patients who presented with only GI symptoms, four of these patients never developed fever or pulmonary symptoms.³

On March 14, the French health minister, Olivier Véran, tweeted that “taking anti-inflammatory drugs (ibuprofen, cortisone ...) could be an aggravating factor for the infection. If you have a fever, take paracetamol.” This was picked up by many news services, and soon became standard recommendations, despite no data.

There is reason for concern for NSAIDs, as regular NSAID use has been tied to more complications in patients with respiratory tract infections.⁴ I have never been a proponent of regular NSAID use in patients who are infected, because the likelihood of toxicity is elevated in patients who are volume depleted or under physiologic stress. But at this time, there is no evidence on problems with episodic NSAID use in patients with COVID-19.

Another widely disseminated decree was that patients with COVID-19 should not use ACE inhibitors and angiotensin II receptor blockers (ARBs). COVID-19 binds to their target cells through ACE2, which is expressed by epithelial cells of the lung, intestine and kidney. Patients who are treated with ACE inhibitors and ARBs have been shown to have more ACE2 expression.

In a letter to the editor by Fang et al. published in Lancet Respiratory Medicine, the authors raised the question of whether patients might be better served to be switched from ACE inhibitors and ARBs to calcium-channel blockers for the treatment of hypertension.⁵ A small study by Meng et al. looked at outcomes of patients on these drugs who had COVID-19 infection.⁶ They looked at 417 patients admitted to a hospital in China with COVID-19 infection. A total of 42 patients were on medications for hypertension. Group 1 were patients on ACE inhibitors/ARBs (17 patients) and group 2 were patients on other antihypertensives (25 patients). During hospitalization 12 patients (48%) in group 2 were categorized as having severe disease and 1 patient died. In group 1 (the ACE inhibitor/ARB–treated patients) only four (23%) were categorized as having severe disease, and no patients in this group died.

Vaduganathan et al. published a special report in the New England Journal of Medicine strongly arguing the point that “[u]ntil further data are available, we think that [renin-angiotensin-aldosterone system] inhibitors should be continued in patients in otherwise stable condition who are at risk for, being evaluated for, or with COVID-19”.⁷ This position is supported by the American Heart Association, the American College of Cardiology, the American College of Physicians, and 11 other medical organizations.
 

Take-home messages

• Testing isn’t perfect – if you have strong suspicion for COVID-19 disease, retest.
• GI symptoms appear to be common, and rarely may be the only symptoms initially.
• NSAIDs are always risky in really sick patients, but data specific to COVID-19 is lacking.
• ACE inhibitors/ARBs should not be avoided in patients with COVID-19.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he 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 Dr. Paauw at [email protected].

References

1. Long C et al. Diagnosis of the Coronavirus disease (COVID-19): rRT-PCR or CT? Eur J Radiol. 2020 Mar 25;126:108961.

2. Zhou F et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: A retrospective cohort study. Lancet. 2020 Mar 28;395(10229):1054-62.

3. Tian Y et al. Review article: Gastrointestinal features in COVID-19 and the possibility of faecal transmission. Aliment Pharmacol Ther. 2020;00:1–9.

4. Voiriot G et al. Risks related to the use of nonsteroidal anti-inflammatory drugs in community-acquired pneumonia in adult and pediatric patients. J Clin Med. 2019;8:E786.

5. Fang L et al. Are patients with hypertension and diabetes mellitus at increased risk for COVID-19 infection? Lancet Respir Med. 2020 Mar 11. doi:10.1016/S2213-2600(20)30116-8.

6. Meng J et al. Renin-angiotensin system inhibitors improve the clinical outcomes of COVID-19 patients with hypertension. Renin-angiotensin system inhibitors improve the clinical outcomes of COVID-19 patients with hypertension. Emerg Microbes Infect. 2020 Dec;9(1):757-60.

7. Vaduganathan M et al. Renin-angiotensin-aldosterone system inhibitors in patients with COVID-19. N Engl J Med. 2020 Mar 30. doi: 10.1056/NEJMsr2005760.

This month, I would like to touch on a few COVID-19 topics that have received much publicity, with some messages about them having been confusing.

Let’s start with a case:

A 37-year-old woman is seen in clinic for a 5-day history of cough, fever, chest tightness, and onset of dyspnea on the day of her office visit.

An exam reveals her blood pressure is 100/60 mm Hg, her pulse is 100 beats per minute, her temperature is 38.7° C, her oxygen saturation is 93%, and her respiratory rate is 20 breaths per minute.

Auscultation of the chest revealed bilateral wheezing and rhonchi. A nasopharyngeal swab is sent for COVID-19 and is negative; she also tests negative for influenza.

Her hemoglobin level is 13 g/dL, hematocrit was 39%, platelet count was 155,000 per mcL of blood, and D-dimer level was 8.4 mcg/mL (normal is less than 0.4 mcg/mL.) Her white blood cell count was 6,000 per mcL of blood (neutrophils, 4,900; lymphocytes, 800; basophils, 200). Her chest x-ray showed bilateral lower lobe infiltrates.
 

What do you recommend?

A. Begin azithromycin plus ceftriaxone

B. Begin azithromycin

C. Begin oseltamivir

D. Obtain chest CT

E. Repeat COVID-19 test

With the massive amount of information coming out every day on COVID-19, it is hard to keep up with all of it, and sort out accurate, reviewed studies. We are in a position where we need to take in what we can and assess the best data available.

In the case above, I think choices D or E would make sense. This patient very likely has COVID-19 based on clinical symptoms and lab parameters. The negative COVID-19 test gives us pause, but several studies show that false negative tests are not uncommon.

Long et al. reported on 36 patients who had received both chest CT and real-time reverse transcription polymerase chain reaction (rRT-PCR) for COVID-19.¹ All were eventually diagnosed with COVID-19 pneumonia. The CT scan had a very high sensitivity (35/36) of 97.2%, whereas the rRT-PCR had a lower sensitivity (30/36) of 83%. All six of the patients with a negative COVID-19 test initially were positive on repeat testing (three on the second test, three on the third test).

There are concerns about what the sensitivity of the rRT-PCR tests being run in the United States are. At this point, I think that, when the pretest probability of COVID-19 infection is very high based on local epidemiology and clinical symptoms, a negative COVID rRT-PCR does not eliminate the diagnosis. In many cases, COVID-19 may still be the most likely diagnosis.

Early in the pandemic, the symptoms that were emphasized were fever, cough, and dyspnea. Those were all crucial symptoms for a disease that causes pneumonia. GI symptoms were initially deemphasized. In an early study released from Wuhan, China, only about 5% of COVID-19 patients had nausea or diarrhea.² In a study of 305 patients focused on gastrointestinal symptoms, half of the patients had diarrhea, half had anorexia and 30% had nausea.³ In a small series of nine patients who presented with only GI symptoms, four of these patients never developed fever or pulmonary symptoms.³

On March 14, the French health minister, Olivier Véran, tweeted that “taking anti-inflammatory drugs (ibuprofen, cortisone ...) could be an aggravating factor for the infection. If you have a fever, take paracetamol.” This was picked up by many news services, and soon became standard recommendations, despite no data.

There is reason for concern for NSAIDs, as regular NSAID use has been tied to more complications in patients with respiratory tract infections.⁴ I have never been a proponent of regular NSAID use in patients who are infected, because the likelihood of toxicity is elevated in patients who are volume depleted or under physiologic stress. But at this time, there is no evidence on problems with episodic NSAID use in patients with COVID-19.

Another widely disseminated decree was that patients with COVID-19 should not use ACE inhibitors and angiotensin II receptor blockers (ARBs). COVID-19 binds to their target cells through ACE2, which is expressed by epithelial cells of the lung, intestine and kidney. Patients who are treated with ACE inhibitors and ARBs have been shown to have more ACE2 expression.

In a letter to the editor by Fang et al. published in Lancet Respiratory Medicine, the authors raised the question of whether patients might be better served to be switched from ACE inhibitors and ARBs to calcium-channel blockers for the treatment of hypertension.⁵ A small study by Meng et al. looked at outcomes of patients on these drugs who had COVID-19 infection.⁶ They looked at 417 patients admitted to a hospital in China with COVID-19 infection. A total of 42 patients were on medications for hypertension. Group 1 were patients on ACE inhibitors/ARBs (17 patients) and group 2 were patients on other antihypertensives (25 patients). During hospitalization 12 patients (48%) in group 2 were categorized as having severe disease and 1 patient died. In group 1 (the ACE inhibitor/ARB–treated patients) only four (23%) were categorized as having severe disease, and no patients in this group died.

Vaduganathan et al. published a special report in the New England Journal of Medicine strongly arguing the point that “[u]ntil further data are available, we think that [renin-angiotensin-aldosterone system] inhibitors should be continued in patients in otherwise stable condition who are at risk for, being evaluated for, or with COVID-19”.⁷ This position is supported by the American Heart Association, the American College of Cardiology, the American College of Physicians, and 11 other medical organizations.
 

Take-home messages

• Testing isn’t perfect – if you have strong suspicion for COVID-19 disease, retest.
• GI symptoms appear to be common, and rarely may be the only symptoms initially.
• NSAIDs are always risky in really sick patients, but data specific to COVID-19 is lacking.
• ACE inhibitors/ARBs should not be avoided in patients with COVID-19.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he 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 Dr. Paauw at [email protected].

References

1. Long C et al. Diagnosis of the Coronavirus disease (COVID-19): rRT-PCR or CT? Eur J Radiol. 2020 Mar 25;126:108961.

2. Zhou F et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: A retrospective cohort study. Lancet. 2020 Mar 28;395(10229):1054-62.

3. Tian Y et al. Review article: Gastrointestinal features in COVID-19 and the possibility of faecal transmission. Aliment Pharmacol Ther. 2020;00:1–9.

4. Voiriot G et al. Risks related to the use of nonsteroidal anti-inflammatory drugs in community-acquired pneumonia in adult and pediatric patients. J Clin Med. 2019;8:E786.

5. Fang L et al. Are patients with hypertension and diabetes mellitus at increased risk for COVID-19 infection? Lancet Respir Med. 2020 Mar 11. doi:10.1016/S2213-2600(20)30116-8.

6. Meng J et al. Renin-angiotensin system inhibitors improve the clinical outcomes of COVID-19 patients with hypertension. Renin-angiotensin system inhibitors improve the clinical outcomes of COVID-19 patients with hypertension. Emerg Microbes Infect. 2020 Dec;9(1):757-60.

7. Vaduganathan M et al. Renin-angiotensin-aldosterone system inhibitors in patients with COVID-19. N Engl J Med. 2020 Mar 30. doi: 10.1056/NEJMsr2005760.

This month, I would like to touch on a few COVID-19 topics that have received much publicity, with some messages about them having been confusing.

Let’s start with a case:

A 37-year-old woman is seen in clinic for a 5-day history of cough, fever, chest tightness, and onset of dyspnea on the day of her office visit.

An exam reveals her blood pressure is 100/60 mm Hg, her pulse is 100 beats per minute, her temperature is 38.7° C, her oxygen saturation is 93%, and her respiratory rate is 20 breaths per minute.

Auscultation of the chest revealed bilateral wheezing and rhonchi. A nasopharyngeal swab is sent for COVID-19 and is negative; she also tests negative for influenza.

Her hemoglobin level is 13 g/dL, hematocrit was 39%, platelet count was 155,000 per mcL of blood, and D-dimer level was 8.4 mcg/mL (normal is less than 0.4 mcg/mL.) Her white blood cell count was 6,000 per mcL of blood (neutrophils, 4,900; lymphocytes, 800; basophils, 200). Her chest x-ray showed bilateral lower lobe infiltrates.
 

What do you recommend?

A. Begin azithromycin plus ceftriaxone

B. Begin azithromycin

C. Begin oseltamivir

D. Obtain chest CT

E. Repeat COVID-19 test

With the massive amount of information coming out every day on COVID-19, it is hard to keep up with all of it, and sort out accurate, reviewed studies. We are in a position where we need to take in what we can and assess the best data available.

In the case above, I think choices D or E would make sense. This patient very likely has COVID-19 based on clinical symptoms and lab parameters. The negative COVID-19 test gives us pause, but several studies show that false negative tests are not uncommon.

Long et al. reported on 36 patients who had received both chest CT and real-time reverse transcription polymerase chain reaction (rRT-PCR) for COVID-19.¹ All were eventually diagnosed with COVID-19 pneumonia. The CT scan had a very high sensitivity (35/36) of 97.2%, whereas the rRT-PCR had a lower sensitivity (30/36) of 83%. All six of the patients with a negative COVID-19 test initially were positive on repeat testing (three on the second test, three on the third test).

There are concerns about what the sensitivity of the rRT-PCR tests being run in the United States are. At this point, I think that, when the pretest probability of COVID-19 infection is very high based on local epidemiology and clinical symptoms, a negative COVID rRT-PCR does not eliminate the diagnosis. In many cases, COVID-19 may still be the most likely diagnosis.

Early in the pandemic, the symptoms that were emphasized were fever, cough, and dyspnea. Those were all crucial symptoms for a disease that causes pneumonia. GI symptoms were initially deemphasized. In an early study released from Wuhan, China, only about 5% of COVID-19 patients had nausea or diarrhea.² In a study of 305 patients focused on gastrointestinal symptoms, half of the patients had diarrhea, half had anorexia and 30% had nausea.³ In a small series of nine patients who presented with only GI symptoms, four of these patients never developed fever or pulmonary symptoms.³

On March 14, the French health minister, Olivier Véran, tweeted that “taking anti-inflammatory drugs (ibuprofen, cortisone ...) could be an aggravating factor for the infection. If you have a fever, take paracetamol.” This was picked up by many news services, and soon became standard recommendations, despite no data.

There is reason for concern for NSAIDs, as regular NSAID use has been tied to more complications in patients with respiratory tract infections.⁴ I have never been a proponent of regular NSAID use in patients who are infected, because the likelihood of toxicity is elevated in patients who are volume depleted or under physiologic stress. But at this time, there is no evidence on problems with episodic NSAID use in patients with COVID-19.

Another widely disseminated decree was that patients with COVID-19 should not use ACE inhibitors and angiotensin II receptor blockers (ARBs). COVID-19 binds to their target cells through ACE2, which is expressed by epithelial cells of the lung, intestine and kidney. Patients who are treated with ACE inhibitors and ARBs have been shown to have more ACE2 expression.

In a letter to the editor by Fang et al. published in Lancet Respiratory Medicine, the authors raised the question of whether patients might be better served to be switched from ACE inhibitors and ARBs to calcium-channel blockers for the treatment of hypertension.⁵ A small study by Meng et al. looked at outcomes of patients on these drugs who had COVID-19 infection.⁶ They looked at 417 patients admitted to a hospital in China with COVID-19 infection. A total of 42 patients were on medications for hypertension. Group 1 were patients on ACE inhibitors/ARBs (17 patients) and group 2 were patients on other antihypertensives (25 patients). During hospitalization 12 patients (48%) in group 2 were categorized as having severe disease and 1 patient died. In group 1 (the ACE inhibitor/ARB–treated patients) only four (23%) were categorized as having severe disease, and no patients in this group died.

Vaduganathan et al. published a special report in the New England Journal of Medicine strongly arguing the point that “[u]ntil further data are available, we think that [renin-angiotensin-aldosterone system] inhibitors should be continued in patients in otherwise stable condition who are at risk for, being evaluated for, or with COVID-19”.⁷ This position is supported by the American Heart Association, the American College of Cardiology, the American College of Physicians, and 11 other medical organizations.
 

Take-home messages

• Testing isn’t perfect – if you have strong suspicion for COVID-19 disease, retest.
• GI symptoms appear to be common, and rarely may be the only symptoms initially.
• NSAIDs are always risky in really sick patients, but data specific to COVID-19 is lacking.
• ACE inhibitors/ARBs should not be avoided in patients with COVID-19.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he 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 Dr. Paauw at [email protected].

References

1. Long C et al. Diagnosis of the Coronavirus disease (COVID-19): rRT-PCR or CT? Eur J Radiol. 2020 Mar 25;126:108961.

2. Zhou F et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: A retrospective cohort study. Lancet. 2020 Mar 28;395(10229):1054-62.

3. Tian Y et al. Review article: Gastrointestinal features in COVID-19 and the possibility of faecal transmission. Aliment Pharmacol Ther. 2020;00:1–9.

4. Voiriot G et al. Risks related to the use of nonsteroidal anti-inflammatory drugs in community-acquired pneumonia in adult and pediatric patients. J Clin Med. 2019;8:E786.

5. Fang L et al. Are patients with hypertension and diabetes mellitus at increased risk for COVID-19 infection? Lancet Respir Med. 2020 Mar 11. doi:10.1016/S2213-2600(20)30116-8.

6. Meng J et al. Renin-angiotensin system inhibitors improve the clinical outcomes of COVID-19 patients with hypertension. Renin-angiotensin system inhibitors improve the clinical outcomes of COVID-19 patients with hypertension. Emerg Microbes Infect. 2020 Dec;9(1):757-60.

7. Vaduganathan M et al. Renin-angiotensin-aldosterone system inhibitors in patients with COVID-19. N Engl J Med. 2020 Mar 30. doi: 10.1056/NEJMsr2005760.

As we are all facing uncertainties in caring for our patients amid the COVID-19 pandemic, I wanted to share some thoughts I have had and some of my own experiences treating patients during this unsettling time. I practice at the University of Washington, Seattle, in an area that initially had the highest prevalence of COVID-19 cases in the United States.

I have never felt better about being a part of the medical profession because of the altruism, compassion, and deep caring I have seen displayed by my colleagues, our nurses, our staff, and our students. I am proud to have worked with all of them while trying to figure out how to practice in this environment.

These times are really difficult and challenging as we face new problems every day. Last week, we had to send our students home, and we switched to phone and telehealth visits to keep our patients and staff safer.

I have had some unanticipated electronic messages from patients during this time. Two of my patients with major medical problems and very dependent on their medications were stranded internationally and running out of medications. I had the family of an incarcerated patient contact me for a letter because that patient was moved to a part of a jail where all patients with upper respiratory infection symptoms were being housed. My patient has severe immunosuppression, and they were requesting an exception for him.

Another of my patients, who has sarcoidosis and is immunosuppressed, informed me that her daughter who lives with her was diagnosed with COVID-19. After 3 days, this patient told me she had become febrile and short of breath. I instructed her patient to go to a hospital, where she was also diagnosed with COVID-19 and was admitted. This patient was discharged within 24 hours, because the utilization review department did not feel she should be in the hospital.

The lack of beds is forcing physicians to frequently make tough decisions like the one made for this patient. This unfortunate reality raises the question of: “How do you manage a patient you are worried about from his or her home?”

In this particular case, I sent my patient an oxygen saturation monitor. We touched base frequently, and I felt okay as long as her saturations on room air were above 90%. So far, she has done okay.

More recently, I received a message from a patient recently diagnosed with Mycobacterium avium complex. I learned that this patient and her disabled husband’s caregiver refused to continue to provide care to them, because my patient had a cough, which began 2 months prior. In this case, a COVID-19 test was done for the explicit purpose of getting the caregiver to return to work.

So how do we face this?

Burnout had been high before this difficult time. But now physicians are being called to care for more and sicker patients without the necessary personal protective gear. Our physicians have demonstrated strength and commitment to patients in their response to this challenge, but they need help from others, including regulators.

I think a first step that needs to be taken is to decrease the volume of documentation physicians are required to make in this time where we are forced to triage to what is most important and drop what isn’t. How is spending so much time documenting instead of seeing the high volumes of patients who need to be seen a good thing? Documentation to the level that Medicare has required isn’t going to work. In fact, it has never been a good thing and is a big driver of burnout.

Our health care system was broken and badly injured before this crisis, and I think now might be a time when positive changes for the future occur. In fact, COVID-19 has resulted in some temporary changes in medicine that I would like to see outlast this outbreak. The telehealth option is now available, for example, and this kind of care is covered much more broadly by Medicare under the 1135 waiver – this has been needed for years. Being able to conduct regular clinic visits via telehealth without the marked restrictions that were previously in place is a big advance. It is currently in place for this emergency only, but this is the time to start pushing hard to make sure this option will be permanent.

I invite you to help me fight for long-term change. Write a letter to the editor of your local newspaper or blog, share your thoughts on social media, and tweet. (I suggest using #documentationordoctors or, although a bit long, #excessivedocumentationcostslives.) This is an unprecedented time in modern medicine. Traumatic times are when the greatest changes occur. Let’s hope for the better.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He frequently contributes Pearl of the Month and Myth of the Month columns to MDedge, and he serves on the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact Dr. Paauw at [email protected].

As we are all facing uncertainties in caring for our patients amid the COVID-19 pandemic, I wanted to share some thoughts I have had and some of my own experiences treating patients during this unsettling time. I practice at the University of Washington, Seattle, in an area that initially had the highest prevalence of COVID-19 cases in the United States.

I have never felt better about being a part of the medical profession because of the altruism, compassion, and deep caring I have seen displayed by my colleagues, our nurses, our staff, and our students. I am proud to have worked with all of them while trying to figure out how to practice in this environment.

These times are really difficult and challenging as we face new problems every day. Last week, we had to send our students home, and we switched to phone and telehealth visits to keep our patients and staff safer.

I have had some unanticipated electronic messages from patients during this time. Two of my patients with major medical problems and very dependent on their medications were stranded internationally and running out of medications. I had the family of an incarcerated patient contact me for a letter because that patient was moved to a part of a jail where all patients with upper respiratory infection symptoms were being housed. My patient has severe immunosuppression, and they were requesting an exception for him.

Another of my patients, who has sarcoidosis and is immunosuppressed, informed me that her daughter who lives with her was diagnosed with COVID-19. After 3 days, this patient told me she had become febrile and short of breath. I instructed her patient to go to a hospital, where she was also diagnosed with COVID-19 and was admitted. This patient was discharged within 24 hours, because the utilization review department did not feel she should be in the hospital.

The lack of beds is forcing physicians to frequently make tough decisions like the one made for this patient. This unfortunate reality raises the question of: “How do you manage a patient you are worried about from his or her home?”

In this particular case, I sent my patient an oxygen saturation monitor. We touched base frequently, and I felt okay as long as her saturations on room air were above 90%. So far, she has done okay.

More recently, I received a message from a patient recently diagnosed with Mycobacterium avium complex. I learned that this patient and her disabled husband’s caregiver refused to continue to provide care to them, because my patient had a cough, which began 2 months prior. In this case, a COVID-19 test was done for the explicit purpose of getting the caregiver to return to work.

So how do we face this?

Burnout had been high before this difficult time. But now physicians are being called to care for more and sicker patients without the necessary personal protective gear. Our physicians have demonstrated strength and commitment to patients in their response to this challenge, but they need help from others, including regulators.

I think a first step that needs to be taken is to decrease the volume of documentation physicians are required to make in this time where we are forced to triage to what is most important and drop what isn’t. How is spending so much time documenting instead of seeing the high volumes of patients who need to be seen a good thing? Documentation to the level that Medicare has required isn’t going to work. In fact, it has never been a good thing and is a big driver of burnout.

Our health care system was broken and badly injured before this crisis, and I think now might be a time when positive changes for the future occur. In fact, COVID-19 has resulted in some temporary changes in medicine that I would like to see outlast this outbreak. The telehealth option is now available, for example, and this kind of care is covered much more broadly by Medicare under the 1135 waiver – this has been needed for years. Being able to conduct regular clinic visits via telehealth without the marked restrictions that were previously in place is a big advance. It is currently in place for this emergency only, but this is the time to start pushing hard to make sure this option will be permanent.

I invite you to help me fight for long-term change. Write a letter to the editor of your local newspaper or blog, share your thoughts on social media, and tweet. (I suggest using #documentationordoctors or, although a bit long, #excessivedocumentationcostslives.) This is an unprecedented time in modern medicine. Traumatic times are when the greatest changes occur. Let’s hope for the better.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He frequently contributes Pearl of the Month and Myth of the Month columns to MDedge, and he serves on the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact Dr. Paauw at [email protected].

As we are all facing uncertainties in caring for our patients amid the COVID-19 pandemic, I wanted to share some thoughts I have had and some of my own experiences treating patients during this unsettling time. I practice at the University of Washington, Seattle, in an area that initially had the highest prevalence of COVID-19 cases in the United States.

I have never felt better about being a part of the medical profession because of the altruism, compassion, and deep caring I have seen displayed by my colleagues, our nurses, our staff, and our students. I am proud to have worked with all of them while trying to figure out how to practice in this environment.

These times are really difficult and challenging as we face new problems every day. Last week, we had to send our students home, and we switched to phone and telehealth visits to keep our patients and staff safer.

I have had some unanticipated electronic messages from patients during this time. Two of my patients with major medical problems and very dependent on their medications were stranded internationally and running out of medications. I had the family of an incarcerated patient contact me for a letter because that patient was moved to a part of a jail where all patients with upper respiratory infection symptoms were being housed. My patient has severe immunosuppression, and they were requesting an exception for him.

Another of my patients, who has sarcoidosis and is immunosuppressed, informed me that her daughter who lives with her was diagnosed with COVID-19. After 3 days, this patient told me she had become febrile and short of breath. I instructed her patient to go to a hospital, where she was also diagnosed with COVID-19 and was admitted. This patient was discharged within 24 hours, because the utilization review department did not feel she should be in the hospital.

The lack of beds is forcing physicians to frequently make tough decisions like the one made for this patient. This unfortunate reality raises the question of: “How do you manage a patient you are worried about from his or her home?”

In this particular case, I sent my patient an oxygen saturation monitor. We touched base frequently, and I felt okay as long as her saturations on room air were above 90%. So far, she has done okay.

More recently, I received a message from a patient recently diagnosed with Mycobacterium avium complex. I learned that this patient and her disabled husband’s caregiver refused to continue to provide care to them, because my patient had a cough, which began 2 months prior. In this case, a COVID-19 test was done for the explicit purpose of getting the caregiver to return to work.

So how do we face this?

Burnout had been high before this difficult time. But now physicians are being called to care for more and sicker patients without the necessary personal protective gear. Our physicians have demonstrated strength and commitment to patients in their response to this challenge, but they need help from others, including regulators.

I think a first step that needs to be taken is to decrease the volume of documentation physicians are required to make in this time where we are forced to triage to what is most important and drop what isn’t. How is spending so much time documenting instead of seeing the high volumes of patients who need to be seen a good thing? Documentation to the level that Medicare has required isn’t going to work. In fact, it has never been a good thing and is a big driver of burnout.

Our health care system was broken and badly injured before this crisis, and I think now might be a time when positive changes for the future occur. In fact, COVID-19 has resulted in some temporary changes in medicine that I would like to see outlast this outbreak. The telehealth option is now available, for example, and this kind of care is covered much more broadly by Medicare under the 1135 waiver – this has been needed for years. Being able to conduct regular clinic visits via telehealth without the marked restrictions that were previously in place is a big advance. It is currently in place for this emergency only, but this is the time to start pushing hard to make sure this option will be permanent.

I invite you to help me fight for long-term change. Write a letter to the editor of your local newspaper or blog, share your thoughts on social media, and tweet. (I suggest using #documentationordoctors or, although a bit long, #excessivedocumentationcostslives.) This is an unprecedented time in modern medicine. Traumatic times are when the greatest changes occur. Let’s hope for the better.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He frequently contributes Pearl of the Month and Myth of the Month columns to MDedge, and he serves on the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact Dr. Paauw at [email protected].

A 59-year-old man is admitted with abdominal pain. He has a history of pancreatitis. A contrast CT scan is ordered. He reports a history of severe shellfish allergy when the radiology tech checks him in for the procedure. You are paged regarding what to do:

A) Continue with scan as ordered.

B) Switch to MRI scan.

C) Switch to MRI scan with gadolinium.

D) Continue with CT with contrast, give dose of Solu-Medrol.

E) Continue with CT with contrast give IV diphenhydramine.
 

The correct answer here is A, This patient can receive his scan and receive contrast as ordered.

For many years, patients have been asked about shellfish allergy as a proxy for having increased risk when receiving iodine containing contrast. The mistaken thought was that shellfish contains iodine, so allergy to shellfish was likely to portend allergy to iodine.

Allergy to shellfish is caused by individual proteins that are definitely not in iodine-containing contrast.¹ Beaty et al. studied the prevalence of the belief that allergy to shellfish is tied to iodine allergy in a survey given to 231 faculty radiologists and interventional cardiologists.² Almost 70% responded that they inquire about seafood allergy before procedures that require iodine contrast, and 37% reported they would withhold the contrast or premedicate patients if they had a seafood allergy.

In a more recent study, Westermann-Clark and colleagues surveyed 252 health professionals before and after an educational intervention to dispel the myth of shellfish allergy and iodinated contrast reactions.³ Before the intervention, 66% of participants felt it was important to ask about shellfish allergies and 93% felt it was important to ask about iodine allergies; 26% responded that they would withhold iodinated contrast material in patients with a shellfish allergy, and 56% would withhold in patients with an iodine allergy. A total of 62% reported they would premedicate patients with a shellfish allergy and 75% would premedicate patients with an iodine allergy. The numbers declined dramatically after the educational intervention.

Patients who have seafood allergy have a higher rate of reactions to iodinated contrast, but not at a higher rate than do patients with other food allergies or asthma.⁴ Most radiology departments do not screen for other food allergies despite the fact these allergies have the same increased risk as for patients with a seafood/shellfish allergy. These patients are more allergic, and in general, are more likely to have reactions. The American Academy of Allergy, Asthma, and Immunology recommends not routinely ordering low- or iso-osmolar radiocontrast media or pretreating with either antihistamines or steroids in patients with a history of seafood allergy.⁵

• It is unnecessary and unhelpful to ask patients about seafood allergies before ordering radiologic studies involving contrast.
• Iodine allergy does not exist.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Narayan AK et al. Avoiding contrast-enhanced computed tomography scans in patients with shellfish allergies. J Hosp Med. 2016 Jun;11(6):435-7.

2. Beaty AD et al. Seafood allergy and radiocontrast media: Are physicians propagating a myth? Am J Med. 2008 Feb;121(2):158.e1-4.

3. Westermann-Clark E et al. Debunking myths about “allergy” to radiocontrast media in an academic institution. Postgrad Med. 2015 Apr;127(3):295-300.

4. Coakley FV and DM Panicek. Iodine allergy: An oyster without a pearl? AJR Am J Roentgenol. 1997 Oct;169(4):951-2.

5. American Academy of Allergy, Asthma & Immunology recommendations on low- or iso-osmolar radiocontrast media.

6. Schabelman E and M Witting. The relationship of radiocontrast, iodine, and seafood allergies: A medical myth exposed. J Emerg Med. 2010 Nov;39(5):701-7.

7. van Ketel WG and WH van den Berg. Sensitization to povidone-iodine. Dermatol Clin. 1990 Jan;8(1):107-9.

A 59-year-old man is admitted with abdominal pain. He has a history of pancreatitis. A contrast CT scan is ordered. He reports a history of severe shellfish allergy when the radiology tech checks him in for the procedure. You are paged regarding what to do:

A) Continue with scan as ordered.

B) Switch to MRI scan.

C) Switch to MRI scan with gadolinium.

D) Continue with CT with contrast, give dose of Solu-Medrol.

E) Continue with CT with contrast give IV diphenhydramine.
 

The correct answer here is A, This patient can receive his scan and receive contrast as ordered.

For many years, patients have been asked about shellfish allergy as a proxy for having increased risk when receiving iodine containing contrast. The mistaken thought was that shellfish contains iodine, so allergy to shellfish was likely to portend allergy to iodine.

Allergy to shellfish is caused by individual proteins that are definitely not in iodine-containing contrast.¹ Beaty et al. studied the prevalence of the belief that allergy to shellfish is tied to iodine allergy in a survey given to 231 faculty radiologists and interventional cardiologists.² Almost 70% responded that they inquire about seafood allergy before procedures that require iodine contrast, and 37% reported they would withhold the contrast or premedicate patients if they had a seafood allergy.

In a more recent study, Westermann-Clark and colleagues surveyed 252 health professionals before and after an educational intervention to dispel the myth of shellfish allergy and iodinated contrast reactions.³ Before the intervention, 66% of participants felt it was important to ask about shellfish allergies and 93% felt it was important to ask about iodine allergies; 26% responded that they would withhold iodinated contrast material in patients with a shellfish allergy, and 56% would withhold in patients with an iodine allergy. A total of 62% reported they would premedicate patients with a shellfish allergy and 75% would premedicate patients with an iodine allergy. The numbers declined dramatically after the educational intervention.

Patients who have seafood allergy have a higher rate of reactions to iodinated contrast, but not at a higher rate than do patients with other food allergies or asthma.⁴ Most radiology departments do not screen for other food allergies despite the fact these allergies have the same increased risk as for patients with a seafood/shellfish allergy. These patients are more allergic, and in general, are more likely to have reactions. The American Academy of Allergy, Asthma, and Immunology recommends not routinely ordering low- or iso-osmolar radiocontrast media or pretreating with either antihistamines or steroids in patients with a history of seafood allergy.⁵

• It is unnecessary and unhelpful to ask patients about seafood allergies before ordering radiologic studies involving contrast.
• Iodine allergy does not exist.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Narayan AK et al. Avoiding contrast-enhanced computed tomography scans in patients with shellfish allergies. J Hosp Med. 2016 Jun;11(6):435-7.

2. Beaty AD et al. Seafood allergy and radiocontrast media: Are physicians propagating a myth? Am J Med. 2008 Feb;121(2):158.e1-4.

3. Westermann-Clark E et al. Debunking myths about “allergy” to radiocontrast media in an academic institution. Postgrad Med. 2015 Apr;127(3):295-300.

4. Coakley FV and DM Panicek. Iodine allergy: An oyster without a pearl? AJR Am J Roentgenol. 1997 Oct;169(4):951-2.

5. American Academy of Allergy, Asthma & Immunology recommendations on low- or iso-osmolar radiocontrast media.

6. Schabelman E and M Witting. The relationship of radiocontrast, iodine, and seafood allergies: A medical myth exposed. J Emerg Med. 2010 Nov;39(5):701-7.

7. van Ketel WG and WH van den Berg. Sensitization to povidone-iodine. Dermatol Clin. 1990 Jan;8(1):107-9.

A 59-year-old man is admitted with abdominal pain. He has a history of pancreatitis. A contrast CT scan is ordered. He reports a history of severe shellfish allergy when the radiology tech checks him in for the procedure. You are paged regarding what to do:

A) Continue with scan as ordered.

B) Switch to MRI scan.

C) Switch to MRI scan with gadolinium.

D) Continue with CT with contrast, give dose of Solu-Medrol.

E) Continue with CT with contrast give IV diphenhydramine.
 

The correct answer here is A, This patient can receive his scan and receive contrast as ordered.

For many years, patients have been asked about shellfish allergy as a proxy for having increased risk when receiving iodine containing contrast. The mistaken thought was that shellfish contains iodine, so allergy to shellfish was likely to portend allergy to iodine.

Allergy to shellfish is caused by individual proteins that are definitely not in iodine-containing contrast.¹ Beaty et al. studied the prevalence of the belief that allergy to shellfish is tied to iodine allergy in a survey given to 231 faculty radiologists and interventional cardiologists.² Almost 70% responded that they inquire about seafood allergy before procedures that require iodine contrast, and 37% reported they would withhold the contrast or premedicate patients if they had a seafood allergy.

In a more recent study, Westermann-Clark and colleagues surveyed 252 health professionals before and after an educational intervention to dispel the myth of shellfish allergy and iodinated contrast reactions.³ Before the intervention, 66% of participants felt it was important to ask about shellfish allergies and 93% felt it was important to ask about iodine allergies; 26% responded that they would withhold iodinated contrast material in patients with a shellfish allergy, and 56% would withhold in patients with an iodine allergy. A total of 62% reported they would premedicate patients with a shellfish allergy and 75% would premedicate patients with an iodine allergy. The numbers declined dramatically after the educational intervention.

Patients who have seafood allergy have a higher rate of reactions to iodinated contrast, but not at a higher rate than do patients with other food allergies or asthma.⁴ Most radiology departments do not screen for other food allergies despite the fact these allergies have the same increased risk as for patients with a seafood/shellfish allergy. These patients are more allergic, and in general, are more likely to have reactions. The American Academy of Allergy, Asthma, and Immunology recommends not routinely ordering low- or iso-osmolar radiocontrast media or pretreating with either antihistamines or steroids in patients with a history of seafood allergy.⁵

• It is unnecessary and unhelpful to ask patients about seafood allergies before ordering radiologic studies involving contrast.
• Iodine allergy does not exist.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Narayan AK et al. Avoiding contrast-enhanced computed tomography scans in patients with shellfish allergies. J Hosp Med. 2016 Jun;11(6):435-7.

2. Beaty AD et al. Seafood allergy and radiocontrast media: Are physicians propagating a myth? Am J Med. 2008 Feb;121(2):158.e1-4.

3. Westermann-Clark E et al. Debunking myths about “allergy” to radiocontrast media in an academic institution. Postgrad Med. 2015 Apr;127(3):295-300.

4. Coakley FV and DM Panicek. Iodine allergy: An oyster without a pearl? AJR Am J Roentgenol. 1997 Oct;169(4):951-2.

5. American Academy of Allergy, Asthma & Immunology recommendations on low- or iso-osmolar radiocontrast media.

6. Schabelman E and M Witting. The relationship of radiocontrast, iodine, and seafood allergies: A medical myth exposed. J Emerg Med. 2010 Nov;39(5):701-7.

7. van Ketel WG and WH van den Berg. Sensitization to povidone-iodine. Dermatol Clin. 1990 Jan;8(1):107-9.

A 55-year-old woman comes to clinic for follow-up. She reports her family is worried that she isn’t getting enough sleep and is more tired than usual. The patient reports she is sleeping 8 hours a night and wakes up feeling rested, but she has noticed she has been yawning much more frequently than she remembers in the past.

Past medical history: gastroesophageal reflux disease, hypertension, generalized anxiety disorder, hypothyroidism, and osteoporosis. Medications: amlodipine, lansoprazole, irbesartan, escitalopram, levothyroxine, and alendronate. Physical examination: blood pressure 110/70 mm Hg, pulse 60 bpm. Lower extremities: 1+ edema.

What is the likely cause of her increased yawning?

A. Amlodipine.

B. Alendronate.

C. Irbesartan.

D. Escitalopram.

E. Lansoprazole.

The correct answer here is escitalopram. Selective serotonin reuptake inhibitors in general are well tolerated. Given how commonly these drugs are used, however, there are a number of lesser-known side effects that you are likely to see.

In the above case, this patient has yawning caused by her SSRI. Roncero et al. described a case of yawning in a patient on escitalopram that resolved when the dose of escitalopram was reduced.¹ Paroxetine has been reported to cause yawning at both low and high doses.²

In a review of drug-induced yawning, SSRIs as a class were most frequently involved, and sertraline and fluoxetine were implicated in addition to paroxetine.³ The serotonin-norepinephrine reuptake inhibitors duloxetine and venlafaxine have also been associated with yawning.^4,5

Hyperhydrosis has also been linked to SSRIs and SNRIs, and both yawning and hyperhidrosis may occur because of an underlying thermoregulatory dysfunction.⁶

SSRIs have been linked to increased bleeding risk, especially increased risk of upper gastrointestinal hemorrhage. Laporte and colleagues showed an association of SSRI use and risk of bleeding in a meta-analysis of 42 observational studies, with an odds ratio of 1.41 (95% confidence interval, 1.27-1.57; P less than .0001).⁷ The risk of upper gastrointestinal (UGI) bleeding is further increased if patients are also taking NSAIDs.

Anglin et al. looked at 15 case-control studies and 4 cohort studies and found an OR of 1.66 for UGI bleeding with SSRI use, and an OR of 4.25 for UGI bleeding if SSRI use was combined with NSAID use.⁸ The number needed to harm is 3,177 for NSAID use in populations at low risk for GI bleeding, but it is much lower (881) in higher-risk populations.⁸ Make sure to think about patients’ bleeding risks when starting SSRIs.

An issue that comes up frequently is: What is the risk of bleeding in patients on SSRIs who are also on anticoagulants? Dr. Quinn and colleagues looked at the bleeding risk of anticoagulated patients also taking SSRIs in the ROCKET AF trial.⁹ They found 737 patients who received SSRIs and matched them with other patients not on SSRIs in the trial. All patients in the trial were either receiving rivaroxaban or warfarin for stroke prophylaxis. They found no significant increase risk in bleeding in the patients on SSRIs and anticoagulants.
 

Take-home points:

• Yawning and hyperhidrosis are interesting side effects of SSRIs.
• Bleeding risk is increased in patients on SSRIs, especially when combined with NSAIDs.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Neurologia. 2013 Nov-Dec;28(9):589-90.

2. Psychiatry Clin Neurosci. 2006 Apr;60(2):260.

3. Presse Med. 2014 Oct;43(10 Pt 1):1135-6.

4. Prog Neuropsychopharmacol Biol Psychiatry. 2009 Jun 15;33(4):747.

5. Ann Pharmacother. 2011 Oct;45(10):1297-301.

6. Depress Anxiety. 2017 Dec;34(12):1134-46.

7. Pharmacol Res. 2017 Apr;118:19-32.

8. Am J Gastroenterol. 2014 Jun;109(6):811-9.

9. J Am Heart Assoc. 2018 Aug 7;7(15):e008755.

A 55-year-old woman comes to clinic for follow-up. She reports her family is worried that she isn’t getting enough sleep and is more tired than usual. The patient reports she is sleeping 8 hours a night and wakes up feeling rested, but she has noticed she has been yawning much more frequently than she remembers in the past.

Past medical history: gastroesophageal reflux disease, hypertension, generalized anxiety disorder, hypothyroidism, and osteoporosis. Medications: amlodipine, lansoprazole, irbesartan, escitalopram, levothyroxine, and alendronate. Physical examination: blood pressure 110/70 mm Hg, pulse 60 bpm. Lower extremities: 1+ edema.

What is the likely cause of her increased yawning?

A. Amlodipine.

B. Alendronate.

C. Irbesartan.

D. Escitalopram.

E. Lansoprazole.

The correct answer here is escitalopram. Selective serotonin reuptake inhibitors in general are well tolerated. Given how commonly these drugs are used, however, there are a number of lesser-known side effects that you are likely to see.

In the above case, this patient has yawning caused by her SSRI. Roncero et al. described a case of yawning in a patient on escitalopram that resolved when the dose of escitalopram was reduced.¹ Paroxetine has been reported to cause yawning at both low and high doses.²

In a review of drug-induced yawning, SSRIs as a class were most frequently involved, and sertraline and fluoxetine were implicated in addition to paroxetine.³ The serotonin-norepinephrine reuptake inhibitors duloxetine and venlafaxine have also been associated with yawning.^4,5

Hyperhydrosis has also been linked to SSRIs and SNRIs, and both yawning and hyperhidrosis may occur because of an underlying thermoregulatory dysfunction.⁶

SSRIs have been linked to increased bleeding risk, especially increased risk of upper gastrointestinal hemorrhage. Laporte and colleagues showed an association of SSRI use and risk of bleeding in a meta-analysis of 42 observational studies, with an odds ratio of 1.41 (95% confidence interval, 1.27-1.57; P less than .0001).⁷ The risk of upper gastrointestinal (UGI) bleeding is further increased if patients are also taking NSAIDs.

Anglin et al. looked at 15 case-control studies and 4 cohort studies and found an OR of 1.66 for UGI bleeding with SSRI use, and an OR of 4.25 for UGI bleeding if SSRI use was combined with NSAID use.⁸ The number needed to harm is 3,177 for NSAID use in populations at low risk for GI bleeding, but it is much lower (881) in higher-risk populations.⁸ Make sure to think about patients’ bleeding risks when starting SSRIs.

An issue that comes up frequently is: What is the risk of bleeding in patients on SSRIs who are also on anticoagulants? Dr. Quinn and colleagues looked at the bleeding risk of anticoagulated patients also taking SSRIs in the ROCKET AF trial.⁹ They found 737 patients who received SSRIs and matched them with other patients not on SSRIs in the trial. All patients in the trial were either receiving rivaroxaban or warfarin for stroke prophylaxis. They found no significant increase risk in bleeding in the patients on SSRIs and anticoagulants.
 

Take-home points:

• Yawning and hyperhidrosis are interesting side effects of SSRIs.
• Bleeding risk is increased in patients on SSRIs, especially when combined with NSAIDs.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Neurologia. 2013 Nov-Dec;28(9):589-90.

2. Psychiatry Clin Neurosci. 2006 Apr;60(2):260.

3. Presse Med. 2014 Oct;43(10 Pt 1):1135-6.

4. Prog Neuropsychopharmacol Biol Psychiatry. 2009 Jun 15;33(4):747.

5. Ann Pharmacother. 2011 Oct;45(10):1297-301.

6. Depress Anxiety. 2017 Dec;34(12):1134-46.

7. Pharmacol Res. 2017 Apr;118:19-32.

8. Am J Gastroenterol. 2014 Jun;109(6):811-9.

9. J Am Heart Assoc. 2018 Aug 7;7(15):e008755.

A 55-year-old woman comes to clinic for follow-up. She reports her family is worried that she isn’t getting enough sleep and is more tired than usual. The patient reports she is sleeping 8 hours a night and wakes up feeling rested, but she has noticed she has been yawning much more frequently than she remembers in the past.

Past medical history: gastroesophageal reflux disease, hypertension, generalized anxiety disorder, hypothyroidism, and osteoporosis. Medications: amlodipine, lansoprazole, irbesartan, escitalopram, levothyroxine, and alendronate. Physical examination: blood pressure 110/70 mm Hg, pulse 60 bpm. Lower extremities: 1+ edema.

What is the likely cause of her increased yawning?

A. Amlodipine.

B. Alendronate.

C. Irbesartan.

D. Escitalopram.

E. Lansoprazole.

The correct answer here is escitalopram. Selective serotonin reuptake inhibitors in general are well tolerated. Given how commonly these drugs are used, however, there are a number of lesser-known side effects that you are likely to see.

In the above case, this patient has yawning caused by her SSRI. Roncero et al. described a case of yawning in a patient on escitalopram that resolved when the dose of escitalopram was reduced.¹ Paroxetine has been reported to cause yawning at both low and high doses.²

In a review of drug-induced yawning, SSRIs as a class were most frequently involved, and sertraline and fluoxetine were implicated in addition to paroxetine.³ The serotonin-norepinephrine reuptake inhibitors duloxetine and venlafaxine have also been associated with yawning.^4,5

Hyperhydrosis has also been linked to SSRIs and SNRIs, and both yawning and hyperhidrosis may occur because of an underlying thermoregulatory dysfunction.⁶

SSRIs have been linked to increased bleeding risk, especially increased risk of upper gastrointestinal hemorrhage. Laporte and colleagues showed an association of SSRI use and risk of bleeding in a meta-analysis of 42 observational studies, with an odds ratio of 1.41 (95% confidence interval, 1.27-1.57; P less than .0001).⁷ The risk of upper gastrointestinal (UGI) bleeding is further increased if patients are also taking NSAIDs.

Anglin et al. looked at 15 case-control studies and 4 cohort studies and found an OR of 1.66 for UGI bleeding with SSRI use, and an OR of 4.25 for UGI bleeding if SSRI use was combined with NSAID use.⁸ The number needed to harm is 3,177 for NSAID use in populations at low risk for GI bleeding, but it is much lower (881) in higher-risk populations.⁸ Make sure to think about patients’ bleeding risks when starting SSRIs.

An issue that comes up frequently is: What is the risk of bleeding in patients on SSRIs who are also on anticoagulants? Dr. Quinn and colleagues looked at the bleeding risk of anticoagulated patients also taking SSRIs in the ROCKET AF trial.⁹ They found 737 patients who received SSRIs and matched them with other patients not on SSRIs in the trial. All patients in the trial were either receiving rivaroxaban or warfarin for stroke prophylaxis. They found no significant increase risk in bleeding in the patients on SSRIs and anticoagulants.
 

Take-home points:

• Yawning and hyperhidrosis are interesting side effects of SSRIs.
• Bleeding risk is increased in patients on SSRIs, especially when combined with NSAIDs.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Neurologia. 2013 Nov-Dec;28(9):589-90.

2. Psychiatry Clin Neurosci. 2006 Apr;60(2):260.

3. Presse Med. 2014 Oct;43(10 Pt 1):1135-6.

4. Prog Neuropsychopharmacol Biol Psychiatry. 2009 Jun 15;33(4):747.

5. Ann Pharmacother. 2011 Oct;45(10):1297-301.

6. Depress Anxiety. 2017 Dec;34(12):1134-46.

7. Pharmacol Res. 2017 Apr;118:19-32.

8. Am J Gastroenterol. 2014 Jun;109(6):811-9.

9. J Am Heart Assoc. 2018 Aug 7;7(15):e008755.

I practice in Seattle, where many of my patients are interested in natural treatment options. I am always puzzled that so many people assume that natural treatment options would be safer than prescription medications. Tsunamis, wildfires, flooding, and earthquakes are all natural and are deadly. There are certainly many natural poisons. There are a number of natural treatments that are very helpful, and recommending them are an important part of my practice. I want to share a few with you.

A useful vein pursuit?

Case: A 60-year-old woman presents to clinic with increasing pain in her left leg. She had a deep vein thrombosis in her left leg 2 years ago, which involved a large portion of her superficial femoral vein. She has noticed edema over the past few weeks, and pain has been more severe over the past 3 months. On exam, varicosities on left lower extremity with grade 2+ edema. Duplex of the lower extremity does not show deep vein thrombosis, but does show a great deal of venous valvular incompetence. She has tried compression stockings for the past 2 weeks. What is the best treatment option?

A) Turmeric

B) Amitriptyline

C) Vitamin B12

D) Horse chestnut

The treatment option with positive data for this problem is horse chestnut. What is horse chestnut? Horse chestnut is a kind of tree, and the seed extract contains aescin which is believed to be the active ingredient. Diehm et al. studied horse chestnut seed extract (HCSE), compared with compression stockings and placebo for edema from chronic venous insufficiency in a study of 240 patients.¹ Lower-leg volume decreased by 43 mL with HCSE, 46 mL with compression stockings, and increased by 9 mL with placebo (P less than .005 for HCSE and P less than .002 for compression). In a Cochrane review, HCSE was considered efficacious and safe for the short-term therapy for chronic venous insufficiency.² Studies have shown both an improvement in pain as well as swelling in patients with chronic venous insufficiency.

The question of UTIs

Probably the most popular natural treatment for prevention and treatment of urinary tract infections (UTIs) in women is cranberry juice (or cranberry extract). Unfortunately, there is little evidence that this treatment is helpful. In a Cochrane analysis, the conclusion was, based on current evidence, cranberry juice cannot currently be recommended for the prevention of UTIs.³ A natural product that appears to be more promising is the sugar D-mannose. Kranjčec et al. studied 308 women with acute UTI who had a history of recurrent UTI.⁴ All the women were treated for their symptomatic infection with ciprofloxacin (500 mg twice daily for 1 week). The women were allocated equally to three groups for 6 months: D-mannose 2 g daily, nitrofurantoin 50 mg daily, or no prophylaxis. About 60% of the women who received no prophylaxis had a UTI during the study period, compared with 20% in the nitrofurantoin group and 15% in the D-mannose group. The relative risk for D-mannose, compared with no prophylaxis, was 0.24 and for nitrofurantoin was 0.34 (P less than .0001), compared with no prophylaxis.

Made for migraines?

Migraine prophylaxis is challenging because all medications that are commonly used have side effects that often limit patient adherence. Tricyclic antidepressants (dry mouth, dizziness and weight gain), beta-blockers (fatigue, decreased exercise tolerance), valproate (weight gain and fatigue), and topiramate (parasthesias and mental slowing) all have troubling side effects. Riboflavin is a vitamin with evidence of effectiveness for migraine prophylaxis. It is extremely well tolerated. In a recent study in children with migraines, Talebian et al. studied 90 children with migraines who were randomized to three groups (200 mg of riboflavin a day, 100 mg of riboflavin a day, or placebo) after observation during a 1-month baseline period.⁵ There was a significant reduction in migraine frequency and duration in patients receiving 200 mg of riboflavin daily, compared with placebo. Rahimdel et al. published an interesting study comparing high-dose riboflavin with valproate for migraine prophylaxis. A total of 90 patients were randomized to receive 400 mg of riboflavin or 500 mg of valproate over a 12-month study.⁶ Both treatments resulted in marked reduction in frequency, duration, and severity of migraines (not statistically significantly different from each other). The reduction in migraine frequency for the riboflavin group was from 9.2 headache days per month to 2.4. The American Academy of Neurology rates the level of evidence for riboflavin as B.

Pearl

Horse chestnut, D-mannose, and riboflavin are safe alternative therapies that can be helpful for several common problems we see frequently in primary care.

References

1. Diehm C et al. Lancet. 1996;347(8997):292-4.

2. Pittler MH, Ernst E. Cochrane Database Syst Rev. 2012 Nov 14;11:CD003230.

3. Jepson RG et al. Cochrane Database Syst Rev. 2012;10:CD001321.

4. Kranjčec B et al. World J Urol. 2014 Feb;32(1):79-84.

5. Talebian A et al. Electron Physician. Feb 25;10(2):6279-85.

6. Rahimdel A et al. Electron Physician. 2015 Oct 19;7(6):1344-8.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

I practice in Seattle, where many of my patients are interested in natural treatment options. I am always puzzled that so many people assume that natural treatment options would be safer than prescription medications. Tsunamis, wildfires, flooding, and earthquakes are all natural and are deadly. There are certainly many natural poisons. There are a number of natural treatments that are very helpful, and recommending them are an important part of my practice. I want to share a few with you.

A useful vein pursuit?

Case: A 60-year-old woman presents to clinic with increasing pain in her left leg. She had a deep vein thrombosis in her left leg 2 years ago, which involved a large portion of her superficial femoral vein. She has noticed edema over the past few weeks, and pain has been more severe over the past 3 months. On exam, varicosities on left lower extremity with grade 2+ edema. Duplex of the lower extremity does not show deep vein thrombosis, but does show a great deal of venous valvular incompetence. She has tried compression stockings for the past 2 weeks. What is the best treatment option?

A) Turmeric

B) Amitriptyline

C) Vitamin B12

D) Horse chestnut

The treatment option with positive data for this problem is horse chestnut. What is horse chestnut? Horse chestnut is a kind of tree, and the seed extract contains aescin which is believed to be the active ingredient. Diehm et al. studied horse chestnut seed extract (HCSE), compared with compression stockings and placebo for edema from chronic venous insufficiency in a study of 240 patients.¹ Lower-leg volume decreased by 43 mL with HCSE, 46 mL with compression stockings, and increased by 9 mL with placebo (P less than .005 for HCSE and P less than .002 for compression). In a Cochrane review, HCSE was considered efficacious and safe for the short-term therapy for chronic venous insufficiency.² Studies have shown both an improvement in pain as well as swelling in patients with chronic venous insufficiency.

The question of UTIs

Probably the most popular natural treatment for prevention and treatment of urinary tract infections (UTIs) in women is cranberry juice (or cranberry extract). Unfortunately, there is little evidence that this treatment is helpful. In a Cochrane analysis, the conclusion was, based on current evidence, cranberry juice cannot currently be recommended for the prevention of UTIs.³ A natural product that appears to be more promising is the sugar D-mannose. Kranjčec et al. studied 308 women with acute UTI who had a history of recurrent UTI.⁴ All the women were treated for their symptomatic infection with ciprofloxacin (500 mg twice daily for 1 week). The women were allocated equally to three groups for 6 months: D-mannose 2 g daily, nitrofurantoin 50 mg daily, or no prophylaxis. About 60% of the women who received no prophylaxis had a UTI during the study period, compared with 20% in the nitrofurantoin group and 15% in the D-mannose group. The relative risk for D-mannose, compared with no prophylaxis, was 0.24 and for nitrofurantoin was 0.34 (P less than .0001), compared with no prophylaxis.

Made for migraines?

Migraine prophylaxis is challenging because all medications that are commonly used have side effects that often limit patient adherence. Tricyclic antidepressants (dry mouth, dizziness and weight gain), beta-blockers (fatigue, decreased exercise tolerance), valproate (weight gain and fatigue), and topiramate (parasthesias and mental slowing) all have troubling side effects. Riboflavin is a vitamin with evidence of effectiveness for migraine prophylaxis. It is extremely well tolerated. In a recent study in children with migraines, Talebian et al. studied 90 children with migraines who were randomized to three groups (200 mg of riboflavin a day, 100 mg of riboflavin a day, or placebo) after observation during a 1-month baseline period.⁵ There was a significant reduction in migraine frequency and duration in patients receiving 200 mg of riboflavin daily, compared with placebo. Rahimdel et al. published an interesting study comparing high-dose riboflavin with valproate for migraine prophylaxis. A total of 90 patients were randomized to receive 400 mg of riboflavin or 500 mg of valproate over a 12-month study.⁶ Both treatments resulted in marked reduction in frequency, duration, and severity of migraines (not statistically significantly different from each other). The reduction in migraine frequency for the riboflavin group was from 9.2 headache days per month to 2.4. The American Academy of Neurology rates the level of evidence for riboflavin as B.

Pearl

Horse chestnut, D-mannose, and riboflavin are safe alternative therapies that can be helpful for several common problems we see frequently in primary care.

References

1. Diehm C et al. Lancet. 1996;347(8997):292-4.

2. Pittler MH, Ernst E. Cochrane Database Syst Rev. 2012 Nov 14;11:CD003230.

3. Jepson RG et al. Cochrane Database Syst Rev. 2012;10:CD001321.

4. Kranjčec B et al. World J Urol. 2014 Feb;32(1):79-84.

5. Talebian A et al. Electron Physician. Feb 25;10(2):6279-85.

6. Rahimdel A et al. Electron Physician. 2015 Oct 19;7(6):1344-8.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

I practice in Seattle, where many of my patients are interested in natural treatment options. I am always puzzled that so many people assume that natural treatment options would be safer than prescription medications. Tsunamis, wildfires, flooding, and earthquakes are all natural and are deadly. There are certainly many natural poisons. There are a number of natural treatments that are very helpful, and recommending them are an important part of my practice. I want to share a few with you.

A useful vein pursuit?

Case: A 60-year-old woman presents to clinic with increasing pain in her left leg. She had a deep vein thrombosis in her left leg 2 years ago, which involved a large portion of her superficial femoral vein. She has noticed edema over the past few weeks, and pain has been more severe over the past 3 months. On exam, varicosities on left lower extremity with grade 2+ edema. Duplex of the lower extremity does not show deep vein thrombosis, but does show a great deal of venous valvular incompetence. She has tried compression stockings for the past 2 weeks. What is the best treatment option?

A) Turmeric

B) Amitriptyline

C) Vitamin B12

D) Horse chestnut

The treatment option with positive data for this problem is horse chestnut. What is horse chestnut? Horse chestnut is a kind of tree, and the seed extract contains aescin which is believed to be the active ingredient. Diehm et al. studied horse chestnut seed extract (HCSE), compared with compression stockings and placebo for edema from chronic venous insufficiency in a study of 240 patients.¹ Lower-leg volume decreased by 43 mL with HCSE, 46 mL with compression stockings, and increased by 9 mL with placebo (P less than .005 for HCSE and P less than .002 for compression). In a Cochrane review, HCSE was considered efficacious and safe for the short-term therapy for chronic venous insufficiency.² Studies have shown both an improvement in pain as well as swelling in patients with chronic venous insufficiency.

The question of UTIs

Probably the most popular natural treatment for prevention and treatment of urinary tract infections (UTIs) in women is cranberry juice (or cranberry extract). Unfortunately, there is little evidence that this treatment is helpful. In a Cochrane analysis, the conclusion was, based on current evidence, cranberry juice cannot currently be recommended for the prevention of UTIs.³ A natural product that appears to be more promising is the sugar D-mannose. Kranjčec et al. studied 308 women with acute UTI who had a history of recurrent UTI.⁴ All the women were treated for their symptomatic infection with ciprofloxacin (500 mg twice daily for 1 week). The women were allocated equally to three groups for 6 months: D-mannose 2 g daily, nitrofurantoin 50 mg daily, or no prophylaxis. About 60% of the women who received no prophylaxis had a UTI during the study period, compared with 20% in the nitrofurantoin group and 15% in the D-mannose group. The relative risk for D-mannose, compared with no prophylaxis, was 0.24 and for nitrofurantoin was 0.34 (P less than .0001), compared with no prophylaxis.

Made for migraines?

Migraine prophylaxis is challenging because all medications that are commonly used have side effects that often limit patient adherence. Tricyclic antidepressants (dry mouth, dizziness and weight gain), beta-blockers (fatigue, decreased exercise tolerance), valproate (weight gain and fatigue), and topiramate (parasthesias and mental slowing) all have troubling side effects. Riboflavin is a vitamin with evidence of effectiveness for migraine prophylaxis. It is extremely well tolerated. In a recent study in children with migraines, Talebian et al. studied 90 children with migraines who were randomized to three groups (200 mg of riboflavin a day, 100 mg of riboflavin a day, or placebo) after observation during a 1-month baseline period.⁵ There was a significant reduction in migraine frequency and duration in patients receiving 200 mg of riboflavin daily, compared with placebo. Rahimdel et al. published an interesting study comparing high-dose riboflavin with valproate for migraine prophylaxis. A total of 90 patients were randomized to receive 400 mg of riboflavin or 500 mg of valproate over a 12-month study.⁶ Both treatments resulted in marked reduction in frequency, duration, and severity of migraines (not statistically significantly different from each other). The reduction in migraine frequency for the riboflavin group was from 9.2 headache days per month to 2.4. The American Academy of Neurology rates the level of evidence for riboflavin as B.

Pearl

Horse chestnut, D-mannose, and riboflavin are safe alternative therapies that can be helpful for several common problems we see frequently in primary care.

References

1. Diehm C et al. Lancet. 1996;347(8997):292-4.

2. Pittler MH, Ernst E. Cochrane Database Syst Rev. 2012 Nov 14;11:CD003230.

3. Jepson RG et al. Cochrane Database Syst Rev. 2012;10:CD001321.

4. Kranjčec B et al. World J Urol. 2014 Feb;32(1):79-84.

5. Talebian A et al. Electron Physician. Feb 25;10(2):6279-85.

6. Rahimdel A et al. Electron Physician. 2015 Oct 19;7(6):1344-8.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

An 88-year-old man with hypertension, chronic obstructive pulmonary disease, and atrial fibrillation presents with severe cerebral palsy and is diagnosed with a non–ST-elevation MI. He is found to have 90% left anterior descending artery occlusion and receives a drug-eluting stent. His current medications include warfarin, tiotropium, amlodipine, aspirin, and lisinopril. What anticoagulant therapy should he receive?

A) Clopidogrel, warfarin, and aspirin

B) Clopidogrel and aspirin

C) Clopidogrel and warfarin

D) Warfarin

E) Warfarin and aspirin

This issue comes up frequently with our patients with atrial fibrillation who are on anticoagulation, then have a coronary event and have a stent placed. What is the best approach to anticoagulation? I think for this patient adding clopidogrel, continuing warfarin, and stopping aspirin would be the best of the options presented.

Elderly patients have a higher risk of bleeding. They also have a greater chance of accumulating cardiovascular disease (atrial fibrillation, cardiac allograft vasculopathy, and valvular disease) that requires anticoagulation. Dewilde et al. studied the difference in bleeding risk in patients who were on oral anticoagulants who then underwent a percutaneous coronary intervention.¹ Patients were assigned clopidogrel alone or clopidogrel plus aspirin in addition to their oral anticoagulant (warfarin). There was a significant increase in all-cause mortality in the patients who received clopidogrel plus aspirin (P = .027), and no significant difference in cardiac mortality between the two groups. There was a much higher risk of bleeding (44.4%) in the patients receiving triple therapy, compared with the double-therapy group (19.4%; P less than .0001).

In a large meta-analysis of over 7,000 patients by D’Ascenzo et al., there was no difference in thrombotic risk between double and triple therapy, and lower bleeding risk in patients who received double therapy.²

In a recently published article, Lopes et al. looked at the benefits and risks of antithrombotic therapy after acute coronary syndrome or percutaneous coronary intervention in patients with atrial fibrillation.³ The study included 4,614 patients, all of whom received a P2Y12 inhibitor. In addition, they received either apixaban or warfarin, and either aspirin or placebo. The patients who received apixaban had a lower risk of bleeding than those receiving warfarin (P less than .001), and those receiving aspirin had a higher risk than those receiving placebo (hazard ratio, 1.89; P less than .001). Patients using the combination of apixaban plus placebo had the lowest event rate per 100 years (16.8), followed by warfarin plus placebo (26.7), then apixaban plus aspirin (33.6), with warfarin plus aspirin having the highest event rate (49.1). The conclusion for the study was that regimens with apixaban without aspirin had less bleeding and hospitalizations without increased ischemic events, compared with regimens of warfarin with or without aspirin.

I think it is best to avoid aspirin in patients who are anticoagulated with warfarin, and likely this extends to Xa inhibitors as well.

Pearl: Avoid using triple anticoagulant therapy by eliminating aspirin.

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. Contact Dr. Paauw at [email protected].

References

1. Dewilde WJ et al. Use of clopidogrel with or without aspirin in patients taking oral anticoagulant therapy and undergoing percutaneous coronary intervention: An open-label, randomised, controlled trial. Lancet. 2013 Mar 30;381(9872):1107-15.

2. D’Ascenzo F et al. Meta-analysis of randomized controlled trials and adjusted observational results of use of clopidogrel, aspirin, and oral anticoagulants in patients undergoing percutaneous coronary intervention. Am J Cardiol. 2015 May 1;115(9):1185-93.

3. Lopes RD et al. Antithrombotic therapy after acute coronary syndrome or PCI in atrial fibrillation. N Engl J Med. 2019 Apr 18;380(16):1509-24.

An 88-year-old man with hypertension, chronic obstructive pulmonary disease, and atrial fibrillation presents with severe cerebral palsy and is diagnosed with a non–ST-elevation MI. He is found to have 90% left anterior descending artery occlusion and receives a drug-eluting stent. His current medications include warfarin, tiotropium, amlodipine, aspirin, and lisinopril. What anticoagulant therapy should he receive?

A) Clopidogrel, warfarin, and aspirin

B) Clopidogrel and aspirin

C) Clopidogrel and warfarin

D) Warfarin

E) Warfarin and aspirin

This issue comes up frequently with our patients with atrial fibrillation who are on anticoagulation, then have a coronary event and have a stent placed. What is the best approach to anticoagulation? I think for this patient adding clopidogrel, continuing warfarin, and stopping aspirin would be the best of the options presented.

Elderly patients have a higher risk of bleeding. They also have a greater chance of accumulating cardiovascular disease (atrial fibrillation, cardiac allograft vasculopathy, and valvular disease) that requires anticoagulation. Dewilde et al. studied the difference in bleeding risk in patients who were on oral anticoagulants who then underwent a percutaneous coronary intervention.¹ Patients were assigned clopidogrel alone or clopidogrel plus aspirin in addition to their oral anticoagulant (warfarin). There was a significant increase in all-cause mortality in the patients who received clopidogrel plus aspirin (P = .027), and no significant difference in cardiac mortality between the two groups. There was a much higher risk of bleeding (44.4%) in the patients receiving triple therapy, compared with the double-therapy group (19.4%; P less than .0001).

In a large meta-analysis of over 7,000 patients by D’Ascenzo et al., there was no difference in thrombotic risk between double and triple therapy, and lower bleeding risk in patients who received double therapy.²

In a recently published article, Lopes et al. looked at the benefits and risks of antithrombotic therapy after acute coronary syndrome or percutaneous coronary intervention in patients with atrial fibrillation.³ The study included 4,614 patients, all of whom received a P2Y12 inhibitor. In addition, they received either apixaban or warfarin, and either aspirin or placebo. The patients who received apixaban had a lower risk of bleeding than those receiving warfarin (P less than .001), and those receiving aspirin had a higher risk than those receiving placebo (hazard ratio, 1.89; P less than .001). Patients using the combination of apixaban plus placebo had the lowest event rate per 100 years (16.8), followed by warfarin plus placebo (26.7), then apixaban plus aspirin (33.6), with warfarin plus aspirin having the highest event rate (49.1). The conclusion for the study was that regimens with apixaban without aspirin had less bleeding and hospitalizations without increased ischemic events, compared with regimens of warfarin with or without aspirin.

I think it is best to avoid aspirin in patients who are anticoagulated with warfarin, and likely this extends to Xa inhibitors as well.

Pearl: Avoid using triple anticoagulant therapy by eliminating aspirin.

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. Contact Dr. Paauw at [email protected].

References

1. Dewilde WJ et al. Use of clopidogrel with or without aspirin in patients taking oral anticoagulant therapy and undergoing percutaneous coronary intervention: An open-label, randomised, controlled trial. Lancet. 2013 Mar 30;381(9872):1107-15.

2. D’Ascenzo F et al. Meta-analysis of randomized controlled trials and adjusted observational results of use of clopidogrel, aspirin, and oral anticoagulants in patients undergoing percutaneous coronary intervention. Am J Cardiol. 2015 May 1;115(9):1185-93.

3. Lopes RD et al. Antithrombotic therapy after acute coronary syndrome or PCI in atrial fibrillation. N Engl J Med. 2019 Apr 18;380(16):1509-24.

An 88-year-old man with hypertension, chronic obstructive pulmonary disease, and atrial fibrillation presents with severe cerebral palsy and is diagnosed with a non–ST-elevation MI. He is found to have 90% left anterior descending artery occlusion and receives a drug-eluting stent. His current medications include warfarin, tiotropium, amlodipine, aspirin, and lisinopril. What anticoagulant therapy should he receive?

A) Clopidogrel, warfarin, and aspirin

B) Clopidogrel and aspirin

C) Clopidogrel and warfarin

D) Warfarin

E) Warfarin and aspirin

This issue comes up frequently with our patients with atrial fibrillation who are on anticoagulation, then have a coronary event and have a stent placed. What is the best approach to anticoagulation? I think for this patient adding clopidogrel, continuing warfarin, and stopping aspirin would be the best of the options presented.

Elderly patients have a higher risk of bleeding. They also have a greater chance of accumulating cardiovascular disease (atrial fibrillation, cardiac allograft vasculopathy, and valvular disease) that requires anticoagulation. Dewilde et al. studied the difference in bleeding risk in patients who were on oral anticoagulants who then underwent a percutaneous coronary intervention.¹ Patients were assigned clopidogrel alone or clopidogrel plus aspirin in addition to their oral anticoagulant (warfarin). There was a significant increase in all-cause mortality in the patients who received clopidogrel plus aspirin (P = .027), and no significant difference in cardiac mortality between the two groups. There was a much higher risk of bleeding (44.4%) in the patients receiving triple therapy, compared with the double-therapy group (19.4%; P less than .0001).

In a large meta-analysis of over 7,000 patients by D’Ascenzo et al., there was no difference in thrombotic risk between double and triple therapy, and lower bleeding risk in patients who received double therapy.²

In a recently published article, Lopes et al. looked at the benefits and risks of antithrombotic therapy after acute coronary syndrome or percutaneous coronary intervention in patients with atrial fibrillation.³ The study included 4,614 patients, all of whom received a P2Y12 inhibitor. In addition, they received either apixaban or warfarin, and either aspirin or placebo. The patients who received apixaban had a lower risk of bleeding than those receiving warfarin (P less than .001), and those receiving aspirin had a higher risk than those receiving placebo (hazard ratio, 1.89; P less than .001). Patients using the combination of apixaban plus placebo had the lowest event rate per 100 years (16.8), followed by warfarin plus placebo (26.7), then apixaban plus aspirin (33.6), with warfarin plus aspirin having the highest event rate (49.1). The conclusion for the study was that regimens with apixaban without aspirin had less bleeding and hospitalizations without increased ischemic events, compared with regimens of warfarin with or without aspirin.

I think it is best to avoid aspirin in patients who are anticoagulated with warfarin, and likely this extends to Xa inhibitors as well.

Pearl: Avoid using triple anticoagulant therapy by eliminating aspirin.

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. Contact Dr. Paauw at [email protected].

References

1. Dewilde WJ et al. Use of clopidogrel with or without aspirin in patients taking oral anticoagulant therapy and undergoing percutaneous coronary intervention: An open-label, randomised, controlled trial. Lancet. 2013 Mar 30;381(9872):1107-15.

2. D’Ascenzo F et al. Meta-analysis of randomized controlled trials and adjusted observational results of use of clopidogrel, aspirin, and oral anticoagulants in patients undergoing percutaneous coronary intervention. Am J Cardiol. 2015 May 1;115(9):1185-93.

3. Lopes RD et al. Antithrombotic therapy after acute coronary syndrome or PCI in atrial fibrillation. N Engl J Med. 2019 Apr 18;380(16):1509-24.

A 50-year-old woman returns for routine follow-up. She has a 15-year history of hypothyroidism, pernicious anemia, and celiac disease. She has had some recent abdominal pain, but no changes in her bowel patterns, and she has not experienced any problems with chest pain, palpitations, or weakness recently. The only medication she is taking is levothyroxine 125 mcg. She has reported no recent weight loss, her blood pressure is 100/60 mm Hg, pulse is 66 beats per minute, temperature is 36.8 degrees Celsius, body mass index is 20, and she does not have a neck goiter. Her cardiac exam was normal and her neurological exam revealed no tremor. Her lab for thyroid-stimulating hormone (TSH) was less than 0.03, and her lab for free thyroxine (FT4) was 2.2, while her TSH level had been 1.4 a year ago. Her levothyroxine dose was decreased to 100 mcg/day, and her repeat lab for TSH, which occurred 12 weeks later, was still less than 0.03. What is the best explanation for why this patient’s labs look like hyperthyroidism, but this patient clinically does not appear to have hyperthyroidism?

A) She was initially given too much levothyroxine; her TSH response is lagging to dose reduction.

B) She has Graves’ disease.

C) She has acute thyroiditis.

D) She is taking extra thyroid hormone.

E) She is taking biotin.

This patient has a history that includes multiple autoimmune diseases including hypothyroidism. It would be extremely unlikely that she would develop Graves' disease or develop acute thyroiditis in the setting of a gland that has been underfunctioning for years. She has no symptoms suggesting that she has hyperthyroidism, which makes taking more thyroid hormone than she is reporting less likely, although this could be possible. The TSH response can lag after dose adjustments of thyroid, but usually a 6-week interval is adequate. This patient’s testing was done 12 weeks after dose reduction making this very unlikely.

The cause for the labs that look like hyperthyroidism in this patient who appears clinically euthyroid is that she is taking biotin. Biotin (vitamin B₇) has become a very popular supplement in the past few years for thin hair, brittle nails, and fatigue. The RDA for biotin is 30 mcg. It is widely available in high doses – 5,000-10,000 mcg – which are common doses for supplements.

Biotin has been used extensively as a key component of immunoassays. Streptavidin, a protein produced by the bacteria Streptomyces avidinii, binds biotin with an extremely high affinity, and this binding is utilized in a number of immunoassays, including the assays for thyroid hormone and TSH.¹

Pearls

Consider biotin supplement use when you have patients whose labs look like hyperthyroidism, but clinically do not appear to be hyperthyroid.

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. Contact Dr. Paauw at [email protected].

References

1. Charles S, Agrawal N, and Blum M. Erroneous thyroid diagnosis due to over-the-counter biotin. Nutrition 2019;57:257-8.

2. Elston MS et al. Factitious Graves’ disease due to a biotin immunoassay interference – a case and review of the literature. J Clin Endocrinol Metab 2016;101:3251-5.

3. Barbesino G. Misdiagnosis of Graves ’disease with apparent severe hyperthyroidism in a patient taking biotin megadoses. Thyroid 2016;26(6):860-3.

4. Katzman et al. Prevalence of biotin supplement usage in outpatients and plasma biotin concentrations in patients presenting to the emergency department. Clin Biochem. 2018 Sep;60:11-16.

5. “The FDA Warns that Biotin May Interfere with Lab Tests: FDA Safety Communication,” Nov. 28, 2017.

6. Trambas et al. Characterization of the scope and magnitude of biotin interference in susceptible Roche Elecsys competitive and sandwich immunoassays. Ann Clin Biochem. 2018 Mar;55(2):205-15.

7. Frame IJ et al. Susceptibility of cardiac troponin assays to biotin interference. Am J Clin Pathol. 2019 Apr 2;151(5):486-93.

A 50-year-old woman returns for routine follow-up. She has a 15-year history of hypothyroidism, pernicious anemia, and celiac disease. She has had some recent abdominal pain, but no changes in her bowel patterns, and she has not experienced any problems with chest pain, palpitations, or weakness recently. The only medication she is taking is levothyroxine 125 mcg. She has reported no recent weight loss, her blood pressure is 100/60 mm Hg, pulse is 66 beats per minute, temperature is 36.8 degrees Celsius, body mass index is 20, and she does not have a neck goiter. Her cardiac exam was normal and her neurological exam revealed no tremor. Her lab for thyroid-stimulating hormone (TSH) was less than 0.03, and her lab for free thyroxine (FT4) was 2.2, while her TSH level had been 1.4 a year ago. Her levothyroxine dose was decreased to 100 mcg/day, and her repeat lab for TSH, which occurred 12 weeks later, was still less than 0.03. What is the best explanation for why this patient’s labs look like hyperthyroidism, but this patient clinically does not appear to have hyperthyroidism?

A) She was initially given too much levothyroxine; her TSH response is lagging to dose reduction.

B) She has Graves’ disease.

C) She has acute thyroiditis.

D) She is taking extra thyroid hormone.

E) She is taking biotin.

This patient has a history that includes multiple autoimmune diseases including hypothyroidism. It would be extremely unlikely that she would develop Graves' disease or develop acute thyroiditis in the setting of a gland that has been underfunctioning for years. She has no symptoms suggesting that she has hyperthyroidism, which makes taking more thyroid hormone than she is reporting less likely, although this could be possible. The TSH response can lag after dose adjustments of thyroid, but usually a 6-week interval is adequate. This patient’s testing was done 12 weeks after dose reduction making this very unlikely.

The cause for the labs that look like hyperthyroidism in this patient who appears clinically euthyroid is that she is taking biotin. Biotin (vitamin B₇) has become a very popular supplement in the past few years for thin hair, brittle nails, and fatigue. The RDA for biotin is 30 mcg. It is widely available in high doses – 5,000-10,000 mcg – which are common doses for supplements.

Biotin has been used extensively as a key component of immunoassays. Streptavidin, a protein produced by the bacteria Streptomyces avidinii, binds biotin with an extremely high affinity, and this binding is utilized in a number of immunoassays, including the assays for thyroid hormone and TSH.¹

Pearls

Consider biotin supplement use when you have patients whose labs look like hyperthyroidism, but clinically do not appear to be hyperthyroid.

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. Contact Dr. Paauw at [email protected].

References

1. Charles S, Agrawal N, and Blum M. Erroneous thyroid diagnosis due to over-the-counter biotin. Nutrition 2019;57:257-8.

2. Elston MS et al. Factitious Graves’ disease due to a biotin immunoassay interference – a case and review of the literature. J Clin Endocrinol Metab 2016;101:3251-5.

3. Barbesino G. Misdiagnosis of Graves ’disease with apparent severe hyperthyroidism in a patient taking biotin megadoses. Thyroid 2016;26(6):860-3.

4. Katzman et al. Prevalence of biotin supplement usage in outpatients and plasma biotin concentrations in patients presenting to the emergency department. Clin Biochem. 2018 Sep;60:11-16.

5. “The FDA Warns that Biotin May Interfere with Lab Tests: FDA Safety Communication,” Nov. 28, 2017.

6. Trambas et al. Characterization of the scope and magnitude of biotin interference in susceptible Roche Elecsys competitive and sandwich immunoassays. Ann Clin Biochem. 2018 Mar;55(2):205-15.

7. Frame IJ et al. Susceptibility of cardiac troponin assays to biotin interference. Am J Clin Pathol. 2019 Apr 2;151(5):486-93.

A 50-year-old woman returns for routine follow-up. She has a 15-year history of hypothyroidism, pernicious anemia, and celiac disease. She has had some recent abdominal pain, but no changes in her bowel patterns, and she has not experienced any problems with chest pain, palpitations, or weakness recently. The only medication she is taking is levothyroxine 125 mcg. She has reported no recent weight loss, her blood pressure is 100/60 mm Hg, pulse is 66 beats per minute, temperature is 36.8 degrees Celsius, body mass index is 20, and she does not have a neck goiter. Her cardiac exam was normal and her neurological exam revealed no tremor. Her lab for thyroid-stimulating hormone (TSH) was less than 0.03, and her lab for free thyroxine (FT4) was 2.2, while her TSH level had been 1.4 a year ago. Her levothyroxine dose was decreased to 100 mcg/day, and her repeat lab for TSH, which occurred 12 weeks later, was still less than 0.03. What is the best explanation for why this patient’s labs look like hyperthyroidism, but this patient clinically does not appear to have hyperthyroidism?

A) She was initially given too much levothyroxine; her TSH response is lagging to dose reduction.

B) She has Graves’ disease.

C) She has acute thyroiditis.

D) She is taking extra thyroid hormone.

E) She is taking biotin.

This patient has a history that includes multiple autoimmune diseases including hypothyroidism. It would be extremely unlikely that she would develop Graves' disease or develop acute thyroiditis in the setting of a gland that has been underfunctioning for years. She has no symptoms suggesting that she has hyperthyroidism, which makes taking more thyroid hormone than she is reporting less likely, although this could be possible. The TSH response can lag after dose adjustments of thyroid, but usually a 6-week interval is adequate. This patient’s testing was done 12 weeks after dose reduction making this very unlikely.

The cause for the labs that look like hyperthyroidism in this patient who appears clinically euthyroid is that she is taking biotin. Biotin (vitamin B₇) has become a very popular supplement in the past few years for thin hair, brittle nails, and fatigue. The RDA for biotin is 30 mcg. It is widely available in high doses – 5,000-10,000 mcg – which are common doses for supplements.

Biotin has been used extensively as a key component of immunoassays. Streptavidin, a protein produced by the bacteria Streptomyces avidinii, binds biotin with an extremely high affinity, and this binding is utilized in a number of immunoassays, including the assays for thyroid hormone and TSH.¹

Pearls

Consider biotin supplement use when you have patients whose labs look like hyperthyroidism, but clinically do not appear to be hyperthyroid.

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. Contact Dr. Paauw at [email protected].

References

1. Charles S, Agrawal N, and Blum M. Erroneous thyroid diagnosis due to over-the-counter biotin. Nutrition 2019;57:257-8.

2. Elston MS et al. Factitious Graves’ disease due to a biotin immunoassay interference – a case and review of the literature. J Clin Endocrinol Metab 2016;101:3251-5.

3. Barbesino G. Misdiagnosis of Graves ’disease with apparent severe hyperthyroidism in a patient taking biotin megadoses. Thyroid 2016;26(6):860-3.

4. Katzman et al. Prevalence of biotin supplement usage in outpatients and plasma biotin concentrations in patients presenting to the emergency department. Clin Biochem. 2018 Sep;60:11-16.

5. “The FDA Warns that Biotin May Interfere with Lab Tests: FDA Safety Communication,” Nov. 28, 2017.

6. Trambas et al. Characterization of the scope and magnitude of biotin interference in susceptible Roche Elecsys competitive and sandwich immunoassays. Ann Clin Biochem. 2018 Mar;55(2):205-15.

7. Frame IJ et al. Susceptibility of cardiac troponin assays to biotin interference. Am J Clin Pathol. 2019 Apr 2;151(5):486-93.

Almost 30 years ago a young woman made an appointment to see me. I had just started my internal medicine practice and almost all the patients who saw me were new to me. I assumed she was establishing care with me. Her first words to me were “Hello Dr. Paauw, I would like to interview you to see if you will be a good fit as my doctor.” We talked for the 40-minute appointment time. I asked her about her health, her life, and what she wanted out of both. We shared with each other that we both were parents of young children. When the appointment was over, she said she would really like for me to be her doctor. She told me that the main thing she appreciated about me was that I listened, and that her previous physician never sat down at her appointments and often had his hand on the door handle for much of the visit. Physicians and patients both agree that compassionate care is essential for good patient care, yet about half of patients and 60% of doctors believe it is lacking in our medical system.¹

Remember the golden first minutes

When you step in the room and greet the patient, make sure the first few minutes are about connecting with a new patient or reconnecting with a patient who has visited your office in the past. I often start by asking the patient to give me an update on how they are doing. This lets me know what is important to them. I do not touch the computer until after this initial check-in.

Use the computer as a bond to strengthen your patient relationship

Many studies have shown patients find the computer gets between the doctor and patient. It is especially problematic if it breaks eye contact with the patient. People are less likely to share scary, sensitive, or embarrassing information if someone is looking at a computer and typing. As you look up tests, radiology reports, or consultant notes, let the patient in on what you are doing. Explain why you are searching in the record, and if it helps make an important point, show your findings to the patient. Offer to print out results, so they have something to carry with them.

Explain what you are looking for and what you find on the physical exam

Being a patient is scary. We all want reassurance that our fears are not true. When you find normal findings on exam, share those with the patient. Hearing “your heart sounds good, your pulses are strong” really helps patients. Explaining what we are doing when we examine is also helpful. Explain why you are feeling for lymph nodes in the neck, why we percuss the abdomen. Patients are often fascinated by getting a window into how we are thinking. I usually have medical students with me, which offers another avenue to explaining the how and why behind the exam. In asking and explaining to students, the patient is also taught why we do what we do.

Make sure that we cover what they are afraid of, not just what their symptom is

Patients come in not just to get symptom relief but to rest their mind from their fears of what it could be. I find it helpful to ask the patient what they think is the cause of the problem, or if they are worried about any specific diagnosis. With certain symptoms this is particularly important (for example, headaches, fatigue, or abdominal pain).

None of these suggestions are easy to do in busy, time-pressured clinic visits. I have found though that when patients feel cared about, listened to and can have their fears addressed they value our advice more, and less time is needed to negotiate the plan, as it has been developed together.

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. Contact Dr. Paauw at [email protected].

Reference

Lown BA et al. Health Aff (Millwood). 2011 Sep;30(9):1772-8.

Almost 30 years ago a young woman made an appointment to see me. I had just started my internal medicine practice and almost all the patients who saw me were new to me. I assumed she was establishing care with me. Her first words to me were “Hello Dr. Paauw, I would like to interview you to see if you will be a good fit as my doctor.” We talked for the 40-minute appointment time. I asked her about her health, her life, and what she wanted out of both. We shared with each other that we both were parents of young children. When the appointment was over, she said she would really like for me to be her doctor. She told me that the main thing she appreciated about me was that I listened, and that her previous physician never sat down at her appointments and often had his hand on the door handle for much of the visit. Physicians and patients both agree that compassionate care is essential for good patient care, yet about half of patients and 60% of doctors believe it is lacking in our medical system.¹

Remember the golden first minutes

When you step in the room and greet the patient, make sure the first few minutes are about connecting with a new patient or reconnecting with a patient who has visited your office in the past. I often start by asking the patient to give me an update on how they are doing. This lets me know what is important to them. I do not touch the computer until after this initial check-in.

Use the computer as a bond to strengthen your patient relationship

Many studies have shown patients find the computer gets between the doctor and patient. It is especially problematic if it breaks eye contact with the patient. People are less likely to share scary, sensitive, or embarrassing information if someone is looking at a computer and typing. As you look up tests, radiology reports, or consultant notes, let the patient in on what you are doing. Explain why you are searching in the record, and if it helps make an important point, show your findings to the patient. Offer to print out results, so they have something to carry with them.

Explain what you are looking for and what you find on the physical exam

Being a patient is scary. We all want reassurance that our fears are not true. When you find normal findings on exam, share those with the patient. Hearing “your heart sounds good, your pulses are strong” really helps patients. Explaining what we are doing when we examine is also helpful. Explain why you are feeling for lymph nodes in the neck, why we percuss the abdomen. Patients are often fascinated by getting a window into how we are thinking. I usually have medical students with me, which offers another avenue to explaining the how and why behind the exam. In asking and explaining to students, the patient is also taught why we do what we do.

Make sure that we cover what they are afraid of, not just what their symptom is

Patients come in not just to get symptom relief but to rest their mind from their fears of what it could be. I find it helpful to ask the patient what they think is the cause of the problem, or if they are worried about any specific diagnosis. With certain symptoms this is particularly important (for example, headaches, fatigue, or abdominal pain).

None of these suggestions are easy to do in busy, time-pressured clinic visits. I have found though that when patients feel cared about, listened to and can have their fears addressed they value our advice more, and less time is needed to negotiate the plan, as it has been developed together.

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. Contact Dr. Paauw at [email protected].

Reference

Lown BA et al. Health Aff (Millwood). 2011 Sep;30(9):1772-8.

Almost 30 years ago a young woman made an appointment to see me. I had just started my internal medicine practice and almost all the patients who saw me were new to me. I assumed she was establishing care with me. Her first words to me were “Hello Dr. Paauw, I would like to interview you to see if you will be a good fit as my doctor.” We talked for the 40-minute appointment time. I asked her about her health, her life, and what she wanted out of both. We shared with each other that we both were parents of young children. When the appointment was over, she said she would really like for me to be her doctor. She told me that the main thing she appreciated about me was that I listened, and that her previous physician never sat down at her appointments and often had his hand on the door handle for much of the visit. Physicians and patients both agree that compassionate care is essential for good patient care, yet about half of patients and 60% of doctors believe it is lacking in our medical system.¹

Remember the golden first minutes

When you step in the room and greet the patient, make sure the first few minutes are about connecting with a new patient or reconnecting with a patient who has visited your office in the past. I often start by asking the patient to give me an update on how they are doing. This lets me know what is important to them. I do not touch the computer until after this initial check-in.

Use the computer as a bond to strengthen your patient relationship

Many studies have shown patients find the computer gets between the doctor and patient. It is especially problematic if it breaks eye contact with the patient. People are less likely to share scary, sensitive, or embarrassing information if someone is looking at a computer and typing. As you look up tests, radiology reports, or consultant notes, let the patient in on what you are doing. Explain why you are searching in the record, and if it helps make an important point, show your findings to the patient. Offer to print out results, so they have something to carry with them.

Explain what you are looking for and what you find on the physical exam

Being a patient is scary. We all want reassurance that our fears are not true. When you find normal findings on exam, share those with the patient. Hearing “your heart sounds good, your pulses are strong” really helps patients. Explaining what we are doing when we examine is also helpful. Explain why you are feeling for lymph nodes in the neck, why we percuss the abdomen. Patients are often fascinated by getting a window into how we are thinking. I usually have medical students with me, which offers another avenue to explaining the how and why behind the exam. In asking and explaining to students, the patient is also taught why we do what we do.

Make sure that we cover what they are afraid of, not just what their symptom is

Patients come in not just to get symptom relief but to rest their mind from their fears of what it could be. I find it helpful to ask the patient what they think is the cause of the problem, or if they are worried about any specific diagnosis. With certain symptoms this is particularly important (for example, headaches, fatigue, or abdominal pain).

None of these suggestions are easy to do in busy, time-pressured clinic visits. I have found though that when patients feel cared about, listened to and can have their fears addressed they value our advice more, and less time is needed to negotiate the plan, as it has been developed together.

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. Contact Dr. Paauw at [email protected].

Reference

Lown BA et al. Health Aff (Millwood). 2011 Sep;30(9):1772-8.