Douglas S. Paauw, MD

For this month’s column, I wanted to share some frustrations I have had about the current state of primary care. We all find those things that are going on in medicine that seem crazy and we just have to find a way to adapt to them. It is good to be able to share some of these thoughts with a community as distinguished as you readers. I know some of these are issues that you all struggle with and I wanted to give a voice to them. I wish I had answers to fix them.

Faxes from insurance companies

I find faxes from insurance companies immensely annoying. First, it takes time to go through lots of unwanted faxes but these faxes are extremely inaccurate. Today I received a fax telling me I might want to consider starting a statin in my 64-year-old HIV patient who has hypertension. He has been on a statin for 10 years.

Another fax warned me to not combine ACE inhibitors and angiotensin II receptor blockers (ARBs) in a patient who was switched from an ACE inhibitor in July to an ARB because of a cough. The fax that was sent to me has a documented end date for the ACE inhibitor before the start date of the ARB.

We only have so much time in the day and piles of faxes are not helpful.

Speaking of faxes: Why do physical therapy offices and nursing homes fax the same form every day? Physicians do not always work in clinic every single day and it increases the workload and burden when you have to sort through three copies of the same fax. I once worked in a world where these would be sent by mail, and mailed back a week later, which seemed to work just fine.
 

Misinformation

Our patients have many sources of health information. Much of the information they get comes from family, friends, social media posts, and Internet sites. The accuracy of the information is often questionable, and in some cases, they are victims of intentional misinformation.

It is frustrating and time consuming to counter the bogus, unsubstantiated information patients receive. It is especially difficult when patients have done their own research on proven therapies (such as statins) and do not want to use them because of the many websites they have looked at that make unscientific claims about the dangers of the proposed therapy. I share evidence-based websites with my patients for their research; my favorite is medlineplus.gov.
 

Access crisis

The availability of specialty care is extremely limited now. In my health care system, there is up to a 6-month wait for appointments in neurology, cardiology, and endocrinology. This puts the burden on the primary care professional to manage the patient’s health, even when the patient really needs specialty care. It also increases the calls we receive to interpret the echocardiograms, MRIs, or lab tests ordered by specialists who do not share the interpretation of the results with their patients.

What can be done to improve this situation? Automatic consults in the hospital should be limited. Every patient who has a transient ischemic attack with a negative workup does not need neurology follow-up. The same goes for patients who have chest pain but a negative cardiac workup in the hospital – they do not need follow-up by a cardiologist, nor do those who have stable, well-managed coronary disease. We have to find a way to keep our specialists seeing the patients whom they can help the most and available for consultation in a timely fashion.

Please share your pet peeves with me. I will try to give them voice in the future. Hang in there, you are the glue that keeps this flawed system together.

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 dpaauw@uw.edu.

For this month’s column, I wanted to share some frustrations I have had about the current state of primary care. We all find those things that are going on in medicine that seem crazy and we just have to find a way to adapt to them. It is good to be able to share some of these thoughts with a community as distinguished as you readers. I know some of these are issues that you all struggle with and I wanted to give a voice to them. I wish I had answers to fix them.

Faxes from insurance companies

I find faxes from insurance companies immensely annoying. First, it takes time to go through lots of unwanted faxes but these faxes are extremely inaccurate. Today I received a fax telling me I might want to consider starting a statin in my 64-year-old HIV patient who has hypertension. He has been on a statin for 10 years.

Another fax warned me to not combine ACE inhibitors and angiotensin II receptor blockers (ARBs) in a patient who was switched from an ACE inhibitor in July to an ARB because of a cough. The fax that was sent to me has a documented end date for the ACE inhibitor before the start date of the ARB.

We only have so much time in the day and piles of faxes are not helpful.

Speaking of faxes: Why do physical therapy offices and nursing homes fax the same form every day? Physicians do not always work in clinic every single day and it increases the workload and burden when you have to sort through three copies of the same fax. I once worked in a world where these would be sent by mail, and mailed back a week later, which seemed to work just fine.
 

Misinformation

Our patients have many sources of health information. Much of the information they get comes from family, friends, social media posts, and Internet sites. The accuracy of the information is often questionable, and in some cases, they are victims of intentional misinformation.

It is frustrating and time consuming to counter the bogus, unsubstantiated information patients receive. It is especially difficult when patients have done their own research on proven therapies (such as statins) and do not want to use them because of the many websites they have looked at that make unscientific claims about the dangers of the proposed therapy. I share evidence-based websites with my patients for their research; my favorite is medlineplus.gov.
 

Access crisis

The availability of specialty care is extremely limited now. In my health care system, there is up to a 6-month wait for appointments in neurology, cardiology, and endocrinology. This puts the burden on the primary care professional to manage the patient’s health, even when the patient really needs specialty care. It also increases the calls we receive to interpret the echocardiograms, MRIs, or lab tests ordered by specialists who do not share the interpretation of the results with their patients.

What can be done to improve this situation? Automatic consults in the hospital should be limited. Every patient who has a transient ischemic attack with a negative workup does not need neurology follow-up. The same goes for patients who have chest pain but a negative cardiac workup in the hospital – they do not need follow-up by a cardiologist, nor do those who have stable, well-managed coronary disease. We have to find a way to keep our specialists seeing the patients whom they can help the most and available for consultation in a timely fashion.

Please share your pet peeves with me. I will try to give them voice in the future. Hang in there, you are the glue that keeps this flawed system together.

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 dpaauw@uw.edu.

For this month’s column, I wanted to share some frustrations I have had about the current state of primary care. We all find those things that are going on in medicine that seem crazy and we just have to find a way to adapt to them. It is good to be able to share some of these thoughts with a community as distinguished as you readers. I know some of these are issues that you all struggle with and I wanted to give a voice to them. I wish I had answers to fix them.

Faxes from insurance companies

I find faxes from insurance companies immensely annoying. First, it takes time to go through lots of unwanted faxes but these faxes are extremely inaccurate. Today I received a fax telling me I might want to consider starting a statin in my 64-year-old HIV patient who has hypertension. He has been on a statin for 10 years.

Another fax warned me to not combine ACE inhibitors and angiotensin II receptor blockers (ARBs) in a patient who was switched from an ACE inhibitor in July to an ARB because of a cough. The fax that was sent to me has a documented end date for the ACE inhibitor before the start date of the ARB.

We only have so much time in the day and piles of faxes are not helpful.

Speaking of faxes: Why do physical therapy offices and nursing homes fax the same form every day? Physicians do not always work in clinic every single day and it increases the workload and burden when you have to sort through three copies of the same fax. I once worked in a world where these would be sent by mail, and mailed back a week later, which seemed to work just fine.
 

Misinformation

Our patients have many sources of health information. Much of the information they get comes from family, friends, social media posts, and Internet sites. The accuracy of the information is often questionable, and in some cases, they are victims of intentional misinformation.

It is frustrating and time consuming to counter the bogus, unsubstantiated information patients receive. It is especially difficult when patients have done their own research on proven therapies (such as statins) and do not want to use them because of the many websites they have looked at that make unscientific claims about the dangers of the proposed therapy. I share evidence-based websites with my patients for their research; my favorite is medlineplus.gov.
 

Access crisis

The availability of specialty care is extremely limited now. In my health care system, there is up to a 6-month wait for appointments in neurology, cardiology, and endocrinology. This puts the burden on the primary care professional to manage the patient’s health, even when the patient really needs specialty care. It also increases the calls we receive to interpret the echocardiograms, MRIs, or lab tests ordered by specialists who do not share the interpretation of the results with their patients.

What can be done to improve this situation? Automatic consults in the hospital should be limited. Every patient who has a transient ischemic attack with a negative workup does not need neurology follow-up. The same goes for patients who have chest pain but a negative cardiac workup in the hospital – they do not need follow-up by a cardiologist, nor do those who have stable, well-managed coronary disease. We have to find a way to keep our specialists seeing the patients whom they can help the most and available for consultation in a timely fashion.

Please share your pet peeves with me. I will try to give them voice in the future. Hang in there, you are the glue that keeps this flawed system together.

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 dpaauw@uw.edu.

A patient inquires about whether he or she can use an EpiPen after the expiration date. What should you advise?

A. The EpiPen is unlikely to be effective after the expiration date.

B. The EpiPen may be dangerous to use after the expiration date.

C. The EpiPen is likely to be okay up to 2 years past the expiration date.

I think that choice C is the most accurate and will get to all the evidence shortly. The expiration date is not the date that the drug stops being effective or potentially becomes toxic. It is a date, required by law, that the manufacturer can guarantee greater than 90% original potency of the medication.

Epinephrine is a costly drug and is usually replaced when the Epipen expires. Weir and colleagues studied six epinephrine syringes 30 months past their expiration date.¹ Three of the syringes and one control, nonexpired syringe were analyzed using liquid chromatography-mass spectrometry and nuclear magnetic resonance to determine epinephrine content. The contents of the other three syringes of epinephrine were cultured for bacteria and fungus, which yielded no microbial growth. The study showed that the content of epinephrine present in the original sample remained unchanged, compared with the control.

Rachid et al. looked at 35 EpiPens 3-36 months past their expiration dates.² The percentage of epinephrine found remained 84%-101%, with all EpiPens less than 24 months past expiration having > 90% of the labeled epinephrine dose. Cantrell and colleagues evaluated a combination of 40 EpiPens and Epipen Jrs that were 1-50 months past expiration.³ These pens had not been kept in ideal conditions, as some had been in cars, outdoor cabins, and other environments without temperature control. Sixty-one percent of the Epipens and 56% of the EpiPen Juniors had > 90% of the labeled epinephrine content. I think expired Epipens can be used as a back-up option – that is, they are safe to use if there is not an Epipen available that is not expired.
 

Shelf life extension program

Lyon and colleagues reported data from the Shelf Life Extension Program (SLEP).⁴ A total of 122 drugs were studied representing 3,005 lots. Based on testing and stability assessment, 88% of the lots were extended at least 1 year beyond their original expiration date for an average extension of 66 months, but the additional stability period was highly variable. Several antibiotics were studied, including ciprofloxacin (mean extension, 55 months), amoxicillin (mean extension, 23 months), and doxycycline (mean extension, 50 months).

What about other drugs not in pill form?

I am frequently asked about the longevity of medication formulations that are not in pill form. For example, I have been asked about using expired eye drops. There are few data on this. Reis at al. studied whether travoprost that was past the expiration date still lowered intraocular pressures.⁵ Intraocular pressures in glaucoma patients treated with travoprost 6 weeks after the seal was broken were compared with pressures when drops were used immediately after the container seal was broken. There was no significant difference in intraocular pressure between the two treatment groups during the study.

I found one case report of harm from using expired eye medications. Use of expired eye drops was associated with a case of bilateral toxic epithelial keratopathy.⁶ Eye drops can be contaminated and cause irritation from the breakdown products of preservatives.

Many people use inhalers for many years. This is especially true for albuterol, which is often used for very intermittent symptoms. I found one recent study on the stability of albuterol. Kutty et al. studied expired albuterol inhalers and solutions up to 20 years past expiration.⁷ Almost all lots of albuterol maintained > 90% of product (73%-103%), many years past their expiration date. Even at 73% retained activity, the dose would likely be effective.
 

Pearl: Expired epinephrine and albuterol appear to retain activity several years past expiration.

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 has no conflicts of interest. Contact Dr. Paauw at dpaauw@uw.edu.

References

1. Weir WB et al. Prehosp Emerg Care. 2018 Jul-Aug;22(4):414-8.

2. Rachid O et al. Ann Allergy Asthma Immunol. 2015 Apr;114(4):354-6.

3. Cantrell FL et al. Ann Intern Med. 2017 Jun 20;166(12):918-9.

4. Lyon RC et al. J Pharmaceut Sci. 2006;95(7):1549-60.

5. Reis R et al. Clin Ther. 2004 Dec;26(12):2121-7.

6. AlGhadeer H, AlHumaiden A. J Clin Pharm Ther. 2022 Dec;47(12):2379-82.

7. Kutty RG et al. Heliyon. 2022 Aug 5;8(8):e10104.

A patient inquires about whether he or she can use an EpiPen after the expiration date. What should you advise?

A. The EpiPen is unlikely to be effective after the expiration date.

B. The EpiPen may be dangerous to use after the expiration date.

C. The EpiPen is likely to be okay up to 2 years past the expiration date.

I think that choice C is the most accurate and will get to all the evidence shortly. The expiration date is not the date that the drug stops being effective or potentially becomes toxic. It is a date, required by law, that the manufacturer can guarantee greater than 90% original potency of the medication.

Epinephrine is a costly drug and is usually replaced when the Epipen expires. Weir and colleagues studied six epinephrine syringes 30 months past their expiration date.¹ Three of the syringes and one control, nonexpired syringe were analyzed using liquid chromatography-mass spectrometry and nuclear magnetic resonance to determine epinephrine content. The contents of the other three syringes of epinephrine were cultured for bacteria and fungus, which yielded no microbial growth. The study showed that the content of epinephrine present in the original sample remained unchanged, compared with the control.

Rachid et al. looked at 35 EpiPens 3-36 months past their expiration dates.² The percentage of epinephrine found remained 84%-101%, with all EpiPens less than 24 months past expiration having > 90% of the labeled epinephrine dose. Cantrell and colleagues evaluated a combination of 40 EpiPens and Epipen Jrs that were 1-50 months past expiration.³ These pens had not been kept in ideal conditions, as some had been in cars, outdoor cabins, and other environments without temperature control. Sixty-one percent of the Epipens and 56% of the EpiPen Juniors had > 90% of the labeled epinephrine content. I think expired Epipens can be used as a back-up option – that is, they are safe to use if there is not an Epipen available that is not expired.
 

Shelf life extension program

Lyon and colleagues reported data from the Shelf Life Extension Program (SLEP).⁴ A total of 122 drugs were studied representing 3,005 lots. Based on testing and stability assessment, 88% of the lots were extended at least 1 year beyond their original expiration date for an average extension of 66 months, but the additional stability period was highly variable. Several antibiotics were studied, including ciprofloxacin (mean extension, 55 months), amoxicillin (mean extension, 23 months), and doxycycline (mean extension, 50 months).

What about other drugs not in pill form?

I am frequently asked about the longevity of medication formulations that are not in pill form. For example, I have been asked about using expired eye drops. There are few data on this. Reis at al. studied whether travoprost that was past the expiration date still lowered intraocular pressures.⁵ Intraocular pressures in glaucoma patients treated with travoprost 6 weeks after the seal was broken were compared with pressures when drops were used immediately after the container seal was broken. There was no significant difference in intraocular pressure between the two treatment groups during the study.

I found one case report of harm from using expired eye medications. Use of expired eye drops was associated with a case of bilateral toxic epithelial keratopathy.⁶ Eye drops can be contaminated and cause irritation from the breakdown products of preservatives.

Many people use inhalers for many years. This is especially true for albuterol, which is often used for very intermittent symptoms. I found one recent study on the stability of albuterol. Kutty et al. studied expired albuterol inhalers and solutions up to 20 years past expiration.⁷ Almost all lots of albuterol maintained > 90% of product (73%-103%), many years past their expiration date. Even at 73% retained activity, the dose would likely be effective.
 

Pearl: Expired epinephrine and albuterol appear to retain activity several years past expiration.

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 has no conflicts of interest. Contact Dr. Paauw at dpaauw@uw.edu.

References

1. Weir WB et al. Prehosp Emerg Care. 2018 Jul-Aug;22(4):414-8.

2. Rachid O et al. Ann Allergy Asthma Immunol. 2015 Apr;114(4):354-6.

3. Cantrell FL et al. Ann Intern Med. 2017 Jun 20;166(12):918-9.

4. Lyon RC et al. J Pharmaceut Sci. 2006;95(7):1549-60.

5. Reis R et al. Clin Ther. 2004 Dec;26(12):2121-7.

6. AlGhadeer H, AlHumaiden A. J Clin Pharm Ther. 2022 Dec;47(12):2379-82.

7. Kutty RG et al. Heliyon. 2022 Aug 5;8(8):e10104.

A patient inquires about whether he or she can use an EpiPen after the expiration date. What should you advise?

A. The EpiPen is unlikely to be effective after the expiration date.

B. The EpiPen may be dangerous to use after the expiration date.

C. The EpiPen is likely to be okay up to 2 years past the expiration date.

I think that choice C is the most accurate and will get to all the evidence shortly. The expiration date is not the date that the drug stops being effective or potentially becomes toxic. It is a date, required by law, that the manufacturer can guarantee greater than 90% original potency of the medication.

Epinephrine is a costly drug and is usually replaced when the Epipen expires. Weir and colleagues studied six epinephrine syringes 30 months past their expiration date.¹ Three of the syringes and one control, nonexpired syringe were analyzed using liquid chromatography-mass spectrometry and nuclear magnetic resonance to determine epinephrine content. The contents of the other three syringes of epinephrine were cultured for bacteria and fungus, which yielded no microbial growth. The study showed that the content of epinephrine present in the original sample remained unchanged, compared with the control.

Rachid et al. looked at 35 EpiPens 3-36 months past their expiration dates.² The percentage of epinephrine found remained 84%-101%, with all EpiPens less than 24 months past expiration having > 90% of the labeled epinephrine dose. Cantrell and colleagues evaluated a combination of 40 EpiPens and Epipen Jrs that were 1-50 months past expiration.³ These pens had not been kept in ideal conditions, as some had been in cars, outdoor cabins, and other environments without temperature control. Sixty-one percent of the Epipens and 56% of the EpiPen Juniors had > 90% of the labeled epinephrine content. I think expired Epipens can be used as a back-up option – that is, they are safe to use if there is not an Epipen available that is not expired.
 

Shelf life extension program

Lyon and colleagues reported data from the Shelf Life Extension Program (SLEP).⁴ A total of 122 drugs were studied representing 3,005 lots. Based on testing and stability assessment, 88% of the lots were extended at least 1 year beyond their original expiration date for an average extension of 66 months, but the additional stability period was highly variable. Several antibiotics were studied, including ciprofloxacin (mean extension, 55 months), amoxicillin (mean extension, 23 months), and doxycycline (mean extension, 50 months).

What about other drugs not in pill form?

I am frequently asked about the longevity of medication formulations that are not in pill form. For example, I have been asked about using expired eye drops. There are few data on this. Reis at al. studied whether travoprost that was past the expiration date still lowered intraocular pressures.⁵ Intraocular pressures in glaucoma patients treated with travoprost 6 weeks after the seal was broken were compared with pressures when drops were used immediately after the container seal was broken. There was no significant difference in intraocular pressure between the two treatment groups during the study.

I found one case report of harm from using expired eye medications. Use of expired eye drops was associated with a case of bilateral toxic epithelial keratopathy.⁶ Eye drops can be contaminated and cause irritation from the breakdown products of preservatives.

Many people use inhalers for many years. This is especially true for albuterol, which is often used for very intermittent symptoms. I found one recent study on the stability of albuterol. Kutty et al. studied expired albuterol inhalers and solutions up to 20 years past expiration.⁷ Almost all lots of albuterol maintained > 90% of product (73%-103%), many years past their expiration date. Even at 73% retained activity, the dose would likely be effective.
 

Pearl: Expired epinephrine and albuterol appear to retain activity several years past expiration.

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 has no conflicts of interest. Contact Dr. Paauw at dpaauw@uw.edu.

References

1. Weir WB et al. Prehosp Emerg Care. 2018 Jul-Aug;22(4):414-8.

2. Rachid O et al. Ann Allergy Asthma Immunol. 2015 Apr;114(4):354-6.

3. Cantrell FL et al. Ann Intern Med. 2017 Jun 20;166(12):918-9.

4. Lyon RC et al. J Pharmaceut Sci. 2006;95(7):1549-60.

5. Reis R et al. Clin Ther. 2004 Dec;26(12):2121-7.

6. AlGhadeer H, AlHumaiden A. J Clin Pharm Ther. 2022 Dec;47(12):2379-82.

7. Kutty RG et al. Heliyon. 2022 Aug 5;8(8):e10104.

A 45-year-old women presents for evaluation of fatigue. She has been tired for the past 6 months. She has had no problems with sleep and no other new symptoms. Her physical exam is unremarkable. Her Patient Health Questionnaire–9 score is 4. Lab results are as follows: hemoglobin, 13 g/dL; hematocrit, 39%; mean corpuscular volume, 90 fL; blood urea nitrogen, 10 mg/dL; Cr, 1.0 mg/dL; AST, 20 IU/L; ALT, 15 IU/L; ferritin, 35 mcg/mL; thyroid-stimulating hormone, 3.5 mIU/L.

What would you recommend?

A. Sertraline

B. Sleep study

C. Iron supplementation

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 dpaauw@uw.edu.

References

1. Verdon F et al. BMJ. 2003 May 24;326(7399):1124. .

2. Houston BL et al. BMJ Open. 2018 Apr 5;8(4):e019240.

3. Almohanna HM et al. Dermatol Ther (Heidelb). 2019 Mar;9(1):51-70. .

4. Hard S. Acta Derm Venereol. 1963;43:562-9.

5. Kantor J et al. J Invest Dermatol. 2003 Nov;121(5):985-8. .

6. Allen RP et al. Sleep Med. 2018 Jan;41:27-44. .

A 45-year-old women presents for evaluation of fatigue. She has been tired for the past 6 months. She has had no problems with sleep and no other new symptoms. Her physical exam is unremarkable. Her Patient Health Questionnaire–9 score is 4. Lab results are as follows: hemoglobin, 13 g/dL; hematocrit, 39%; mean corpuscular volume, 90 fL; blood urea nitrogen, 10 mg/dL; Cr, 1.0 mg/dL; AST, 20 IU/L; ALT, 15 IU/L; ferritin, 35 mcg/mL; thyroid-stimulating hormone, 3.5 mIU/L.

What would you recommend?

A. Sertraline

B. Sleep study

C. Iron supplementation

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 dpaauw@uw.edu.

References

1. Verdon F et al. BMJ. 2003 May 24;326(7399):1124. .

2. Houston BL et al. BMJ Open. 2018 Apr 5;8(4):e019240.

3. Almohanna HM et al. Dermatol Ther (Heidelb). 2019 Mar;9(1):51-70. .

4. Hard S. Acta Derm Venereol. 1963;43:562-9.

5. Kantor J et al. J Invest Dermatol. 2003 Nov;121(5):985-8. .

6. Allen RP et al. Sleep Med. 2018 Jan;41:27-44. .

A 45-year-old women presents for evaluation of fatigue. She has been tired for the past 6 months. She has had no problems with sleep and no other new symptoms. Her physical exam is unremarkable. Her Patient Health Questionnaire–9 score is 4. Lab results are as follows: hemoglobin, 13 g/dL; hematocrit, 39%; mean corpuscular volume, 90 fL; blood urea nitrogen, 10 mg/dL; Cr, 1.0 mg/dL; AST, 20 IU/L; ALT, 15 IU/L; ferritin, 35 mcg/mL; thyroid-stimulating hormone, 3.5 mIU/L.

What would you recommend?

A. Sertraline

B. Sleep study

C. Iron supplementation

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 dpaauw@uw.edu.

References

1. Verdon F et al. BMJ. 2003 May 24;326(7399):1124. .

2. Houston BL et al. BMJ Open. 2018 Apr 5;8(4):e019240.

3. Almohanna HM et al. Dermatol Ther (Heidelb). 2019 Mar;9(1):51-70. .

4. Hard S. Acta Derm Venereol. 1963;43:562-9.

5. Kantor J et al. J Invest Dermatol. 2003 Nov;121(5):985-8. .

6. Allen RP et al. Sleep Med. 2018 Jan;41:27-44. .

As we all face remarkable challenges in giving great care to our patients and maintaining great care for ourselves, I wanted to share a few thoughts I have had regarding difficult things I have seen in the past few months.

• Call centers: Yikes! I think this is an overlooked stress on the primary care system. In a cost-cutting effort, organizations have gone to call centers to handle incoming calls, and hold times can be enormous. My own organization often has wait times longer than 30 minutes. I recently called another organization and had a wait time more than 30 minutes. Patients become frustrated and will message their primary care team to intervene for scheduling issues then will arrive at their appointments frustrated by all the hassles.
• Difficult encounters: We all have visits that we know will be challenging. I think it is even more difficult when we enter the visit stressed and tired. I have always found that, when I am in a calm place, even the most difficult visits go much better. Our patients arrive at clinic visits more stressed and tired too, as they face the challenge of a stretched and overwhelmed primary care system.
• Limited availability of specialists: My organization has had a sharp increase in wait times for specialty care over the past few years. Waits for some specialties can be almost a year. A study by Reddy and colleagues found a wait time of 3 months for patients referred to gastroenterologists.¹ The lack of timely access to specialists adds to the stress and burden of primary care professionals. Managing problems deemed in need of subspecialty care as patients wait for appointments is difficult.
• Patient portals: Some practices are starting to figure this out this problem, others aren’t. Budd reviewed all the factors with the EHR that contribute to physician burnout.² Portals have added another source of patient care outside face-to-face visits that adds to physician work load; for many practices is not appropriately accounted for in effort or productivity measures. Some practices are now starting to charge for patient messaging, but this may require even more physician time in documentation and billing. Unless this directly helps the physician reduce work hours or improve compensation, then it may make the problem worse.

There is little mystery why it seems so hard ... it is! Many things have been added to the plate of primary care professionals (increased messaging, calming patients frustrated with the medical system, and increased need for bridging care while patients wait for specialty appointments). Our patients need us now more than ever to give excellent, compassionate care in a poorly functioning system. We need to be emotionally and physically healthy enough to be there for our patients. Prioritize your own needs.

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 dpaauw@uw.edu.

References

1. Reddy K et al. Health Equity. 2018 Jun 1;2(1):103-8.

2. Budd J. J Prim Care Community Health. 2023 Apr 19.

As we all face remarkable challenges in giving great care to our patients and maintaining great care for ourselves, I wanted to share a few thoughts I have had regarding difficult things I have seen in the past few months.

• Call centers: Yikes! I think this is an overlooked stress on the primary care system. In a cost-cutting effort, organizations have gone to call centers to handle incoming calls, and hold times can be enormous. My own organization often has wait times longer than 30 minutes. I recently called another organization and had a wait time more than 30 minutes. Patients become frustrated and will message their primary care team to intervene for scheduling issues then will arrive at their appointments frustrated by all the hassles.
• Difficult encounters: We all have visits that we know will be challenging. I think it is even more difficult when we enter the visit stressed and tired. I have always found that, when I am in a calm place, even the most difficult visits go much better. Our patients arrive at clinic visits more stressed and tired too, as they face the challenge of a stretched and overwhelmed primary care system.
• Limited availability of specialists: My organization has had a sharp increase in wait times for specialty care over the past few years. Waits for some specialties can be almost a year. A study by Reddy and colleagues found a wait time of 3 months for patients referred to gastroenterologists.¹ The lack of timely access to specialists adds to the stress and burden of primary care professionals. Managing problems deemed in need of subspecialty care as patients wait for appointments is difficult.
• Patient portals: Some practices are starting to figure this out this problem, others aren’t. Budd reviewed all the factors with the EHR that contribute to physician burnout.² Portals have added another source of patient care outside face-to-face visits that adds to physician work load; for many practices is not appropriately accounted for in effort or productivity measures. Some practices are now starting to charge for patient messaging, but this may require even more physician time in documentation and billing. Unless this directly helps the physician reduce work hours or improve compensation, then it may make the problem worse.

There is little mystery why it seems so hard ... it is! Many things have been added to the plate of primary care professionals (increased messaging, calming patients frustrated with the medical system, and increased need for bridging care while patients wait for specialty appointments). Our patients need us now more than ever to give excellent, compassionate care in a poorly functioning system. We need to be emotionally and physically healthy enough to be there for our patients. Prioritize your own needs.

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 dpaauw@uw.edu.

References

1. Reddy K et al. Health Equity. 2018 Jun 1;2(1):103-8.

2. Budd J. J Prim Care Community Health. 2023 Apr 19.

As we all face remarkable challenges in giving great care to our patients and maintaining great care for ourselves, I wanted to share a few thoughts I have had regarding difficult things I have seen in the past few months.

• Call centers: Yikes! I think this is an overlooked stress on the primary care system. In a cost-cutting effort, organizations have gone to call centers to handle incoming calls, and hold times can be enormous. My own organization often has wait times longer than 30 minutes. I recently called another organization and had a wait time more than 30 minutes. Patients become frustrated and will message their primary care team to intervene for scheduling issues then will arrive at their appointments frustrated by all the hassles.
• Difficult encounters: We all have visits that we know will be challenging. I think it is even more difficult when we enter the visit stressed and tired. I have always found that, when I am in a calm place, even the most difficult visits go much better. Our patients arrive at clinic visits more stressed and tired too, as they face the challenge of a stretched and overwhelmed primary care system.
• Limited availability of specialists: My organization has had a sharp increase in wait times for specialty care over the past few years. Waits for some specialties can be almost a year. A study by Reddy and colleagues found a wait time of 3 months for patients referred to gastroenterologists.¹ The lack of timely access to specialists adds to the stress and burden of primary care professionals. Managing problems deemed in need of subspecialty care as patients wait for appointments is difficult.
• Patient portals: Some practices are starting to figure this out this problem, others aren’t. Budd reviewed all the factors with the EHR that contribute to physician burnout.² Portals have added another source of patient care outside face-to-face visits that adds to physician work load; for many practices is not appropriately accounted for in effort or productivity measures. Some practices are now starting to charge for patient messaging, but this may require even more physician time in documentation and billing. Unless this directly helps the physician reduce work hours or improve compensation, then it may make the problem worse.

There is little mystery why it seems so hard ... it is! Many things have been added to the plate of primary care professionals (increased messaging, calming patients frustrated with the medical system, and increased need for bridging care while patients wait for specialty appointments). Our patients need us now more than ever to give excellent, compassionate care in a poorly functioning system. We need to be emotionally and physically healthy enough to be there for our patients. Prioritize your own needs.

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 dpaauw@uw.edu.

References

1. Reddy K et al. Health Equity. 2018 Jun 1;2(1):103-8.

2. Budd J. J Prim Care Community Health. 2023 Apr 19.

An 85-year-old woman is brought to the emergency department after a syncopal episode. Her caregivers report a similar episode 2 weeks ago, but she recovered so quickly they did not seek evaluation for her.

Medications: Omeprazole 20 mg, pravastatin 40 mg, citalopram 10 mg, albuterol, donepezil 10 mg, isosorbide mononitrate 60 mg, and calcium. On exam, blood pressure is 100/60 mm Hg, pulse 55. ECG indicates bradycardia with normal intervals. What drug most likely caused her syncope?

A. Citalopram

B. Pravastatin

C. Donepezil

D. Isosorbide

E. Calcium

This woman’s syncope is likely caused by donepezil. Citalopram can lengthen the QT interval, especially in elderly patients, but the normal intervals on ECG eliminate this possibility. Donepezil can cause bradycardia, which can contribute to syncope.

Hernandez and colleagues evaluated a cohort of veterans with dementia over an 8-year period.¹ They found that there was a 1.4-fold increased risk of bradycardia in patients with dementia treated with an acetylcholine inhibitor (compared with that in patients who were not taking these medications) and that there was a dose-dependent increase in risk for patients on donepezil.

Park-Wyllie et al. found in a study of 1.4 million older adults a greater than twofold risk of hospitalization for bradycardia in patients treated with a cholinesterase inhibitor.² Gill and colleagues performed a population-based cohort study of 19,803 elderly patients with dementia who were prescribed cholinesterase inhibitors, and compared them to age-matched controls.³ They found increased hospital visits for syncope in people receiving cholinesterase inhibitors (hazard ratio, 1.76; 95% confidence interval, 1.57-1.98). Other syncope-related events were also more common in people receiving cholinesterase inhibitors, compared with controls: hospital visits for bradycardia (HR, 1.69; 95% CI, 1.32-2.15), permanent pacemaker insertion (HR, 1.49; 95% CI, 1.12-2.00), and hip fracture (HR, 1.18; (95% CI, 1.04-1.34).

Nausea, vomiting, and weight loss are much more common than the rarer side effects of bradycardia and syncope. The frequency of gastroenterological side effects is up to 25%. Cholinesterase inhibitors have modest effects on cognitive function with a high number needed to treat (NNT) of 10, and an NNT as high as 100 for global function. The number needed to harm (NNH) is 4, when gastrointestinal symptoms are added in.⁴ Another important, problematic side effect of cholinesterase inhibitors is urinary incontinence. This often leads to patients receiving medications, to combat this side effect, that may worsen cognitive function.

Another commonly used medication that scares me in certain circumstances is trimethoprim-sulfamethoxazole. My main concern is when it is used in patients who are elderly, have chronic kidney disease, or are taking other medications that can cause hyperkalemia (ACEIs, ARBs, potassium-sparing diuretics including spironolactone). Hyperkalemia is a real concern in these patient populations. Trimethoprim reduces renal potassium excretion through the competitive inhibition of sodium channels in the distal nephron, in a manner similar to the potassium-sparing diuretic amiloride. Hospitalizations for hyperkalemia are more common in patients who take ACEIs and ARBs and are prescribed trimethoprim-sulfamethoxazole, compared with other antibiotics.⁵

Sudden cardiac death is also more common in patients who are taking ACEIs or ARBs and receive trimethoprim-sulfamethoxazole.⁶ Trimethoprim-sulfamethoxazole also has a powerful interaction with warfarin, both displacing warfarin from albumin and inhibiting its metabolism. It raises the INR (international normalized ratio) in warfarin-treated patients much greater than do other antibiotics.⁷
 

Pearls

• Think carefully about the use of cholinesterase inhibitors because of the unfavorable NNH vs. NNT.
• Use caution prescribing trimethoprim for patients who are elderly, especially if they are on an ACEI, an ARB, or spironolactone, and in patients with chronic kidney disease.

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 dpaauw@uw.edu.

References

1. Hernandez RK et al. J Am Geriatr Soc. 2009;57:1997-2003.

2. Park-Wyllie LY et al. PLoS Med. 2009;6:e1000157.

3. Gill SS et al. Arch Intern Med 2009;169:867-73.

4. Peters KR. J Am Geriatr Soc. 2013 Jul;61(7):1170-4.

5. Antoniou TN et al. Arch Intern Med. 2010;170(12):1045-9.

6. Fralick M et al. BMJ. 2014 Oct 30;349:g6196.

7. Glasheen JJ et al. J Gen Intern Med. 2005 Jul;20(7):653-6.

An 85-year-old woman is brought to the emergency department after a syncopal episode. Her caregivers report a similar episode 2 weeks ago, but she recovered so quickly they did not seek evaluation for her.

Medications: Omeprazole 20 mg, pravastatin 40 mg, citalopram 10 mg, albuterol, donepezil 10 mg, isosorbide mononitrate 60 mg, and calcium. On exam, blood pressure is 100/60 mm Hg, pulse 55. ECG indicates bradycardia with normal intervals. What drug most likely caused her syncope?

A. Citalopram

B. Pravastatin

C. Donepezil

D. Isosorbide

E. Calcium

This woman’s syncope is likely caused by donepezil. Citalopram can lengthen the QT interval, especially in elderly patients, but the normal intervals on ECG eliminate this possibility. Donepezil can cause bradycardia, which can contribute to syncope.

Hernandez and colleagues evaluated a cohort of veterans with dementia over an 8-year period.¹ They found that there was a 1.4-fold increased risk of bradycardia in patients with dementia treated with an acetylcholine inhibitor (compared with that in patients who were not taking these medications) and that there was a dose-dependent increase in risk for patients on donepezil.

Park-Wyllie et al. found in a study of 1.4 million older adults a greater than twofold risk of hospitalization for bradycardia in patients treated with a cholinesterase inhibitor.² Gill and colleagues performed a population-based cohort study of 19,803 elderly patients with dementia who were prescribed cholinesterase inhibitors, and compared them to age-matched controls.³ They found increased hospital visits for syncope in people receiving cholinesterase inhibitors (hazard ratio, 1.76; 95% confidence interval, 1.57-1.98). Other syncope-related events were also more common in people receiving cholinesterase inhibitors, compared with controls: hospital visits for bradycardia (HR, 1.69; 95% CI, 1.32-2.15), permanent pacemaker insertion (HR, 1.49; 95% CI, 1.12-2.00), and hip fracture (HR, 1.18; (95% CI, 1.04-1.34).

Nausea, vomiting, and weight loss are much more common than the rarer side effects of bradycardia and syncope. The frequency of gastroenterological side effects is up to 25%. Cholinesterase inhibitors have modest effects on cognitive function with a high number needed to treat (NNT) of 10, and an NNT as high as 100 for global function. The number needed to harm (NNH) is 4, when gastrointestinal symptoms are added in.⁴ Another important, problematic side effect of cholinesterase inhibitors is urinary incontinence. This often leads to patients receiving medications, to combat this side effect, that may worsen cognitive function.

Another commonly used medication that scares me in certain circumstances is trimethoprim-sulfamethoxazole. My main concern is when it is used in patients who are elderly, have chronic kidney disease, or are taking other medications that can cause hyperkalemia (ACEIs, ARBs, potassium-sparing diuretics including spironolactone). Hyperkalemia is a real concern in these patient populations. Trimethoprim reduces renal potassium excretion through the competitive inhibition of sodium channels in the distal nephron, in a manner similar to the potassium-sparing diuretic amiloride. Hospitalizations for hyperkalemia are more common in patients who take ACEIs and ARBs and are prescribed trimethoprim-sulfamethoxazole, compared with other antibiotics.⁵

Sudden cardiac death is also more common in patients who are taking ACEIs or ARBs and receive trimethoprim-sulfamethoxazole.⁶ Trimethoprim-sulfamethoxazole also has a powerful interaction with warfarin, both displacing warfarin from albumin and inhibiting its metabolism. It raises the INR (international normalized ratio) in warfarin-treated patients much greater than do other antibiotics.⁷
 

Pearls

• Think carefully about the use of cholinesterase inhibitors because of the unfavorable NNH vs. NNT.
• Use caution prescribing trimethoprim for patients who are elderly, especially if they are on an ACEI, an ARB, or spironolactone, and in patients with chronic kidney disease.

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 dpaauw@uw.edu.

References

1. Hernandez RK et al. J Am Geriatr Soc. 2009;57:1997-2003.

2. Park-Wyllie LY et al. PLoS Med. 2009;6:e1000157.

3. Gill SS et al. Arch Intern Med 2009;169:867-73.

4. Peters KR. J Am Geriatr Soc. 2013 Jul;61(7):1170-4.

5. Antoniou TN et al. Arch Intern Med. 2010;170(12):1045-9.

6. Fralick M et al. BMJ. 2014 Oct 30;349:g6196.

7. Glasheen JJ et al. J Gen Intern Med. 2005 Jul;20(7):653-6.

An 85-year-old woman is brought to the emergency department after a syncopal episode. Her caregivers report a similar episode 2 weeks ago, but she recovered so quickly they did not seek evaluation for her.

Medications: Omeprazole 20 mg, pravastatin 40 mg, citalopram 10 mg, albuterol, donepezil 10 mg, isosorbide mononitrate 60 mg, and calcium. On exam, blood pressure is 100/60 mm Hg, pulse 55. ECG indicates bradycardia with normal intervals. What drug most likely caused her syncope?

A. Citalopram

B. Pravastatin

C. Donepezil

D. Isosorbide

E. Calcium

This woman’s syncope is likely caused by donepezil. Citalopram can lengthen the QT interval, especially in elderly patients, but the normal intervals on ECG eliminate this possibility. Donepezil can cause bradycardia, which can contribute to syncope.

Hernandez and colleagues evaluated a cohort of veterans with dementia over an 8-year period.¹ They found that there was a 1.4-fold increased risk of bradycardia in patients with dementia treated with an acetylcholine inhibitor (compared with that in patients who were not taking these medications) and that there was a dose-dependent increase in risk for patients on donepezil.

Park-Wyllie et al. found in a study of 1.4 million older adults a greater than twofold risk of hospitalization for bradycardia in patients treated with a cholinesterase inhibitor.² Gill and colleagues performed a population-based cohort study of 19,803 elderly patients with dementia who were prescribed cholinesterase inhibitors, and compared them to age-matched controls.³ They found increased hospital visits for syncope in people receiving cholinesterase inhibitors (hazard ratio, 1.76; 95% confidence interval, 1.57-1.98). Other syncope-related events were also more common in people receiving cholinesterase inhibitors, compared with controls: hospital visits for bradycardia (HR, 1.69; 95% CI, 1.32-2.15), permanent pacemaker insertion (HR, 1.49; 95% CI, 1.12-2.00), and hip fracture (HR, 1.18; (95% CI, 1.04-1.34).

Nausea, vomiting, and weight loss are much more common than the rarer side effects of bradycardia and syncope. The frequency of gastroenterological side effects is up to 25%. Cholinesterase inhibitors have modest effects on cognitive function with a high number needed to treat (NNT) of 10, and an NNT as high as 100 for global function. The number needed to harm (NNH) is 4, when gastrointestinal symptoms are added in.⁴ Another important, problematic side effect of cholinesterase inhibitors is urinary incontinence. This often leads to patients receiving medications, to combat this side effect, that may worsen cognitive function.

Another commonly used medication that scares me in certain circumstances is trimethoprim-sulfamethoxazole. My main concern is when it is used in patients who are elderly, have chronic kidney disease, or are taking other medications that can cause hyperkalemia (ACEIs, ARBs, potassium-sparing diuretics including spironolactone). Hyperkalemia is a real concern in these patient populations. Trimethoprim reduces renal potassium excretion through the competitive inhibition of sodium channels in the distal nephron, in a manner similar to the potassium-sparing diuretic amiloride. Hospitalizations for hyperkalemia are more common in patients who take ACEIs and ARBs and are prescribed trimethoprim-sulfamethoxazole, compared with other antibiotics.⁵

Sudden cardiac death is also more common in patients who are taking ACEIs or ARBs and receive trimethoprim-sulfamethoxazole.⁶ Trimethoprim-sulfamethoxazole also has a powerful interaction with warfarin, both displacing warfarin from albumin and inhibiting its metabolism. It raises the INR (international normalized ratio) in warfarin-treated patients much greater than do other antibiotics.⁷
 

Pearls

• Think carefully about the use of cholinesterase inhibitors because of the unfavorable NNH vs. NNT.
• Use caution prescribing trimethoprim for patients who are elderly, especially if they are on an ACEI, an ARB, or spironolactone, and in patients with chronic kidney disease.

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 dpaauw@uw.edu.

References

1. Hernandez RK et al. J Am Geriatr Soc. 2009;57:1997-2003.

2. Park-Wyllie LY et al. PLoS Med. 2009;6:e1000157.

3. Gill SS et al. Arch Intern Med 2009;169:867-73.

4. Peters KR. J Am Geriatr Soc. 2013 Jul;61(7):1170-4.

5. Antoniou TN et al. Arch Intern Med. 2010;170(12):1045-9.

6. Fralick M et al. BMJ. 2014 Oct 30;349:g6196.

7. Glasheen JJ et al. J Gen Intern Med. 2005 Jul;20(7):653-6.

A 43-year-old man presents to the emergency department with dizziness and a 6-hour history of passing maroon stool. He has been in good health with the only medical problem in his history being depression.

He is taking sertraline. On exam, his blood pressure is 100/60, and his pulse is 100, both while lying down. His blood pressure while standing is 90/60 and his pulse while standing is 130. The rest of his exam is normal. His lab values include hemoglobin of 10, hematocrit of 30, white blood cell of 4.6, platelet count of 175,000, sodium of 142, chloride of 100, bicarbonate of 24, potassium of 3.8, blood urea nitrogen (BUN) of 38, and creatinine clearance (Cr) of 1.1.

What is the most likely source of his bleeding?

A. Gastric ulcer

B. Meckel’s diverticulum

C. Arteriovenous malformation

D. Diverticulosis

E. Hemorrhoids

What makes the most sense

The most likely cause of this patient’s maroon stool is an upper gastrointestinal bleed, so it would make the most sense for a gastric ulcer to be the source of his bleeding. The clue here is the very high BUN/Cr ratio.

We were all taught early in our training that a high BUN/Cr ratio represented volume depletion. This is certainly the most common cause, but very high BUN/Cr ratios (over 30) can represent causes beyond volume depletion.

Witting and colleagues studied factors that predicted upper GI bleeding in patients presenting without hematemesis. They found that the three strongest predictors were black stool (odds ratio, 16.6), BUN/Cr ratio greater than 30 (OR, 10), and age greater than 50 (OR, 8.4).¹

Srygley and colleagues reviewed high-quality studies of factors associated with upper GI bleeding.² Factors that were found to increase the likelihood of an upper gastrointestinal bleed were Melenic stool on exam (likelihood ratio, 25), blood or coffee grounds on nasogastric aspiration (LR, 9.6), and BUN/Cr ratio greater than 30 (LR, 7.5).

Very high BUN/Cr ratios can indicate problems other than UGI bleeding and volume depletion. High BUN/Cr ratios are seen in patients with heart failure.

Zhang and colleagues studied if a high BUN/Cr ratio helped distinguish heart failure from asthma and chronic obstructive pulmonary disease (COPD).³ They found that, compared with those in the asthma group, the BUN/Cr ratios were significantly increased in the heart failure group (P < .05), whereas no significant differences in BUN/Cr ratios were found between the asthma and COPD groups.

Cheang and colleagues conducted their own study, as well as a meta-analysis, looking to see if high BUN/Cr ratios predicted increased mortality in patients with acute heart failure.⁴ In the meta-analysis of 8 studies (including their own), they found that the highest BUN/Cr ratio category was associated with an 77% higher all-cause mortality than the lowest category (hazard ratio, 1.77; 95% confidence interval, 1.52-2.07).

High dose corticosteroids can raise BUN levels, especially in patients with chronic kidney disease, and cause unexpectedly high BUN/Cr ratios.
 

Pearl

Very high BUN/Cr ratios (greater than 30) can signify upper GI bleeding, heart failure, or high-dose corticosteroid use.

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 dpaauw@uw.edu.

References

1. Am J Emerg Med. 2006 May;24(3):280-5.

2. JAMA. 2012;307(10):1072-9.

3. Comput Math Methods Med. 2022 Jul 21. doi: 10.1155/2022/4586458.

4. Cardiorenal Med. 2020;10:415-28.

A 43-year-old man presents to the emergency department with dizziness and a 6-hour history of passing maroon stool. He has been in good health with the only medical problem in his history being depression.

He is taking sertraline. On exam, his blood pressure is 100/60, and his pulse is 100, both while lying down. His blood pressure while standing is 90/60 and his pulse while standing is 130. The rest of his exam is normal. His lab values include hemoglobin of 10, hematocrit of 30, white blood cell of 4.6, platelet count of 175,000, sodium of 142, chloride of 100, bicarbonate of 24, potassium of 3.8, blood urea nitrogen (BUN) of 38, and creatinine clearance (Cr) of 1.1.

What is the most likely source of his bleeding?

A. Gastric ulcer

B. Meckel’s diverticulum

C. Arteriovenous malformation

D. Diverticulosis

E. Hemorrhoids

What makes the most sense

The most likely cause of this patient’s maroon stool is an upper gastrointestinal bleed, so it would make the most sense for a gastric ulcer to be the source of his bleeding. The clue here is the very high BUN/Cr ratio.

We were all taught early in our training that a high BUN/Cr ratio represented volume depletion. This is certainly the most common cause, but very high BUN/Cr ratios (over 30) can represent causes beyond volume depletion.

Witting and colleagues studied factors that predicted upper GI bleeding in patients presenting without hematemesis. They found that the three strongest predictors were black stool (odds ratio, 16.6), BUN/Cr ratio greater than 30 (OR, 10), and age greater than 50 (OR, 8.4).¹

Srygley and colleagues reviewed high-quality studies of factors associated with upper GI bleeding.² Factors that were found to increase the likelihood of an upper gastrointestinal bleed were Melenic stool on exam (likelihood ratio, 25), blood or coffee grounds on nasogastric aspiration (LR, 9.6), and BUN/Cr ratio greater than 30 (LR, 7.5).

Very high BUN/Cr ratios can indicate problems other than UGI bleeding and volume depletion. High BUN/Cr ratios are seen in patients with heart failure.

Zhang and colleagues studied if a high BUN/Cr ratio helped distinguish heart failure from asthma and chronic obstructive pulmonary disease (COPD).³ They found that, compared with those in the asthma group, the BUN/Cr ratios were significantly increased in the heart failure group (P < .05), whereas no significant differences in BUN/Cr ratios were found between the asthma and COPD groups.

Cheang and colleagues conducted their own study, as well as a meta-analysis, looking to see if high BUN/Cr ratios predicted increased mortality in patients with acute heart failure.⁴ In the meta-analysis of 8 studies (including their own), they found that the highest BUN/Cr ratio category was associated with an 77% higher all-cause mortality than the lowest category (hazard ratio, 1.77; 95% confidence interval, 1.52-2.07).

High dose corticosteroids can raise BUN levels, especially in patients with chronic kidney disease, and cause unexpectedly high BUN/Cr ratios.
 

Pearl

Very high BUN/Cr ratios (greater than 30) can signify upper GI bleeding, heart failure, or high-dose corticosteroid use.

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 dpaauw@uw.edu.

References

1. Am J Emerg Med. 2006 May;24(3):280-5.

2. JAMA. 2012;307(10):1072-9.

3. Comput Math Methods Med. 2022 Jul 21. doi: 10.1155/2022/4586458.

4. Cardiorenal Med. 2020;10:415-28.

A 43-year-old man presents to the emergency department with dizziness and a 6-hour history of passing maroon stool. He has been in good health with the only medical problem in his history being depression.

He is taking sertraline. On exam, his blood pressure is 100/60, and his pulse is 100, both while lying down. His blood pressure while standing is 90/60 and his pulse while standing is 130. The rest of his exam is normal. His lab values include hemoglobin of 10, hematocrit of 30, white blood cell of 4.6, platelet count of 175,000, sodium of 142, chloride of 100, bicarbonate of 24, potassium of 3.8, blood urea nitrogen (BUN) of 38, and creatinine clearance (Cr) of 1.1.

What is the most likely source of his bleeding?

A. Gastric ulcer

B. Meckel’s diverticulum

C. Arteriovenous malformation

D. Diverticulosis

E. Hemorrhoids

What makes the most sense

The most likely cause of this patient’s maroon stool is an upper gastrointestinal bleed, so it would make the most sense for a gastric ulcer to be the source of his bleeding. The clue here is the very high BUN/Cr ratio.

We were all taught early in our training that a high BUN/Cr ratio represented volume depletion. This is certainly the most common cause, but very high BUN/Cr ratios (over 30) can represent causes beyond volume depletion.

Witting and colleagues studied factors that predicted upper GI bleeding in patients presenting without hematemesis. They found that the three strongest predictors were black stool (odds ratio, 16.6), BUN/Cr ratio greater than 30 (OR, 10), and age greater than 50 (OR, 8.4).¹

Srygley and colleagues reviewed high-quality studies of factors associated with upper GI bleeding.² Factors that were found to increase the likelihood of an upper gastrointestinal bleed were Melenic stool on exam (likelihood ratio, 25), blood or coffee grounds on nasogastric aspiration (LR, 9.6), and BUN/Cr ratio greater than 30 (LR, 7.5).

Very high BUN/Cr ratios can indicate problems other than UGI bleeding and volume depletion. High BUN/Cr ratios are seen in patients with heart failure.

Zhang and colleagues studied if a high BUN/Cr ratio helped distinguish heart failure from asthma and chronic obstructive pulmonary disease (COPD).³ They found that, compared with those in the asthma group, the BUN/Cr ratios were significantly increased in the heart failure group (P < .05), whereas no significant differences in BUN/Cr ratios were found between the asthma and COPD groups.

Cheang and colleagues conducted their own study, as well as a meta-analysis, looking to see if high BUN/Cr ratios predicted increased mortality in patients with acute heart failure.⁴ In the meta-analysis of 8 studies (including their own), they found that the highest BUN/Cr ratio category was associated with an 77% higher all-cause mortality than the lowest category (hazard ratio, 1.77; 95% confidence interval, 1.52-2.07).

High dose corticosteroids can raise BUN levels, especially in patients with chronic kidney disease, and cause unexpectedly high BUN/Cr ratios.
 

Pearl

Very high BUN/Cr ratios (greater than 30) can signify upper GI bleeding, heart failure, or high-dose corticosteroid use.

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 dpaauw@uw.edu.

References

1. Am J Emerg Med. 2006 May;24(3):280-5.

2. JAMA. 2012;307(10):1072-9.

3. Comput Math Methods Med. 2022 Jul 21. doi: 10.1155/2022/4586458.

4. Cardiorenal Med. 2020;10:415-28.

A common sentiment shared by patients who are happy with their health care professionals is, “I feel heard and understood.” How do we become those professionals and make sure that we are doing a good job connecting and communicating with our patients?

Here are a few suggestions on how to do this.
 

Practice intent listening

When a patient shares their symptoms with you, show genuine curiosity and concern. Ask clarifying questions. Ask how the symptom or problem is affecting their day-to-day life. Avoid quick, rapid-fire questions back at the patient. Do not accept a patient self-diagnosis.

When a patient with a first-time headache says they are having a migraine headache, for example, ask many clarifying questions to make sure you can make a diagnosis of headache type, then use all the information you have gathered to educate the patient on what you believe they have.

It is easy to jump to treatment, but we always want to make sure we have the diagnosis correct first. By intently listening, it also makes it much easier to tell a patient you do not know what is causing their symptoms, but that you and the patient will be vigilant for any future clues that may lead to a diagnosis.
 

Use terminology that patients understand

Rachael Gotlieb, MD, and colleagues published an excellent study with eye-opening results on common phrases we use as health care providers and how often patients do not understand them.

Only 9% of patients understood what was meant when they were asked if they have been febrile. Only 2% understood what was meant by “I am concerned the patient has an occult infection.” Only 21% understood that “your xray findings were quite impressive” was bad news.

It is easy to avoid these medical language traps, we just have to check our doctor speak. Ask, “Do you have a fever?” Say, “I am concerned you may have an infection that is hard to find.”

Several other terms we use all the time in explaining things to patients that I have found most patients do not understand are the terms bilateral, systemic, and significant. Think carefully as you explain things to patients and check back to have them repeat to you what they think you said.
 

Be comfortable saying you don’t know

Many symptoms in medicine end up not being diagnosable. When a patient shares symptoms that do not fit a pattern of a disease, it is important to share with them why you think it is okay to wait and watch, even if you do not have a diagnosis.

Patients find it comforting that you are so honest with them. Doing this also has the benefit of gaining patients’ trust when you are sure about something, because it tells them you don’t have an answer for everything.
 

Ask your patients what they think is causing their symptoms

This way, you know what their big fear is. You can address what they are worried about, even if it isn’t something you are considering.

Patients are often fearful of a disease a close friend or relative has, so when they get new symptoms, they fear diseases that we might not think of. By knowing what they are fearful of, you can reassure when appropriate.

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 dpaauw@uw.edu.

A common sentiment shared by patients who are happy with their health care professionals is, “I feel heard and understood.” How do we become those professionals and make sure that we are doing a good job connecting and communicating with our patients?

Here are a few suggestions on how to do this.
 

Practice intent listening

When a patient shares their symptoms with you, show genuine curiosity and concern. Ask clarifying questions. Ask how the symptom or problem is affecting their day-to-day life. Avoid quick, rapid-fire questions back at the patient. Do not accept a patient self-diagnosis.

When a patient with a first-time headache says they are having a migraine headache, for example, ask many clarifying questions to make sure you can make a diagnosis of headache type, then use all the information you have gathered to educate the patient on what you believe they have.

It is easy to jump to treatment, but we always want to make sure we have the diagnosis correct first. By intently listening, it also makes it much easier to tell a patient you do not know what is causing their symptoms, but that you and the patient will be vigilant for any future clues that may lead to a diagnosis.
 

Use terminology that patients understand

Rachael Gotlieb, MD, and colleagues published an excellent study with eye-opening results on common phrases we use as health care providers and how often patients do not understand them.

Only 9% of patients understood what was meant when they were asked if they have been febrile. Only 2% understood what was meant by “I am concerned the patient has an occult infection.” Only 21% understood that “your xray findings were quite impressive” was bad news.

It is easy to avoid these medical language traps, we just have to check our doctor speak. Ask, “Do you have a fever?” Say, “I am concerned you may have an infection that is hard to find.”

Several other terms we use all the time in explaining things to patients that I have found most patients do not understand are the terms bilateral, systemic, and significant. Think carefully as you explain things to patients and check back to have them repeat to you what they think you said.
 

Be comfortable saying you don’t know

Many symptoms in medicine end up not being diagnosable. When a patient shares symptoms that do not fit a pattern of a disease, it is important to share with them why you think it is okay to wait and watch, even if you do not have a diagnosis.

Patients find it comforting that you are so honest with them. Doing this also has the benefit of gaining patients’ trust when you are sure about something, because it tells them you don’t have an answer for everything.
 

Ask your patients what they think is causing their symptoms

This way, you know what their big fear is. You can address what they are worried about, even if it isn’t something you are considering.

Patients are often fearful of a disease a close friend or relative has, so when they get new symptoms, they fear diseases that we might not think of. By knowing what they are fearful of, you can reassure when appropriate.

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 dpaauw@uw.edu.

A common sentiment shared by patients who are happy with their health care professionals is, “I feel heard and understood.” How do we become those professionals and make sure that we are doing a good job connecting and communicating with our patients?

Here are a few suggestions on how to do this.
 

Practice intent listening

When a patient shares their symptoms with you, show genuine curiosity and concern. Ask clarifying questions. Ask how the symptom or problem is affecting their day-to-day life. Avoid quick, rapid-fire questions back at the patient. Do not accept a patient self-diagnosis.

When a patient with a first-time headache says they are having a migraine headache, for example, ask many clarifying questions to make sure you can make a diagnosis of headache type, then use all the information you have gathered to educate the patient on what you believe they have.

It is easy to jump to treatment, but we always want to make sure we have the diagnosis correct first. By intently listening, it also makes it much easier to tell a patient you do not know what is causing their symptoms, but that you and the patient will be vigilant for any future clues that may lead to a diagnosis.
 

Use terminology that patients understand

Rachael Gotlieb, MD, and colleagues published an excellent study with eye-opening results on common phrases we use as health care providers and how often patients do not understand them.

Only 9% of patients understood what was meant when they were asked if they have been febrile. Only 2% understood what was meant by “I am concerned the patient has an occult infection.” Only 21% understood that “your xray findings were quite impressive” was bad news.

It is easy to avoid these medical language traps, we just have to check our doctor speak. Ask, “Do you have a fever?” Say, “I am concerned you may have an infection that is hard to find.”

Several other terms we use all the time in explaining things to patients that I have found most patients do not understand are the terms bilateral, systemic, and significant. Think carefully as you explain things to patients and check back to have them repeat to you what they think you said.
 

Be comfortable saying you don’t know

Many symptoms in medicine end up not being diagnosable. When a patient shares symptoms that do not fit a pattern of a disease, it is important to share with them why you think it is okay to wait and watch, even if you do not have a diagnosis.

Patients find it comforting that you are so honest with them. Doing this also has the benefit of gaining patients’ trust when you are sure about something, because it tells them you don’t have an answer for everything.
 

Ask your patients what they think is causing their symptoms

This way, you know what their big fear is. You can address what they are worried about, even if it isn’t something you are considering.

Patients are often fearful of a disease a close friend or relative has, so when they get new symptoms, they fear diseases that we might not think of. By knowing what they are fearful of, you can reassure when appropriate.

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 dpaauw@uw.edu.

A 70-year-old man with a history of coronary artery disease (CAD) is seen for concerns about erectile dysfunction (ED). He is requesting sildenafil. He has stable angina, having chest pain with exercise. He uses sublingual nitroglycerin (SL NTG prn) about three times a month. His blood pressure is 140/70 mm Hg. His pulse is 60 beats per minute. His current medications are lisinopril, atorvastatin, aspirin, and SL NTG tablets as needed.

What would you recommend?

A. No sildenafil; refer to urologist for other ED options.

B. Okay to use sildenafil if greater than 6 hours from NTG use.

C. Recommend tadalafil.

Is coprescribing nitrates and phosphodiesterase inhibitors safe?

The FDA warns against the use of phosphodiesterase inhibitors in patients taking nitrates. Combining nitrates with phosphodiesterase type 5 (PDE5) inhibitors is contraindicated because of a synergistic blood pressure lowering effect.¹ This warning/contraindication was based on theoretical concerns, as well as concern that of the first 130 deaths reported in patients who took sildenafil, 16 of the patients also were taking nitrates.²

Parker and colleagues studied the safety of giving IV nitroglycerin to patients with coronary artery disease (CAD) who have taken sildenafil.³ The study was a randomized, placebo-controlled, crossover trial. Participants received sildenafil 100 mg or placebo, then received intravenous NTG. Patients who received sildenafil had a 4-6 mm Hg systolic BP drop compared with those who took the placebo. There was no difference in severe events between the sildenafil and placebo groups. The blood levels of nitroglycerin in this study were very likely much higher than the levels that occur with SL NTG.

A recent study by Holt et al. looked at overall cardiovascular outcomes with coprescribing nitrates and phosphodiesterase inhibitors.⁴ The study was a case crossover design, using a nationwide Danish health registry over the period of 2000-2018. In 2000, the rate of coprescribing of phosphodiesterase inhibitors in ischemic heart disease patients on nitrates was .9 per 100 persons/year and rose to 19.5 prescriptions per 100 persons/year in 2018. During this same time, no statistically significant association was found between the coprescription of nitrates with PDE5 inhibitors and the risk for MI, cardiac arrest, syncope, stroke, or an adverse drug event.
 

Does nitroglycerin response help determine cause of chest pain?

Nitroglycerin response has long been used as a clinical indicator on whether a patient’s chest pain is cardiac or not. Eric A. Shry, MD, and his colleagues looked at the usefulness of nitroglycerin response in the treatment of chest pain as a predictor of ischemic chest pain in an emergency department setting.⁵

The study was a retrospective review of 223 patients who presented to the emergency department over a 5-month period with ongoing chest pain. They looked at patients who had ongoing chest pain in the emergency department, received nitroglycerin, and did not receive any therapy other than aspirin within 10 minutes of receiving nitroglycerin. Response to the drug was compared with the final diagnosis of cardiac versus noncardiac chest pain.

Of the patients with a final determination of cardiac chest pain, 88% had a nitroglycerin response, whereas 92% of the patients with noncardiac chest pain had a nitroglycerin response (P = .50).

Deborah B. Diercks, MD, and her colleagues looked at improvement in chest pain scores in the emergency department in patients treated with nitroglycerin and whether it correlated with a cardiac etiology of chest pain.⁶ The study was a prospective, observational study of 664 patients in an urban tertiary care emergency department over a 16-month period. An 11-point numeric chest pain scale was assessed and recorded by research assistants before and 5 minutes after receiving nitroglycerin. The scale ranged from 0 (no pain) to 10 (worst pain imaginable).

A final diagnosis of a cardiac etiology for chest pain was found in 18% of the patients in the study. Of the patients who had cardiac-related chest pain, 20% had no reduction in pain with nitroglycerin, compared with 19% of the patients without cardiac-related chest pain.

A complete or significant reduction in chest pain occurred with nitroglycerin in 31% of patients with cardiac chest pain and 27% of the patients without cardiac chest pain (P = .76).

Nitroglycerin response does not appear to be helpful in distinguishing cardiac from noncardiac chest pain, but a study by His and colleagues offers an interesting twist.⁷

The authors of this research studied 118 patients looking to see if the side effect of headache with nitroglycerin was more common in patients who did not have CAD than in those who did. All the patients had a varying degree of relief of chest pain with NTG administration within 10 minutes. In patients with normal coronary arteries or minimal CAD, 73% had headache caused by NTG, whereas in patients with obstructive CAD, only 23% had headache after NTG use.
 

Take-home messages

• Short acting nitroglycerin may not be a contraindication for phosphodiesterase inhibitor use.
• More data are still needed.
• Nitroglycerin response does not help distinguish chest pain from CAD from noncardiac causes.

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 imnews@mdedge.com.

References

1. Schwartz BG, Kloner RA. Drug interactions with phosphodiesterase-5 inhibitors used for the treatment of erectile dysfunction or pulmonary hypertension. Circulation. 2010;122:88-95.

2. Kloner RA, Zusman RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999 Sep 9;84(5B):11N-17N.

3. Parker JD et al. Safety of intravenous nitroglycerin after administration of sildenafil citrate to men with coronary artery disease: A double-blind, placebo-controlled, randomized, crossover trial. Crit Care Med. 2007;35:1863-8.

4. Holt A et al. Adverse events associated with coprescription of phosphodiesterase type inhibitors and oral organic nitrates in male patients with ischemic heart disease. Ann Intern Med. 2022 Jun;175(6):774-82.

5. Shry EA et al. Usefulness of the response to sublingual nitroglycerin as a predictor of ischemic chest pain in the emergency department. Am J Cardiol. 2002 Dec 1;90(11):1264-6.

6. Diercks DB et al. Changes in the numeric descriptive scale for pain after sublingual nitroglycerin do not predict cardiac etiology of chest pain. Ann Emerg Med. 2005 Jun;45(6):581-5.

7. His DH et al. Headache response to glyceryl trinitrate in patients with and without obstructive coronary artery disease. Heart 2005;91:1164-6.

A 70-year-old man with a history of coronary artery disease (CAD) is seen for concerns about erectile dysfunction (ED). He is requesting sildenafil. He has stable angina, having chest pain with exercise. He uses sublingual nitroglycerin (SL NTG prn) about three times a month. His blood pressure is 140/70 mm Hg. His pulse is 60 beats per minute. His current medications are lisinopril, atorvastatin, aspirin, and SL NTG tablets as needed.

What would you recommend?

A. No sildenafil; refer to urologist for other ED options.

B. Okay to use sildenafil if greater than 6 hours from NTG use.

C. Recommend tadalafil.

Is coprescribing nitrates and phosphodiesterase inhibitors safe?

The FDA warns against the use of phosphodiesterase inhibitors in patients taking nitrates. Combining nitrates with phosphodiesterase type 5 (PDE5) inhibitors is contraindicated because of a synergistic blood pressure lowering effect.¹ This warning/contraindication was based on theoretical concerns, as well as concern that of the first 130 deaths reported in patients who took sildenafil, 16 of the patients also were taking nitrates.²

Parker and colleagues studied the safety of giving IV nitroglycerin to patients with coronary artery disease (CAD) who have taken sildenafil.³ The study was a randomized, placebo-controlled, crossover trial. Participants received sildenafil 100 mg or placebo, then received intravenous NTG. Patients who received sildenafil had a 4-6 mm Hg systolic BP drop compared with those who took the placebo. There was no difference in severe events between the sildenafil and placebo groups. The blood levels of nitroglycerin in this study were very likely much higher than the levels that occur with SL NTG.

A recent study by Holt et al. looked at overall cardiovascular outcomes with coprescribing nitrates and phosphodiesterase inhibitors.⁴ The study was a case crossover design, using a nationwide Danish health registry over the period of 2000-2018. In 2000, the rate of coprescribing of phosphodiesterase inhibitors in ischemic heart disease patients on nitrates was .9 per 100 persons/year and rose to 19.5 prescriptions per 100 persons/year in 2018. During this same time, no statistically significant association was found between the coprescription of nitrates with PDE5 inhibitors and the risk for MI, cardiac arrest, syncope, stroke, or an adverse drug event.
 

Does nitroglycerin response help determine cause of chest pain?

Nitroglycerin response has long been used as a clinical indicator on whether a patient’s chest pain is cardiac or not. Eric A. Shry, MD, and his colleagues looked at the usefulness of nitroglycerin response in the treatment of chest pain as a predictor of ischemic chest pain in an emergency department setting.⁵

The study was a retrospective review of 223 patients who presented to the emergency department over a 5-month period with ongoing chest pain. They looked at patients who had ongoing chest pain in the emergency department, received nitroglycerin, and did not receive any therapy other than aspirin within 10 minutes of receiving nitroglycerin. Response to the drug was compared with the final diagnosis of cardiac versus noncardiac chest pain.

Of the patients with a final determination of cardiac chest pain, 88% had a nitroglycerin response, whereas 92% of the patients with noncardiac chest pain had a nitroglycerin response (P = .50).

Deborah B. Diercks, MD, and her colleagues looked at improvement in chest pain scores in the emergency department in patients treated with nitroglycerin and whether it correlated with a cardiac etiology of chest pain.⁶ The study was a prospective, observational study of 664 patients in an urban tertiary care emergency department over a 16-month period. An 11-point numeric chest pain scale was assessed and recorded by research assistants before and 5 minutes after receiving nitroglycerin. The scale ranged from 0 (no pain) to 10 (worst pain imaginable).

A final diagnosis of a cardiac etiology for chest pain was found in 18% of the patients in the study. Of the patients who had cardiac-related chest pain, 20% had no reduction in pain with nitroglycerin, compared with 19% of the patients without cardiac-related chest pain.

A complete or significant reduction in chest pain occurred with nitroglycerin in 31% of patients with cardiac chest pain and 27% of the patients without cardiac chest pain (P = .76).

Nitroglycerin response does not appear to be helpful in distinguishing cardiac from noncardiac chest pain, but a study by His and colleagues offers an interesting twist.⁷

The authors of this research studied 118 patients looking to see if the side effect of headache with nitroglycerin was more common in patients who did not have CAD than in those who did. All the patients had a varying degree of relief of chest pain with NTG administration within 10 minutes. In patients with normal coronary arteries or minimal CAD, 73% had headache caused by NTG, whereas in patients with obstructive CAD, only 23% had headache after NTG use.
 

Take-home messages

• Short acting nitroglycerin may not be a contraindication for phosphodiesterase inhibitor use.
• More data are still needed.
• Nitroglycerin response does not help distinguish chest pain from CAD from noncardiac causes.

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 imnews@mdedge.com.

References

1. Schwartz BG, Kloner RA. Drug interactions with phosphodiesterase-5 inhibitors used for the treatment of erectile dysfunction or pulmonary hypertension. Circulation. 2010;122:88-95.

2. Kloner RA, Zusman RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999 Sep 9;84(5B):11N-17N.

3. Parker JD et al. Safety of intravenous nitroglycerin after administration of sildenafil citrate to men with coronary artery disease: A double-blind, placebo-controlled, randomized, crossover trial. Crit Care Med. 2007;35:1863-8.

4. Holt A et al. Adverse events associated with coprescription of phosphodiesterase type inhibitors and oral organic nitrates in male patients with ischemic heart disease. Ann Intern Med. 2022 Jun;175(6):774-82.

5. Shry EA et al. Usefulness of the response to sublingual nitroglycerin as a predictor of ischemic chest pain in the emergency department. Am J Cardiol. 2002 Dec 1;90(11):1264-6.

6. Diercks DB et al. Changes in the numeric descriptive scale for pain after sublingual nitroglycerin do not predict cardiac etiology of chest pain. Ann Emerg Med. 2005 Jun;45(6):581-5.

7. His DH et al. Headache response to glyceryl trinitrate in patients with and without obstructive coronary artery disease. Heart 2005;91:1164-6.

A 70-year-old man with a history of coronary artery disease (CAD) is seen for concerns about erectile dysfunction (ED). He is requesting sildenafil. He has stable angina, having chest pain with exercise. He uses sublingual nitroglycerin (SL NTG prn) about three times a month. His blood pressure is 140/70 mm Hg. His pulse is 60 beats per minute. His current medications are lisinopril, atorvastatin, aspirin, and SL NTG tablets as needed.

What would you recommend?

A. No sildenafil; refer to urologist for other ED options.

B. Okay to use sildenafil if greater than 6 hours from NTG use.

C. Recommend tadalafil.

Is coprescribing nitrates and phosphodiesterase inhibitors safe?

The FDA warns against the use of phosphodiesterase inhibitors in patients taking nitrates. Combining nitrates with phosphodiesterase type 5 (PDE5) inhibitors is contraindicated because of a synergistic blood pressure lowering effect.¹ This warning/contraindication was based on theoretical concerns, as well as concern that of the first 130 deaths reported in patients who took sildenafil, 16 of the patients also were taking nitrates.²

Parker and colleagues studied the safety of giving IV nitroglycerin to patients with coronary artery disease (CAD) who have taken sildenafil.³ The study was a randomized, placebo-controlled, crossover trial. Participants received sildenafil 100 mg or placebo, then received intravenous NTG. Patients who received sildenafil had a 4-6 mm Hg systolic BP drop compared with those who took the placebo. There was no difference in severe events between the sildenafil and placebo groups. The blood levels of nitroglycerin in this study were very likely much higher than the levels that occur with SL NTG.

A recent study by Holt et al. looked at overall cardiovascular outcomes with coprescribing nitrates and phosphodiesterase inhibitors.⁴ The study was a case crossover design, using a nationwide Danish health registry over the period of 2000-2018. In 2000, the rate of coprescribing of phosphodiesterase inhibitors in ischemic heart disease patients on nitrates was .9 per 100 persons/year and rose to 19.5 prescriptions per 100 persons/year in 2018. During this same time, no statistically significant association was found between the coprescription of nitrates with PDE5 inhibitors and the risk for MI, cardiac arrest, syncope, stroke, or an adverse drug event.
 

Does nitroglycerin response help determine cause of chest pain?

Nitroglycerin response has long been used as a clinical indicator on whether a patient’s chest pain is cardiac or not. Eric A. Shry, MD, and his colleagues looked at the usefulness of nitroglycerin response in the treatment of chest pain as a predictor of ischemic chest pain in an emergency department setting.⁵

The study was a retrospective review of 223 patients who presented to the emergency department over a 5-month period with ongoing chest pain. They looked at patients who had ongoing chest pain in the emergency department, received nitroglycerin, and did not receive any therapy other than aspirin within 10 minutes of receiving nitroglycerin. Response to the drug was compared with the final diagnosis of cardiac versus noncardiac chest pain.

Of the patients with a final determination of cardiac chest pain, 88% had a nitroglycerin response, whereas 92% of the patients with noncardiac chest pain had a nitroglycerin response (P = .50).

Deborah B. Diercks, MD, and her colleagues looked at improvement in chest pain scores in the emergency department in patients treated with nitroglycerin and whether it correlated with a cardiac etiology of chest pain.⁶ The study was a prospective, observational study of 664 patients in an urban tertiary care emergency department over a 16-month period. An 11-point numeric chest pain scale was assessed and recorded by research assistants before and 5 minutes after receiving nitroglycerin. The scale ranged from 0 (no pain) to 10 (worst pain imaginable).

A final diagnosis of a cardiac etiology for chest pain was found in 18% of the patients in the study. Of the patients who had cardiac-related chest pain, 20% had no reduction in pain with nitroglycerin, compared with 19% of the patients without cardiac-related chest pain.

A complete or significant reduction in chest pain occurred with nitroglycerin in 31% of patients with cardiac chest pain and 27% of the patients without cardiac chest pain (P = .76).

Nitroglycerin response does not appear to be helpful in distinguishing cardiac from noncardiac chest pain, but a study by His and colleagues offers an interesting twist.⁷

The authors of this research studied 118 patients looking to see if the side effect of headache with nitroglycerin was more common in patients who did not have CAD than in those who did. All the patients had a varying degree of relief of chest pain with NTG administration within 10 minutes. In patients with normal coronary arteries or minimal CAD, 73% had headache caused by NTG, whereas in patients with obstructive CAD, only 23% had headache after NTG use.
 

Take-home messages

• Short acting nitroglycerin may not be a contraindication for phosphodiesterase inhibitor use.
• More data are still needed.
• Nitroglycerin response does not help distinguish chest pain from CAD from noncardiac causes.

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 imnews@mdedge.com.

References

1. Schwartz BG, Kloner RA. Drug interactions with phosphodiesterase-5 inhibitors used for the treatment of erectile dysfunction or pulmonary hypertension. Circulation. 2010;122:88-95.

2. Kloner RA, Zusman RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999 Sep 9;84(5B):11N-17N.

3. Parker JD et al. Safety of intravenous nitroglycerin after administration of sildenafil citrate to men with coronary artery disease: A double-blind, placebo-controlled, randomized, crossover trial. Crit Care Med. 2007;35:1863-8.

4. Holt A et al. Adverse events associated with coprescription of phosphodiesterase type inhibitors and oral organic nitrates in male patients with ischemic heart disease. Ann Intern Med. 2022 Jun;175(6):774-82.

5. Shry EA et al. Usefulness of the response to sublingual nitroglycerin as a predictor of ischemic chest pain in the emergency department. Am J Cardiol. 2002 Dec 1;90(11):1264-6.

6. Diercks DB et al. Changes in the numeric descriptive scale for pain after sublingual nitroglycerin do not predict cardiac etiology of chest pain. Ann Emerg Med. 2005 Jun;45(6):581-5.

7. His DH et al. Headache response to glyceryl trinitrate in patients with and without obstructive coronary artery disease. Heart 2005;91:1164-6.

A 67-year-old man asks about what he can do to prevent dementia. He reports his mother had dementia, and he wants to do everything he can to prevent it. Which of the following has evidence of benefit?

A) Thiamine

B) Vitamin E

C) Multivitamin (MV)

D) Keto diet

E) Red wine
 

FDA-approved therapies for dementia

To date the actual therapies for dementia have been disappointing. Donepezil, the most prescribed medication for the treatment of dementia has a number-needed-to treat (NNT) over 17, and causes frequent side effects. Aducanumab was recently approved by the Food and Drug Administration for the treatment of Alzheimer’s disease (AD), but controversy has arisen, as the clinical results were modest, and the price tag will be large – estimated at $30,000-$50,000/year.

Preventive options that may decrease the likelihood of dementia

Patients often ask the question stated above. Regarding how to respond to that question, choice C, MV, has some recent evidence of benefit. Baker and colleagues studied the effect of cocoa extract and multivitamins on cognitive function in the COSMOS-Mind trial.¹ A total of 2,262 people were enrolled, and over 90% completed baseline and at least one annual cognitive assessment. Cocoa extract had no impact on global cognition (confidence interval [CI], –.02-.08, P = .28), but MV supplementation did have a statistically significant impact on global cognition (CI, .02-.12, P less than .007).

Vitamin E has been enthusiastically endorsed in the past as a treatment to prevent cognitive decline. The most recent Cochrane review on vitamin E concluded there was no evidence that the alpha-tocopherol form of vitamin E given to people with MCI prevents progression to dementia, or that it improves cognitive function in people with MCI or dementia due to AD.²

Exercise has long been a mainstay of our advice to patients as something they can do to help prevent dementia. Yu and colleagues did a meta-analysis of almost 400 randomized controlled trials and observational studies to grade the evidence on different interventions.³ They gave exercise a grade B for evidence of benefit.

A recent study addressed this issue, and I think it is helpful on quantifying how much exercise is needed. Del Pozo Cruz and colleagues did a prospective population-based cohort study of 78,000 adults aged 40-79, with an average of 6.9 years of follow up.⁴ The optimal step count was 9,826 steps (hazard ratio [HR], 0.49; 95% CI, 0.39-0.62) and the minimal step count for benefit was 3,826 steps (HR, 0.75; 95% CI, 0.67-0.83).
 

Modifiable factors

The other major modifiable factors to consider are problems with special senses. Both vision loss and hearing loss have been associated with cognitive impairment.

Shang and colleagues published a meta-analysis of 14 cohort studies addressing vision impairment and cognitive function involving more than 6 million individuals.⁵ They concluded that vision impairment is associated with an increased risk of both dementia and cognitive impairment in older adults.

Loughrey and colleagues performed a meta-analysis of 36 studies addressing hearing loss and cognitive decline.⁶ They reported that, among cross-sectional studies, a significant association was found for cognitive impairment (odds ratio [OR], 2.00; 95% CI, 1.39-2.89) and dementia (OR, 2.42; 95% CI, 1.24-4.72). A similar finding was present in prospective cohort studies with a significant association being found for cognitive impairment (OR, 1.22; 95% CI, 1.09-1.36) and dementia (OR, 1.28; 95% CI, 1.02-1.59).

A 25-year prospective, population-based study of patients with hearing loss revealed a difference in the rate of change in MMSE score over the 25-year follow-up between participants with hearing loss not using hearing aids matched with controls who didn’t have hearing loss. Those with untreated hearing loss had more cognitive decline than that of patients without hearing loss.⁷ The subjects with hearing loss using a hearing aid had no difference in cognitive decline from controls.
 

Pearl

Several simple and safe interventions may protect our patients from cognitive decline. These include taking a daily multivitamin, walking more than 4,000 steps a day, and optimizing vision and hearing.

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 dpaauw@uw.edu.

References

1. Baker LD et al. Effects of cocoa extract and a multivitamin on cognitive function: A randomized clinical trial. Alzheimer’s Dement. 2022 Sep 14. doi: 10.1002/alz.12767.

2. Farina N et al. Vitamin E for Alzheimer’s dementia and mild cognitive impairment. Cochrane Database Syst Rev. 2017 Apr 18;4(4):CD002854. doi: 10.1002/14651858.CD002854.pub5.

3. Yu JT et al. Evidence-based prevention of Alzheimer’s disease: Systematic review and meta-analysis of 243 observational prospective studies and 153 randomised controlled trials. J Neurol Neurosurg Psychiatry. 2020 Nov;91(11):1201-9.

4. Del Pozo Cruz B et al. Association of daily step count and intensity with incident dementia in 78,430 adults living in the UK. JAMA Neurol. 2022 Oct 1;79(10):1059-63.

5. Shang X et al. The association between vision impairment and incidence of dementia and cognitive impairment: A systematic review and meta-analysis. Ophthalmology. 2021 Aug;128(8):1135-49.

6. Loughrey DG et al. Association of age-related hearing loss with cognitive function, cognitive impairment, and dementia: A systematic review and meta-analysis. JAMA Otolaryngol Head Neck Surg. 2018 Feb 1;144(2):115-26.

7. Amieva H et al. Self-reported hearing loss, hearing aids, and cognitive decline in elderly adults: A 25-year study. J Am Geriatr Soc. 2015 Oct;63(10):2099-104.

A 67-year-old man asks about what he can do to prevent dementia. He reports his mother had dementia, and he wants to do everything he can to prevent it. Which of the following has evidence of benefit?

A) Thiamine

B) Vitamin E

C) Multivitamin (MV)

D) Keto diet

E) Red wine
 

FDA-approved therapies for dementia

To date the actual therapies for dementia have been disappointing. Donepezil, the most prescribed medication for the treatment of dementia has a number-needed-to treat (NNT) over 17, and causes frequent side effects. Aducanumab was recently approved by the Food and Drug Administration for the treatment of Alzheimer’s disease (AD), but controversy has arisen, as the clinical results were modest, and the price tag will be large – estimated at $30,000-$50,000/year.

Preventive options that may decrease the likelihood of dementia

Patients often ask the question stated above. Regarding how to respond to that question, choice C, MV, has some recent evidence of benefit. Baker and colleagues studied the effect of cocoa extract and multivitamins on cognitive function in the COSMOS-Mind trial.¹ A total of 2,262 people were enrolled, and over 90% completed baseline and at least one annual cognitive assessment. Cocoa extract had no impact on global cognition (confidence interval [CI], –.02-.08, P = .28), but MV supplementation did have a statistically significant impact on global cognition (CI, .02-.12, P less than .007).

Vitamin E has been enthusiastically endorsed in the past as a treatment to prevent cognitive decline. The most recent Cochrane review on vitamin E concluded there was no evidence that the alpha-tocopherol form of vitamin E given to people with MCI prevents progression to dementia, or that it improves cognitive function in people with MCI or dementia due to AD.²

Exercise has long been a mainstay of our advice to patients as something they can do to help prevent dementia. Yu and colleagues did a meta-analysis of almost 400 randomized controlled trials and observational studies to grade the evidence on different interventions.³ They gave exercise a grade B for evidence of benefit.

A recent study addressed this issue, and I think it is helpful on quantifying how much exercise is needed. Del Pozo Cruz and colleagues did a prospective population-based cohort study of 78,000 adults aged 40-79, with an average of 6.9 years of follow up.⁴ The optimal step count was 9,826 steps (hazard ratio [HR], 0.49; 95% CI, 0.39-0.62) and the minimal step count for benefit was 3,826 steps (HR, 0.75; 95% CI, 0.67-0.83).
 

Modifiable factors

The other major modifiable factors to consider are problems with special senses. Both vision loss and hearing loss have been associated with cognitive impairment.

Shang and colleagues published a meta-analysis of 14 cohort studies addressing vision impairment and cognitive function involving more than 6 million individuals.⁵ They concluded that vision impairment is associated with an increased risk of both dementia and cognitive impairment in older adults.

Loughrey and colleagues performed a meta-analysis of 36 studies addressing hearing loss and cognitive decline.⁶ They reported that, among cross-sectional studies, a significant association was found for cognitive impairment (odds ratio [OR], 2.00; 95% CI, 1.39-2.89) and dementia (OR, 2.42; 95% CI, 1.24-4.72). A similar finding was present in prospective cohort studies with a significant association being found for cognitive impairment (OR, 1.22; 95% CI, 1.09-1.36) and dementia (OR, 1.28; 95% CI, 1.02-1.59).

A 25-year prospective, population-based study of patients with hearing loss revealed a difference in the rate of change in MMSE score over the 25-year follow-up between participants with hearing loss not using hearing aids matched with controls who didn’t have hearing loss. Those with untreated hearing loss had more cognitive decline than that of patients without hearing loss.⁷ The subjects with hearing loss using a hearing aid had no difference in cognitive decline from controls.
 

Pearl

Several simple and safe interventions may protect our patients from cognitive decline. These include taking a daily multivitamin, walking more than 4,000 steps a day, and optimizing vision and hearing.

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 dpaauw@uw.edu.

References

1. Baker LD et al. Effects of cocoa extract and a multivitamin on cognitive function: A randomized clinical trial. Alzheimer’s Dement. 2022 Sep 14. doi: 10.1002/alz.12767.

2. Farina N et al. Vitamin E for Alzheimer’s dementia and mild cognitive impairment. Cochrane Database Syst Rev. 2017 Apr 18;4(4):CD002854. doi: 10.1002/14651858.CD002854.pub5.

3. Yu JT et al. Evidence-based prevention of Alzheimer’s disease: Systematic review and meta-analysis of 243 observational prospective studies and 153 randomised controlled trials. J Neurol Neurosurg Psychiatry. 2020 Nov;91(11):1201-9.

4. Del Pozo Cruz B et al. Association of daily step count and intensity with incident dementia in 78,430 adults living in the UK. JAMA Neurol. 2022 Oct 1;79(10):1059-63.

5. Shang X et al. The association between vision impairment and incidence of dementia and cognitive impairment: A systematic review and meta-analysis. Ophthalmology. 2021 Aug;128(8):1135-49.

6. Loughrey DG et al. Association of age-related hearing loss with cognitive function, cognitive impairment, and dementia: A systematic review and meta-analysis. JAMA Otolaryngol Head Neck Surg. 2018 Feb 1;144(2):115-26.

7. Amieva H et al. Self-reported hearing loss, hearing aids, and cognitive decline in elderly adults: A 25-year study. J Am Geriatr Soc. 2015 Oct;63(10):2099-104.

A 67-year-old man asks about what he can do to prevent dementia. He reports his mother had dementia, and he wants to do everything he can to prevent it. Which of the following has evidence of benefit?

A) Thiamine

B) Vitamin E

C) Multivitamin (MV)

D) Keto diet

E) Red wine
 

FDA-approved therapies for dementia

To date the actual therapies for dementia have been disappointing. Donepezil, the most prescribed medication for the treatment of dementia has a number-needed-to treat (NNT) over 17, and causes frequent side effects. Aducanumab was recently approved by the Food and Drug Administration for the treatment of Alzheimer’s disease (AD), but controversy has arisen, as the clinical results were modest, and the price tag will be large – estimated at $30,000-$50,000/year.

Preventive options that may decrease the likelihood of dementia

Patients often ask the question stated above. Regarding how to respond to that question, choice C, MV, has some recent evidence of benefit. Baker and colleagues studied the effect of cocoa extract and multivitamins on cognitive function in the COSMOS-Mind trial.¹ A total of 2,262 people were enrolled, and over 90% completed baseline and at least one annual cognitive assessment. Cocoa extract had no impact on global cognition (confidence interval [CI], –.02-.08, P = .28), but MV supplementation did have a statistically significant impact on global cognition (CI, .02-.12, P less than .007).

Vitamin E has been enthusiastically endorsed in the past as a treatment to prevent cognitive decline. The most recent Cochrane review on vitamin E concluded there was no evidence that the alpha-tocopherol form of vitamin E given to people with MCI prevents progression to dementia, or that it improves cognitive function in people with MCI or dementia due to AD.²

Exercise has long been a mainstay of our advice to patients as something they can do to help prevent dementia. Yu and colleagues did a meta-analysis of almost 400 randomized controlled trials and observational studies to grade the evidence on different interventions.³ They gave exercise a grade B for evidence of benefit.

A recent study addressed this issue, and I think it is helpful on quantifying how much exercise is needed. Del Pozo Cruz and colleagues did a prospective population-based cohort study of 78,000 adults aged 40-79, with an average of 6.9 years of follow up.⁴ The optimal step count was 9,826 steps (hazard ratio [HR], 0.49; 95% CI, 0.39-0.62) and the minimal step count for benefit was 3,826 steps (HR, 0.75; 95% CI, 0.67-0.83).
 

Modifiable factors

The other major modifiable factors to consider are problems with special senses. Both vision loss and hearing loss have been associated with cognitive impairment.

Shang and colleagues published a meta-analysis of 14 cohort studies addressing vision impairment and cognitive function involving more than 6 million individuals.⁵ They concluded that vision impairment is associated with an increased risk of both dementia and cognitive impairment in older adults.

Loughrey and colleagues performed a meta-analysis of 36 studies addressing hearing loss and cognitive decline.⁶ They reported that, among cross-sectional studies, a significant association was found for cognitive impairment (odds ratio [OR], 2.00; 95% CI, 1.39-2.89) and dementia (OR, 2.42; 95% CI, 1.24-4.72). A similar finding was present in prospective cohort studies with a significant association being found for cognitive impairment (OR, 1.22; 95% CI, 1.09-1.36) and dementia (OR, 1.28; 95% CI, 1.02-1.59).

A 25-year prospective, population-based study of patients with hearing loss revealed a difference in the rate of change in MMSE score over the 25-year follow-up between participants with hearing loss not using hearing aids matched with controls who didn’t have hearing loss. Those with untreated hearing loss had more cognitive decline than that of patients without hearing loss.⁷ The subjects with hearing loss using a hearing aid had no difference in cognitive decline from controls.
 

Pearl

Several simple and safe interventions may protect our patients from cognitive decline. These include taking a daily multivitamin, walking more than 4,000 steps a day, and optimizing vision and hearing.

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 dpaauw@uw.edu.

References

1. Baker LD et al. Effects of cocoa extract and a multivitamin on cognitive function: A randomized clinical trial. Alzheimer’s Dement. 2022 Sep 14. doi: 10.1002/alz.12767.

2. Farina N et al. Vitamin E for Alzheimer’s dementia and mild cognitive impairment. Cochrane Database Syst Rev. 2017 Apr 18;4(4):CD002854. doi: 10.1002/14651858.CD002854.pub5.

3. Yu JT et al. Evidence-based prevention of Alzheimer’s disease: Systematic review and meta-analysis of 243 observational prospective studies and 153 randomised controlled trials. J Neurol Neurosurg Psychiatry. 2020 Nov;91(11):1201-9.

4. Del Pozo Cruz B et al. Association of daily step count and intensity with incident dementia in 78,430 adults living in the UK. JAMA Neurol. 2022 Oct 1;79(10):1059-63.

5. Shang X et al. The association between vision impairment and incidence of dementia and cognitive impairment: A systematic review and meta-analysis. Ophthalmology. 2021 Aug;128(8):1135-49.

6. Loughrey DG et al. Association of age-related hearing loss with cognitive function, cognitive impairment, and dementia: A systematic review and meta-analysis. JAMA Otolaryngol Head Neck Surg. 2018 Feb 1;144(2):115-26.

7. Amieva H et al. Self-reported hearing loss, hearing aids, and cognitive decline in elderly adults: A 25-year study. J Am Geriatr Soc. 2015 Oct;63(10):2099-104.

When I worked as a scribe prior to starting medical school, it was commonplace for patients to have fasting labs. I always felt terrible for the patients we saw late in the afternoon that had somehow fasted all day. For many other patients, there was the challenge of finding a time when they could return to have fasting labs drawn.

While in medical school, I have seen the transition of my preceptors’ recommendations, where it seems patients can now have nonfasting labs. However, I have still observed instances when patients need to have fasting labs. We can look at an example case to better understand when and why patients do and do not need to fast prior to having their lipids checked.

Case

A 57-year-old woman presents for an annual wellness visit. She has been healthy this past year with no new concerns. Her blood pressure has been well controlled, and she continues on a statin for hyperlipidemia. She is due for annual labs. She ate breakfast this morning. Which of the following do you recommend?

A. Obtain lipids with her other blood work now.

B. Have her return tomorrow to obtain fasting labs.

In this situation, A is the correct answer. The patient is due for routine screening labs and there are no current indications that fasting labs are necessary.

Studies of fasting vs. nonfasting lipids

Sidhu and Naugler performed a cross-sectional analysis comparing lipid values at fasting intervals of 1 hour to 16 hours.¹ They found the mean total cholesterol and HDL cholesterol values differed by greater than 2%. For LDL cholesterol, the values differed by less than 10% and triglycerides values differed by less than 20%. With this information, the researchers concluded fasting for routine lipids is generally unnecessary.

Mora and colleagues performed a post hoc prospective follow-up of a randomized control

trial to assess if nonfasting lipid measurements could cause misclassification of cardiovascular risk assessment.² Based on 8,270 participants, coronary events associated with fasting vs. nonfasting lipid values were similar when adjusted hazard ratios were compared. They also found an agreement of 94.8% when classifying participants into ASCVD risk categories for fasting and nonfasting lipid values. These outcomes led them to support the use of nonfasting lipid labs for routine cardiovascular risk assessment.

Rahman and colleagues performed a systematic review and found the use of nonfasting lipid values can reliably determine statin management in most situations.³ Circumstances where fasting labs should be used are if patients have a genetic dyslipidemia, if patients have severe hypertriglyceridemia (greater than 500 mg/dL), and if patients have pancreatitis. Triglyceride values fluctuate the most between the fasting and nonfasting state as seen above from Sidhu and Naugler. This could impact triglyceride disorder management and the accuracy of LDL cholesterol estimation (calculated by the Friedewald equation: LDL cholesterol = total cholesterol – HDL cholesterol – triglycerides/5 in mg/dL).³

Benefits of nonfasting lipid labs

There are many benefits of nonfasting labs. For the patients, they do not have to come to their appointments hungry, we can reduce the risk of hypoglycemia for those with diabetes, and they do not have to come back at a later date if they ate something earlier in the day.

For the lab, we can improve efficiency and decrease early morning congestion when patients typically come in for fasting labs.

Lastly, for the provider, nonfasting labs can improve workflow and help decrease the number of patients lost to follow-up who were unable to complete fasting labs the same day as their appointment.
 

Summary

Patients do not need to fast prior to having lipid levels drawn for routine screening. Fasting labs should be considered for patients who have a genetic dyslipidemia or if there is concern for hypertriglyceridemia.

Per the ACC/AHA guidelines, nonfasting lipids can be used to assess ASCVD risk and to establish a baseline LDL cholesterol in adults 20 years and older. If a patient has nonfasting triglycerides greater than 400 mg/dL, repeat fasting lipids should be drawn to assess fasting triglycerides and to establish a baseline LDL cholesterol.⁴
 

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

References

1. Rahman F et al. Curr Atheroscler Rep. 2018;20(3):14. Published 2018 Feb 17.

2. Mora S et al. JAMA Intern Med. 2019;179(7):898-905.

3. Sidhu D and Naugler C. Arch Intern Med. 2012;172(22):1707-10.

4. Hoover LE. Am Fam Physician. 2019 May 1;99(9):589-91.

When I worked as a scribe prior to starting medical school, it was commonplace for patients to have fasting labs. I always felt terrible for the patients we saw late in the afternoon that had somehow fasted all day. For many other patients, there was the challenge of finding a time when they could return to have fasting labs drawn.

While in medical school, I have seen the transition of my preceptors’ recommendations, where it seems patients can now have nonfasting labs. However, I have still observed instances when patients need to have fasting labs. We can look at an example case to better understand when and why patients do and do not need to fast prior to having their lipids checked.

Case

A 57-year-old woman presents for an annual wellness visit. She has been healthy this past year with no new concerns. Her blood pressure has been well controlled, and she continues on a statin for hyperlipidemia. She is due for annual labs. She ate breakfast this morning. Which of the following do you recommend?

A. Obtain lipids with her other blood work now.

B. Have her return tomorrow to obtain fasting labs.

In this situation, A is the correct answer. The patient is due for routine screening labs and there are no current indications that fasting labs are necessary.

Studies of fasting vs. nonfasting lipids

Sidhu and Naugler performed a cross-sectional analysis comparing lipid values at fasting intervals of 1 hour to 16 hours.¹ They found the mean total cholesterol and HDL cholesterol values differed by greater than 2%. For LDL cholesterol, the values differed by less than 10% and triglycerides values differed by less than 20%. With this information, the researchers concluded fasting for routine lipids is generally unnecessary.

Mora and colleagues performed a post hoc prospective follow-up of a randomized control

trial to assess if nonfasting lipid measurements could cause misclassification of cardiovascular risk assessment.² Based on 8,270 participants, coronary events associated with fasting vs. nonfasting lipid values were similar when adjusted hazard ratios were compared. They also found an agreement of 94.8% when classifying participants into ASCVD risk categories for fasting and nonfasting lipid values. These outcomes led them to support the use of nonfasting lipid labs for routine cardiovascular risk assessment.

Rahman and colleagues performed a systematic review and found the use of nonfasting lipid values can reliably determine statin management in most situations.³ Circumstances where fasting labs should be used are if patients have a genetic dyslipidemia, if patients have severe hypertriglyceridemia (greater than 500 mg/dL), and if patients have pancreatitis. Triglyceride values fluctuate the most between the fasting and nonfasting state as seen above from Sidhu and Naugler. This could impact triglyceride disorder management and the accuracy of LDL cholesterol estimation (calculated by the Friedewald equation: LDL cholesterol = total cholesterol – HDL cholesterol – triglycerides/5 in mg/dL).³

Benefits of nonfasting lipid labs

There are many benefits of nonfasting labs. For the patients, they do not have to come to their appointments hungry, we can reduce the risk of hypoglycemia for those with diabetes, and they do not have to come back at a later date if they ate something earlier in the day.

For the lab, we can improve efficiency and decrease early morning congestion when patients typically come in for fasting labs.

Lastly, for the provider, nonfasting labs can improve workflow and help decrease the number of patients lost to follow-up who were unable to complete fasting labs the same day as their appointment.
 

Summary

Patients do not need to fast prior to having lipid levels drawn for routine screening. Fasting labs should be considered for patients who have a genetic dyslipidemia or if there is concern for hypertriglyceridemia.

Per the ACC/AHA guidelines, nonfasting lipids can be used to assess ASCVD risk and to establish a baseline LDL cholesterol in adults 20 years and older. If a patient has nonfasting triglycerides greater than 400 mg/dL, repeat fasting lipids should be drawn to assess fasting triglycerides and to establish a baseline LDL cholesterol.⁴
 

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

References

1. Rahman F et al. Curr Atheroscler Rep. 2018;20(3):14. Published 2018 Feb 17.

2. Mora S et al. JAMA Intern Med. 2019;179(7):898-905.

3. Sidhu D and Naugler C. Arch Intern Med. 2012;172(22):1707-10.

4. Hoover LE. Am Fam Physician. 2019 May 1;99(9):589-91.

When I worked as a scribe prior to starting medical school, it was commonplace for patients to have fasting labs. I always felt terrible for the patients we saw late in the afternoon that had somehow fasted all day. For many other patients, there was the challenge of finding a time when they could return to have fasting labs drawn.

While in medical school, I have seen the transition of my preceptors’ recommendations, where it seems patients can now have nonfasting labs. However, I have still observed instances when patients need to have fasting labs. We can look at an example case to better understand when and why patients do and do not need to fast prior to having their lipids checked.

Case

A 57-year-old woman presents for an annual wellness visit. She has been healthy this past year with no new concerns. Her blood pressure has been well controlled, and she continues on a statin for hyperlipidemia. She is due for annual labs. She ate breakfast this morning. Which of the following do you recommend?

A. Obtain lipids with her other blood work now.

B. Have her return tomorrow to obtain fasting labs.

In this situation, A is the correct answer. The patient is due for routine screening labs and there are no current indications that fasting labs are necessary.

Studies of fasting vs. nonfasting lipids

Sidhu and Naugler performed a cross-sectional analysis comparing lipid values at fasting intervals of 1 hour to 16 hours.¹ They found the mean total cholesterol and HDL cholesterol values differed by greater than 2%. For LDL cholesterol, the values differed by less than 10% and triglycerides values differed by less than 20%. With this information, the researchers concluded fasting for routine lipids is generally unnecessary.

Mora and colleagues performed a post hoc prospective follow-up of a randomized control

trial to assess if nonfasting lipid measurements could cause misclassification of cardiovascular risk assessment.² Based on 8,270 participants, coronary events associated with fasting vs. nonfasting lipid values were similar when adjusted hazard ratios were compared. They also found an agreement of 94.8% when classifying participants into ASCVD risk categories for fasting and nonfasting lipid values. These outcomes led them to support the use of nonfasting lipid labs for routine cardiovascular risk assessment.

Rahman and colleagues performed a systematic review and found the use of nonfasting lipid values can reliably determine statin management in most situations.³ Circumstances where fasting labs should be used are if patients have a genetic dyslipidemia, if patients have severe hypertriglyceridemia (greater than 500 mg/dL), and if patients have pancreatitis. Triglyceride values fluctuate the most between the fasting and nonfasting state as seen above from Sidhu and Naugler. This could impact triglyceride disorder management and the accuracy of LDL cholesterol estimation (calculated by the Friedewald equation: LDL cholesterol = total cholesterol – HDL cholesterol – triglycerides/5 in mg/dL).³

Benefits of nonfasting lipid labs

There are many benefits of nonfasting labs. For the patients, they do not have to come to their appointments hungry, we can reduce the risk of hypoglycemia for those with diabetes, and they do not have to come back at a later date if they ate something earlier in the day.

For the lab, we can improve efficiency and decrease early morning congestion when patients typically come in for fasting labs.

Lastly, for the provider, nonfasting labs can improve workflow and help decrease the number of patients lost to follow-up who were unable to complete fasting labs the same day as their appointment.
 

Summary

Patients do not need to fast prior to having lipid levels drawn for routine screening. Fasting labs should be considered for patients who have a genetic dyslipidemia or if there is concern for hypertriglyceridemia.

Per the ACC/AHA guidelines, nonfasting lipids can be used to assess ASCVD risk and to establish a baseline LDL cholesterol in adults 20 years and older. If a patient has nonfasting triglycerides greater than 400 mg/dL, repeat fasting lipids should be drawn to assess fasting triglycerides and to establish a baseline LDL cholesterol.⁴
 

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

References

1. Rahman F et al. Curr Atheroscler Rep. 2018;20(3):14. Published 2018 Feb 17.

2. Mora S et al. JAMA Intern Med. 2019;179(7):898-905.

3. Sidhu D and Naugler C. Arch Intern Med. 2012;172(22):1707-10.

4. Hoover LE. Am Fam Physician. 2019 May 1;99(9):589-91.