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Practice guidelines highlights from past year
Based on the most recent Infectious Diseases Society of America (IDSA) guidelines, what would be the preferred therapy?
A) Metronidazole
B) Fidaxomicin + bezlotoxumab
C) Vancomycin
D) Fecal microbiota transplant
The recommendations from the 2021 guidelines would be to treat with fidaxomicin and add bezlotoxumab.1 The guidelines highlight the following changes:
- In patients with an initial Clostridioides difficile infections (CDI) fidaxomicin is preferred over vancomycin.
- In patients with a recurrent CDI episode, fidaxomicin is favored over vancomycin. For patients with multiple recurrences, vancomycin in a tapered and pulsed regimen, vancomycin followed by rifaximin, and fecal microbiota transplantation are options in addition to fidaxomicin.
- Addition of bezlotoxumab to standard of care antibiotics is recommended for recurrence of CDI within the first 6 months over standard of care antibiotics alone
The feasibility of these recommendations is up for debate. The cost of a course of fidaxomicin is $2,800, and the cost of bezlotoxumab is about $4,500. Cost effectiveness studies that helped drive the recommendations show a savings by reducing future hospitalizations for C. diff.2 Unfortunately, this enthusiasm is not shared by many insurance companies for outpatient treatment.
Knee osteoarthritis
I will save you the excitement of the new acromegaly guidelines and focus on something we see all the time: knee osteoarthritis. The American Academy of Orthopedic Surgeons has released guidelines for this condition.3 The useful points I found were as follows:
- Topical application of nonsteroidal anti-inflammatory drugs (e.g., diclofenac) should be used to improve function and quality of life in patients with knee osteoarthritis.
- Exercise routines (i.e, supervised, unsupervised, and/or aquatic) are recommended versus no exercise for improving pain and function in patients with knee osteoarthritis.
- Not recommended is the use of oral narcotics (including tramadol), as they are not effective at improving pain or function, and their use results in a significant increased risk of adverse events.
- Not recommended for routine use in symptomatic knee osteoarthritis is intra-articular injection of hyaluronic acid.
I was happy to see topical NSAIDS recommended, as they are a much safer option in older patients than oral NSAIDS (which were also recommended). The recommendation against narcotics, including tramadol, is a shift from the recommendation of tramadol in the 2013 guidelines.4 Acetaminophen was enthusiastically recommended, and is still worth a try.
Sexually transmitted infections
- The dosing for the treatment of gonorrhea has increased to 500 mg of ceftriaxone (was 250 mg in 2015 guidelines), with a dose of 1 gram for patients who weigh more than 150 kg.
- Chlamydia infections should be treated with a 7-day course of doxycycline as the preferred antibiotic, except in pregnant women (where azithromycin is recommended).
- Herpes simplex virus 2 recurrences can be treated with twice-daily dosing of 800 mg of acyclovir for 5 days, or acyclovir 800 mg three times a day for 2 days. The shortest course for recurrence is famciclovir 1 gram twice a day for 1 day.
- The Centers for Disease Control and Prevention has removed the recommendation for avoidance of alcohol when taking metronidazole.
I hope these highlights of guidelines for common issues we see are helpful!
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Johnson S et al. Clinical practice guideline by the Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA): 2021 Focused update guidelines on management of Clostridioides difficile Infection in adults. Clin Infect Dis. 2021 Sep 7;73(5):e1029-e1044.
2. Pabhu VS et al. Cost-effectiveness of bezlotoxumab compared with placebo for the prevention of recurrent Clostridium difficile infection. Clin Infect Dis. 2018 Feb 1;66(3):355-62.
3. American Academy of Orthopaedic Surgeons: Management of osteoarthritis of the knee (non-arthroplasty) – Evidence-based clinical practice guideline (2021 Aug 31. https://www.aaos.org/oak3cpg).
4. Jevsevar DS. Treatment of osteoarthritis of the knee: Evidence-based guideline, 2nd edition. J Am Acad Orthop Surg. 2013: Sep;21(9):571-6.
5. Sexually transmitted infections treatment guidelines, 2021 recommendations and reports. MMWR 2021 Jul 23;70(4):1-187.
Based on the most recent Infectious Diseases Society of America (IDSA) guidelines, what would be the preferred therapy?
A) Metronidazole
B) Fidaxomicin + bezlotoxumab
C) Vancomycin
D) Fecal microbiota transplant
The recommendations from the 2021 guidelines would be to treat with fidaxomicin and add bezlotoxumab.1 The guidelines highlight the following changes:
- In patients with an initial Clostridioides difficile infections (CDI) fidaxomicin is preferred over vancomycin.
- In patients with a recurrent CDI episode, fidaxomicin is favored over vancomycin. For patients with multiple recurrences, vancomycin in a tapered and pulsed regimen, vancomycin followed by rifaximin, and fecal microbiota transplantation are options in addition to fidaxomicin.
- Addition of bezlotoxumab to standard of care antibiotics is recommended for recurrence of CDI within the first 6 months over standard of care antibiotics alone
The feasibility of these recommendations is up for debate. The cost of a course of fidaxomicin is $2,800, and the cost of bezlotoxumab is about $4,500. Cost effectiveness studies that helped drive the recommendations show a savings by reducing future hospitalizations for C. diff.2 Unfortunately, this enthusiasm is not shared by many insurance companies for outpatient treatment.
Knee osteoarthritis
I will save you the excitement of the new acromegaly guidelines and focus on something we see all the time: knee osteoarthritis. The American Academy of Orthopedic Surgeons has released guidelines for this condition.3 The useful points I found were as follows:
- Topical application of nonsteroidal anti-inflammatory drugs (e.g., diclofenac) should be used to improve function and quality of life in patients with knee osteoarthritis.
- Exercise routines (i.e, supervised, unsupervised, and/or aquatic) are recommended versus no exercise for improving pain and function in patients with knee osteoarthritis.
- Not recommended is the use of oral narcotics (including tramadol), as they are not effective at improving pain or function, and their use results in a significant increased risk of adverse events.
- Not recommended for routine use in symptomatic knee osteoarthritis is intra-articular injection of hyaluronic acid.
I was happy to see topical NSAIDS recommended, as they are a much safer option in older patients than oral NSAIDS (which were also recommended). The recommendation against narcotics, including tramadol, is a shift from the recommendation of tramadol in the 2013 guidelines.4 Acetaminophen was enthusiastically recommended, and is still worth a try.
Sexually transmitted infections
- The dosing for the treatment of gonorrhea has increased to 500 mg of ceftriaxone (was 250 mg in 2015 guidelines), with a dose of 1 gram for patients who weigh more than 150 kg.
- Chlamydia infections should be treated with a 7-day course of doxycycline as the preferred antibiotic, except in pregnant women (where azithromycin is recommended).
- Herpes simplex virus 2 recurrences can be treated with twice-daily dosing of 800 mg of acyclovir for 5 days, or acyclovir 800 mg three times a day for 2 days. The shortest course for recurrence is famciclovir 1 gram twice a day for 1 day.
- The Centers for Disease Control and Prevention has removed the recommendation for avoidance of alcohol when taking metronidazole.
I hope these highlights of guidelines for common issues we see are helpful!
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Johnson S et al. Clinical practice guideline by the Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA): 2021 Focused update guidelines on management of Clostridioides difficile Infection in adults. Clin Infect Dis. 2021 Sep 7;73(5):e1029-e1044.
2. Pabhu VS et al. Cost-effectiveness of bezlotoxumab compared with placebo for the prevention of recurrent Clostridium difficile infection. Clin Infect Dis. 2018 Feb 1;66(3):355-62.
3. American Academy of Orthopaedic Surgeons: Management of osteoarthritis of the knee (non-arthroplasty) – Evidence-based clinical practice guideline (2021 Aug 31. https://www.aaos.org/oak3cpg).
4. Jevsevar DS. Treatment of osteoarthritis of the knee: Evidence-based guideline, 2nd edition. J Am Acad Orthop Surg. 2013: Sep;21(9):571-6.
5. Sexually transmitted infections treatment guidelines, 2021 recommendations and reports. MMWR 2021 Jul 23;70(4):1-187.
Based on the most recent Infectious Diseases Society of America (IDSA) guidelines, what would be the preferred therapy?
A) Metronidazole
B) Fidaxomicin + bezlotoxumab
C) Vancomycin
D) Fecal microbiota transplant
The recommendations from the 2021 guidelines would be to treat with fidaxomicin and add bezlotoxumab.1 The guidelines highlight the following changes:
- In patients with an initial Clostridioides difficile infections (CDI) fidaxomicin is preferred over vancomycin.
- In patients with a recurrent CDI episode, fidaxomicin is favored over vancomycin. For patients with multiple recurrences, vancomycin in a tapered and pulsed regimen, vancomycin followed by rifaximin, and fecal microbiota transplantation are options in addition to fidaxomicin.
- Addition of bezlotoxumab to standard of care antibiotics is recommended for recurrence of CDI within the first 6 months over standard of care antibiotics alone
The feasibility of these recommendations is up for debate. The cost of a course of fidaxomicin is $2,800, and the cost of bezlotoxumab is about $4,500. Cost effectiveness studies that helped drive the recommendations show a savings by reducing future hospitalizations for C. diff.2 Unfortunately, this enthusiasm is not shared by many insurance companies for outpatient treatment.
Knee osteoarthritis
I will save you the excitement of the new acromegaly guidelines and focus on something we see all the time: knee osteoarthritis. The American Academy of Orthopedic Surgeons has released guidelines for this condition.3 The useful points I found were as follows:
- Topical application of nonsteroidal anti-inflammatory drugs (e.g., diclofenac) should be used to improve function and quality of life in patients with knee osteoarthritis.
- Exercise routines (i.e, supervised, unsupervised, and/or aquatic) are recommended versus no exercise for improving pain and function in patients with knee osteoarthritis.
- Not recommended is the use of oral narcotics (including tramadol), as they are not effective at improving pain or function, and their use results in a significant increased risk of adverse events.
- Not recommended for routine use in symptomatic knee osteoarthritis is intra-articular injection of hyaluronic acid.
I was happy to see topical NSAIDS recommended, as they are a much safer option in older patients than oral NSAIDS (which were also recommended). The recommendation against narcotics, including tramadol, is a shift from the recommendation of tramadol in the 2013 guidelines.4 Acetaminophen was enthusiastically recommended, and is still worth a try.
Sexually transmitted infections
- The dosing for the treatment of gonorrhea has increased to 500 mg of ceftriaxone (was 250 mg in 2015 guidelines), with a dose of 1 gram for patients who weigh more than 150 kg.
- Chlamydia infections should be treated with a 7-day course of doxycycline as the preferred antibiotic, except in pregnant women (where azithromycin is recommended).
- Herpes simplex virus 2 recurrences can be treated with twice-daily dosing of 800 mg of acyclovir for 5 days, or acyclovir 800 mg three times a day for 2 days. The shortest course for recurrence is famciclovir 1 gram twice a day for 1 day.
- The Centers for Disease Control and Prevention has removed the recommendation for avoidance of alcohol when taking metronidazole.
I hope these highlights of guidelines for common issues we see are helpful!
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Johnson S et al. Clinical practice guideline by the Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA): 2021 Focused update guidelines on management of Clostridioides difficile Infection in adults. Clin Infect Dis. 2021 Sep 7;73(5):e1029-e1044.
2. Pabhu VS et al. Cost-effectiveness of bezlotoxumab compared with placebo for the prevention of recurrent Clostridium difficile infection. Clin Infect Dis. 2018 Feb 1;66(3):355-62.
3. American Academy of Orthopaedic Surgeons: Management of osteoarthritis of the knee (non-arthroplasty) – Evidence-based clinical practice guideline (2021 Aug 31. https://www.aaos.org/oak3cpg).
4. Jevsevar DS. Treatment of osteoarthritis of the knee: Evidence-based guideline, 2nd edition. J Am Acad Orthop Surg. 2013: Sep;21(9):571-6.
5. Sexually transmitted infections treatment guidelines, 2021 recommendations and reports. MMWR 2021 Jul 23;70(4):1-187.
Tips for connecting with your patients
It is a tough time to be a doctor. With the stresses of the pandemic, the continued unfettered rise of insurance company BS, and so many medical groups being bought up that we often don’t even know who makes the decisions, the patient can sometimes be hidden in the equation.
Be curious
When physicians are curious about why patients have symptoms, how those symptoms will affect their lives, and how worried the patient is about them, patients feel cared about.
Ascertaining how concerned patients are about their symptoms will help you make decisions on whether symptoms you are not concerned about actually need to be treated.
Limit use of EHRs when possible
Use of the electronic health record during visits is essential, but focusing on it too much can put a barrier between the physician and the patient.
Marmor and colleagues found there is an inverse relationship between time spent on the EHR by a patient’s physician and the patient’s satisfaction.1
Eye contact with the patient is important, especially when patients are sharing concerns they are scared about and upsetting experiences. There can be awkward pauses when looking things up on the EHR. Fill those pauses by explaining to the patient what you are doing, or chatting with the patient.
Consider teaching medical students
When a medical student works with you, it doubles the time the patient gets with a concerned listener. Students also can do a great job with timely follow-up and checking in with worried patients.
By having the student present in the clinic room, with the patient present, the patient can really feel heard. The student shares all the details the patient shared, and now their physician is hearing an organized, thoughtful report of the patients concerns.
In fact, I was involved in a study that showed that patients preferred in room presentations, and that they were more satisfied when students presented in the room.2
Use healing words
Some words carry loaded emotions. The word chronic, for example, has negative connotations, whereas the term persisting does not.
I will often ask patients how long they have been suffering from a symptom to imply my concern for what they are going through. The term “chief complaint” is outdated, and upsets patients when they see it in their medical record.
As a patient of mine once said to me: “I never complained about that problem, I just brought it to your attention.” No one wants to be seen as a complainer. Substituting the word concern for complaint works well.
Explain as you examine
People love to hear the term normal. When you are examining a patient, let them know when findings are normal.
I also find it helpful to explain to patients why I am doing certain physical exam maneuvers. This helps them assess how thorough we are in our thought process.
When patients feel their physicians are thorough, they have more confidence in them.
In summary
- Be curious.
- Do not overly focus on the EHR.
- Consider teaching a medical student.
- Be careful of word choice.
- “Overexplain” the physical exam.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-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. Marmor RA et al. Appl Clin Inform. 2018 Jan;9(1):11-4.
2. Rogers HD et al. Acad Med. 2003 Sep;78(9):945-9.
It is a tough time to be a doctor. With the stresses of the pandemic, the continued unfettered rise of insurance company BS, and so many medical groups being bought up that we often don’t even know who makes the decisions, the patient can sometimes be hidden in the equation.
Be curious
When physicians are curious about why patients have symptoms, how those symptoms will affect their lives, and how worried the patient is about them, patients feel cared about.
Ascertaining how concerned patients are about their symptoms will help you make decisions on whether symptoms you are not concerned about actually need to be treated.
Limit use of EHRs when possible
Use of the electronic health record during visits is essential, but focusing on it too much can put a barrier between the physician and the patient.
Marmor and colleagues found there is an inverse relationship between time spent on the EHR by a patient’s physician and the patient’s satisfaction.1
Eye contact with the patient is important, especially when patients are sharing concerns they are scared about and upsetting experiences. There can be awkward pauses when looking things up on the EHR. Fill those pauses by explaining to the patient what you are doing, or chatting with the patient.
Consider teaching medical students
When a medical student works with you, it doubles the time the patient gets with a concerned listener. Students also can do a great job with timely follow-up and checking in with worried patients.
By having the student present in the clinic room, with the patient present, the patient can really feel heard. The student shares all the details the patient shared, and now their physician is hearing an organized, thoughtful report of the patients concerns.
In fact, I was involved in a study that showed that patients preferred in room presentations, and that they were more satisfied when students presented in the room.2
Use healing words
Some words carry loaded emotions. The word chronic, for example, has negative connotations, whereas the term persisting does not.
I will often ask patients how long they have been suffering from a symptom to imply my concern for what they are going through. The term “chief complaint” is outdated, and upsets patients when they see it in their medical record.
As a patient of mine once said to me: “I never complained about that problem, I just brought it to your attention.” No one wants to be seen as a complainer. Substituting the word concern for complaint works well.
Explain as you examine
People love to hear the term normal. When you are examining a patient, let them know when findings are normal.
I also find it helpful to explain to patients why I am doing certain physical exam maneuvers. This helps them assess how thorough we are in our thought process.
When patients feel their physicians are thorough, they have more confidence in them.
In summary
- Be curious.
- Do not overly focus on the EHR.
- Consider teaching a medical student.
- Be careful of word choice.
- “Overexplain” the physical exam.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-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. Marmor RA et al. Appl Clin Inform. 2018 Jan;9(1):11-4.
2. Rogers HD et al. Acad Med. 2003 Sep;78(9):945-9.
It is a tough time to be a doctor. With the stresses of the pandemic, the continued unfettered rise of insurance company BS, and so many medical groups being bought up that we often don’t even know who makes the decisions, the patient can sometimes be hidden in the equation.
Be curious
When physicians are curious about why patients have symptoms, how those symptoms will affect their lives, and how worried the patient is about them, patients feel cared about.
Ascertaining how concerned patients are about their symptoms will help you make decisions on whether symptoms you are not concerned about actually need to be treated.
Limit use of EHRs when possible
Use of the electronic health record during visits is essential, but focusing on it too much can put a barrier between the physician and the patient.
Marmor and colleagues found there is an inverse relationship between time spent on the EHR by a patient’s physician and the patient’s satisfaction.1
Eye contact with the patient is important, especially when patients are sharing concerns they are scared about and upsetting experiences. There can be awkward pauses when looking things up on the EHR. Fill those pauses by explaining to the patient what you are doing, or chatting with the patient.
Consider teaching medical students
When a medical student works with you, it doubles the time the patient gets with a concerned listener. Students also can do a great job with timely follow-up and checking in with worried patients.
By having the student present in the clinic room, with the patient present, the patient can really feel heard. The student shares all the details the patient shared, and now their physician is hearing an organized, thoughtful report of the patients concerns.
In fact, I was involved in a study that showed that patients preferred in room presentations, and that they were more satisfied when students presented in the room.2
Use healing words
Some words carry loaded emotions. The word chronic, for example, has negative connotations, whereas the term persisting does not.
I will often ask patients how long they have been suffering from a symptom to imply my concern for what they are going through. The term “chief complaint” is outdated, and upsets patients when they see it in their medical record.
As a patient of mine once said to me: “I never complained about that problem, I just brought it to your attention.” No one wants to be seen as a complainer. Substituting the word concern for complaint works well.
Explain as you examine
People love to hear the term normal. When you are examining a patient, let them know when findings are normal.
I also find it helpful to explain to patients why I am doing certain physical exam maneuvers. This helps them assess how thorough we are in our thought process.
When patients feel their physicians are thorough, they have more confidence in them.
In summary
- Be curious.
- Do not overly focus on the EHR.
- Consider teaching a medical student.
- Be careful of word choice.
- “Overexplain” the physical exam.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-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. Marmor RA et al. Appl Clin Inform. 2018 Jan;9(1):11-4.
2. Rogers HD et al. Acad Med. 2003 Sep;78(9):945-9.
My favorite physical exam pearls
I would like to start the new year off by returning to the past – when the physical exam was emphasized and utilized in decision making. I think a big reason that its use has diminished in recent years is due to the physical exam not having been emphasized in training.
For those seeking to increase their comfort with conducting the physical exam, below are several methods I have found helpful to use in practice.
Examining the pharynx
We were usually taught to ask the patient to say ahhh, with or without a nasty tongue depressor.
When I was on my pediatrics rotation, I was taught to ask the patients to roar like a lion, which always gave a nice look at their posterior pharynx. The kids also really liked doing this, but it might seem a little strange to ask adults to do this.
A technique I have found that works well with adults is to ask them to yawn. I have found that this get me a great look at the pharynx for about half of my patients.
Auscultatory percussion for pleural effusions
Guarino and colleagues described a technique that is easily mastered and very effective for determining the presence of pleural effusions.1 It involves placing the stethoscope 3 cm below the last rib in the mid clavicular line and tapping from the apex down to the last rib.
For patients without effusion, a sharp change to a loud percussion note will occur at the last rib.
If the patient has an effusion, the loud percussion note will start at the top of the effusion.
This method was remarkably successful at finding pleural effusions. In the study, Dr. Guarino found a sensitivity of 96% and a specificity of 100%.
Physical exam for anemia
Look at the nails and see if they look pale. How can we do this?
The first step is to know what your own hematocrit is. You can then compare the color of your nail to that of the patient.
If you have a normal hematocrit and the patient’s nail bed color is lighter than yours, the patient likely has anemia. If you do this frequently, you will get good at estimating hematocrit. This is especially important if you do not have labs readily available.
Another way to assess for anemia is to look at the color tint of the lower conjunctiva. The best way to look for this is to look at whether there is a generous amount of visible capillaries in the lower conjunctiva. Patients without anemia have a darker red color because of these vessels, whereas patients with anemia are a lighter pink.
Strobach and colleagues2 looked at both nail bed rubor and color tint of the lower conjunctiva and found that both reliably predicted presence and degree of anemia.
Determining if clubbing is present
Most physicians are aware of Shamroth sign, and use it to evaluate for clubbing. Shamroth sign is the loss of the diamond that is created by placing the back surfaces of opposite terminal phalanges together.
I have found that it’s easier to diagnose mild clubbing by looking at the finger in profile. If the ratio of the distal phalangeal depth compared to the depth across the distal interphalangeal joint is greater than 1:1, then clubbing is present.3
Pearls
1. Have the patient try yawning to better see the pharynx without using a tongue blade.
2. Try the technique of auscultatory percussion to be more accurate at picking up pleural effusions.
3. Know your hematocrit, so you can better use color shade to assess for anemia.
4. Try looking at fingers in profile to pick up clubbing.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-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. Guarino JR and Guarino JC. Auscultatory percussion: A simple method to detect pleural effusion. J Gen Intern Med. 1994 Feb;9(2):71-4.
2. Strobach RS et al. The value of the physical examination in the diagnosis of anemia. Correlation of the physical findings and the hemoglobin concentration. Arch Intern Med. 1988 Apr;148(4):831-2.
3. Spicknall KE et al. Clubbing: an update on diagnosis, differential diagnosis, pathophysiology, and clinical relevance. J Am Acad Dermatol. 2005 Jun;52(6):1020-8.
I would like to start the new year off by returning to the past – when the physical exam was emphasized and utilized in decision making. I think a big reason that its use has diminished in recent years is due to the physical exam not having been emphasized in training.
For those seeking to increase their comfort with conducting the physical exam, below are several methods I have found helpful to use in practice.
Examining the pharynx
We were usually taught to ask the patient to say ahhh, with or without a nasty tongue depressor.
When I was on my pediatrics rotation, I was taught to ask the patients to roar like a lion, which always gave a nice look at their posterior pharynx. The kids also really liked doing this, but it might seem a little strange to ask adults to do this.
A technique I have found that works well with adults is to ask them to yawn. I have found that this get me a great look at the pharynx for about half of my patients.
Auscultatory percussion for pleural effusions
Guarino and colleagues described a technique that is easily mastered and very effective for determining the presence of pleural effusions.1 It involves placing the stethoscope 3 cm below the last rib in the mid clavicular line and tapping from the apex down to the last rib.
For patients without effusion, a sharp change to a loud percussion note will occur at the last rib.
If the patient has an effusion, the loud percussion note will start at the top of the effusion.
This method was remarkably successful at finding pleural effusions. In the study, Dr. Guarino found a sensitivity of 96% and a specificity of 100%.
Physical exam for anemia
Look at the nails and see if they look pale. How can we do this?
The first step is to know what your own hematocrit is. You can then compare the color of your nail to that of the patient.
If you have a normal hematocrit and the patient’s nail bed color is lighter than yours, the patient likely has anemia. If you do this frequently, you will get good at estimating hematocrit. This is especially important if you do not have labs readily available.
Another way to assess for anemia is to look at the color tint of the lower conjunctiva. The best way to look for this is to look at whether there is a generous amount of visible capillaries in the lower conjunctiva. Patients without anemia have a darker red color because of these vessels, whereas patients with anemia are a lighter pink.
Strobach and colleagues2 looked at both nail bed rubor and color tint of the lower conjunctiva and found that both reliably predicted presence and degree of anemia.
Determining if clubbing is present
Most physicians are aware of Shamroth sign, and use it to evaluate for clubbing. Shamroth sign is the loss of the diamond that is created by placing the back surfaces of opposite terminal phalanges together.
I have found that it’s easier to diagnose mild clubbing by looking at the finger in profile. If the ratio of the distal phalangeal depth compared to the depth across the distal interphalangeal joint is greater than 1:1, then clubbing is present.3
Pearls
1. Have the patient try yawning to better see the pharynx without using a tongue blade.
2. Try the technique of auscultatory percussion to be more accurate at picking up pleural effusions.
3. Know your hematocrit, so you can better use color shade to assess for anemia.
4. Try looking at fingers in profile to pick up clubbing.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-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. Guarino JR and Guarino JC. Auscultatory percussion: A simple method to detect pleural effusion. J Gen Intern Med. 1994 Feb;9(2):71-4.
2. Strobach RS et al. The value of the physical examination in the diagnosis of anemia. Correlation of the physical findings and the hemoglobin concentration. Arch Intern Med. 1988 Apr;148(4):831-2.
3. Spicknall KE et al. Clubbing: an update on diagnosis, differential diagnosis, pathophysiology, and clinical relevance. J Am Acad Dermatol. 2005 Jun;52(6):1020-8.
I would like to start the new year off by returning to the past – when the physical exam was emphasized and utilized in decision making. I think a big reason that its use has diminished in recent years is due to the physical exam not having been emphasized in training.
For those seeking to increase their comfort with conducting the physical exam, below are several methods I have found helpful to use in practice.
Examining the pharynx
We were usually taught to ask the patient to say ahhh, with or without a nasty tongue depressor.
When I was on my pediatrics rotation, I was taught to ask the patients to roar like a lion, which always gave a nice look at their posterior pharynx. The kids also really liked doing this, but it might seem a little strange to ask adults to do this.
A technique I have found that works well with adults is to ask them to yawn. I have found that this get me a great look at the pharynx for about half of my patients.
Auscultatory percussion for pleural effusions
Guarino and colleagues described a technique that is easily mastered and very effective for determining the presence of pleural effusions.1 It involves placing the stethoscope 3 cm below the last rib in the mid clavicular line and tapping from the apex down to the last rib.
For patients without effusion, a sharp change to a loud percussion note will occur at the last rib.
If the patient has an effusion, the loud percussion note will start at the top of the effusion.
This method was remarkably successful at finding pleural effusions. In the study, Dr. Guarino found a sensitivity of 96% and a specificity of 100%.
Physical exam for anemia
Look at the nails and see if they look pale. How can we do this?
The first step is to know what your own hematocrit is. You can then compare the color of your nail to that of the patient.
If you have a normal hematocrit and the patient’s nail bed color is lighter than yours, the patient likely has anemia. If you do this frequently, you will get good at estimating hematocrit. This is especially important if you do not have labs readily available.
Another way to assess for anemia is to look at the color tint of the lower conjunctiva. The best way to look for this is to look at whether there is a generous amount of visible capillaries in the lower conjunctiva. Patients without anemia have a darker red color because of these vessels, whereas patients with anemia are a lighter pink.
Strobach and colleagues2 looked at both nail bed rubor and color tint of the lower conjunctiva and found that both reliably predicted presence and degree of anemia.
Determining if clubbing is present
Most physicians are aware of Shamroth sign, and use it to evaluate for clubbing. Shamroth sign is the loss of the diamond that is created by placing the back surfaces of opposite terminal phalanges together.
I have found that it’s easier to diagnose mild clubbing by looking at the finger in profile. If the ratio of the distal phalangeal depth compared to the depth across the distal interphalangeal joint is greater than 1:1, then clubbing is present.3
Pearls
1. Have the patient try yawning to better see the pharynx without using a tongue blade.
2. Try the technique of auscultatory percussion to be more accurate at picking up pleural effusions.
3. Know your hematocrit, so you can better use color shade to assess for anemia.
4. Try looking at fingers in profile to pick up clubbing.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-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. Guarino JR and Guarino JC. Auscultatory percussion: A simple method to detect pleural effusion. J Gen Intern Med. 1994 Feb;9(2):71-4.
2. Strobach RS et al. The value of the physical examination in the diagnosis of anemia. Correlation of the physical findings and the hemoglobin concentration. Arch Intern Med. 1988 Apr;148(4):831-2.
3. Spicknall KE et al. Clubbing: an update on diagnosis, differential diagnosis, pathophysiology, and clinical relevance. J Am Acad Dermatol. 2005 Jun;52(6):1020-8.
Case: Older patient with T2D has recurrent flushing
He has had no other symptoms. His only abnormalities on physical exam are a blood pressure of 160/100 and mild peripheral edema.
His current medications include: Famotidine 20 mg b.i.d., Pseudoephedrine/guaifenesin SR b.i.d., Metformin 1,000 mg twice a day, Nifedipine 60 mg XL once a day, and Atorvastatin 20 mg once a day.
His laboratory work up includes: blood urea nitrogen: 20, creatinine: 1.3, sodium: 140, Chloride: 104, potassium: 3.9, glucose: 205, white blood cell count: 6,000, hematocrit: 41, 24-hour urine 5-hydroxyindoleacetic acid (5HIAA) test: 12 mg/day (normal 2-8 mg/day), free catecholamines: 80 mg/24 hours (normal less than 100 mg/24 hours).
What is the most likely diagnosis?
A. Drug effect
B. Pheochromocytoma
C. Carcinoid syndrome
D. Mastocytosis
E. Medullary thyroid cancer
The most likely diagnosis is a drug effect. His flushing is likely caused by nifedipine.
Flushing is one of the most common side effects of this drug.1 This patient had lab testing done for carcinoid (urine 5HIAA), presumably because he had flushing. This lab test result was a false positive, likely because of guaifenesin ingestion, which can cause false-positive 5HIAA results.2
Carcinoid syndrome is very rare (estimates from less than 1 patient/100,000), and the vast majority of patients who have it present with metastatic disease at presentation. Drug side effects are common, and usually are much more likely than rare diseases.
Four principles for assisting with making a diagnosis
This case points out the following four principles that I will touch on to help us make diagnoses in challenging cases.
1. Trigger symptoms: These are symptoms that make us think of a rare disease. In this case, the symptom is flushing, which may make you think of carcinoid syndrome.
Another good example of a trigger symptom is night sweats, where you may think of tuberculosis or lymphoma. These symptoms almost always have a much more common and likely cause, which in this case is a common drug side effect.
Trigger symptoms are great to pay attention to, but do not jump to working up the rare diagnosis without more evidence that it is a plausible diagnosis. Working up rare diseases without a reasonable pretest probability will lead to significant false-positive results.
2. Distinguishing features: These are findings, or combinations of findings, that make rarer diseases more likely. For example, flushing, although seen in many patients with carcinoid syndrome, is much more commonly caused by rosacea, medications, or estrogen/testosterone deficiency.
If a patient presents with flushing plus diarrhea, carcinoid syndrome becomes more likely in differentials. An example of a specific distinguishing feature is transient visual obstructions in patients with idiopathic intracranial hypertension (IIH or pseudotumor cerebri).
Sudden transient visual loss is not a symptom we see often, but headaches and obesity are problems we see every day. A patient with headaches and obesity is very likely to have IIH if they have transient visual obstructions along with headaches and obesity.
3. Intentional physical exams: Do the physical exam focusing on what findings will change your diagnostic probabilities. For example, in this case, if you are considering carcinoid, do a careful abdominal exam, with close attention to the liver, as 75% of patients with carcinoid syndrome have liver metastases.
If you are thinking about IIH, a fundoscopic exam is mandatory, as papilledema is a key feature of this diagnosis.
Read about the rare diagnosis you are considering, this will help with targeting your exam.
4. Remember the unusual presentation of a common disease is more common than the common presentation of a rare disease: Good examples of this are sleep apnea and gastroesophageal reflux disease causing night sweats more commonly than finding lymphomas or active tuberculosis (in the United States) as the cause.3
Pearl: Trigger symptoms help us think of rare diseases, but distinguishing features are most helpful in including or excluding the diagnosis.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Gueret P et al. Drugs. 1990;39 Suppl 2:67-72.
2. Corcuff J et al. Endocr Connect. 2017;6:R87.
3. Smith CS and Paauw DS. J Am Board Fam Pract. 2000;13:424-9.
He has had no other symptoms. His only abnormalities on physical exam are a blood pressure of 160/100 and mild peripheral edema.
His current medications include: Famotidine 20 mg b.i.d., Pseudoephedrine/guaifenesin SR b.i.d., Metformin 1,000 mg twice a day, Nifedipine 60 mg XL once a day, and Atorvastatin 20 mg once a day.
His laboratory work up includes: blood urea nitrogen: 20, creatinine: 1.3, sodium: 140, Chloride: 104, potassium: 3.9, glucose: 205, white blood cell count: 6,000, hematocrit: 41, 24-hour urine 5-hydroxyindoleacetic acid (5HIAA) test: 12 mg/day (normal 2-8 mg/day), free catecholamines: 80 mg/24 hours (normal less than 100 mg/24 hours).
What is the most likely diagnosis?
A. Drug effect
B. Pheochromocytoma
C. Carcinoid syndrome
D. Mastocytosis
E. Medullary thyroid cancer
The most likely diagnosis is a drug effect. His flushing is likely caused by nifedipine.
Flushing is one of the most common side effects of this drug.1 This patient had lab testing done for carcinoid (urine 5HIAA), presumably because he had flushing. This lab test result was a false positive, likely because of guaifenesin ingestion, which can cause false-positive 5HIAA results.2
Carcinoid syndrome is very rare (estimates from less than 1 patient/100,000), and the vast majority of patients who have it present with metastatic disease at presentation. Drug side effects are common, and usually are much more likely than rare diseases.
Four principles for assisting with making a diagnosis
This case points out the following four principles that I will touch on to help us make diagnoses in challenging cases.
1. Trigger symptoms: These are symptoms that make us think of a rare disease. In this case, the symptom is flushing, which may make you think of carcinoid syndrome.
Another good example of a trigger symptom is night sweats, where you may think of tuberculosis or lymphoma. These symptoms almost always have a much more common and likely cause, which in this case is a common drug side effect.
Trigger symptoms are great to pay attention to, but do not jump to working up the rare diagnosis without more evidence that it is a plausible diagnosis. Working up rare diseases without a reasonable pretest probability will lead to significant false-positive results.
2. Distinguishing features: These are findings, or combinations of findings, that make rarer diseases more likely. For example, flushing, although seen in many patients with carcinoid syndrome, is much more commonly caused by rosacea, medications, or estrogen/testosterone deficiency.
If a patient presents with flushing plus diarrhea, carcinoid syndrome becomes more likely in differentials. An example of a specific distinguishing feature is transient visual obstructions in patients with idiopathic intracranial hypertension (IIH or pseudotumor cerebri).
Sudden transient visual loss is not a symptom we see often, but headaches and obesity are problems we see every day. A patient with headaches and obesity is very likely to have IIH if they have transient visual obstructions along with headaches and obesity.
3. Intentional physical exams: Do the physical exam focusing on what findings will change your diagnostic probabilities. For example, in this case, if you are considering carcinoid, do a careful abdominal exam, with close attention to the liver, as 75% of patients with carcinoid syndrome have liver metastases.
If you are thinking about IIH, a fundoscopic exam is mandatory, as papilledema is a key feature of this diagnosis.
Read about the rare diagnosis you are considering, this will help with targeting your exam.
4. Remember the unusual presentation of a common disease is more common than the common presentation of a rare disease: Good examples of this are sleep apnea and gastroesophageal reflux disease causing night sweats more commonly than finding lymphomas or active tuberculosis (in the United States) as the cause.3
Pearl: Trigger symptoms help us think of rare diseases, but distinguishing features are most helpful in including or excluding the diagnosis.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Gueret P et al. Drugs. 1990;39 Suppl 2:67-72.
2. Corcuff J et al. Endocr Connect. 2017;6:R87.
3. Smith CS and Paauw DS. J Am Board Fam Pract. 2000;13:424-9.
He has had no other symptoms. His only abnormalities on physical exam are a blood pressure of 160/100 and mild peripheral edema.
His current medications include: Famotidine 20 mg b.i.d., Pseudoephedrine/guaifenesin SR b.i.d., Metformin 1,000 mg twice a day, Nifedipine 60 mg XL once a day, and Atorvastatin 20 mg once a day.
His laboratory work up includes: blood urea nitrogen: 20, creatinine: 1.3, sodium: 140, Chloride: 104, potassium: 3.9, glucose: 205, white blood cell count: 6,000, hematocrit: 41, 24-hour urine 5-hydroxyindoleacetic acid (5HIAA) test: 12 mg/day (normal 2-8 mg/day), free catecholamines: 80 mg/24 hours (normal less than 100 mg/24 hours).
What is the most likely diagnosis?
A. Drug effect
B. Pheochromocytoma
C. Carcinoid syndrome
D. Mastocytosis
E. Medullary thyroid cancer
The most likely diagnosis is a drug effect. His flushing is likely caused by nifedipine.
Flushing is one of the most common side effects of this drug.1 This patient had lab testing done for carcinoid (urine 5HIAA), presumably because he had flushing. This lab test result was a false positive, likely because of guaifenesin ingestion, which can cause false-positive 5HIAA results.2
Carcinoid syndrome is very rare (estimates from less than 1 patient/100,000), and the vast majority of patients who have it present with metastatic disease at presentation. Drug side effects are common, and usually are much more likely than rare diseases.
Four principles for assisting with making a diagnosis
This case points out the following four principles that I will touch on to help us make diagnoses in challenging cases.
1. Trigger symptoms: These are symptoms that make us think of a rare disease. In this case, the symptom is flushing, which may make you think of carcinoid syndrome.
Another good example of a trigger symptom is night sweats, where you may think of tuberculosis or lymphoma. These symptoms almost always have a much more common and likely cause, which in this case is a common drug side effect.
Trigger symptoms are great to pay attention to, but do not jump to working up the rare diagnosis without more evidence that it is a plausible diagnosis. Working up rare diseases without a reasonable pretest probability will lead to significant false-positive results.
2. Distinguishing features: These are findings, or combinations of findings, that make rarer diseases more likely. For example, flushing, although seen in many patients with carcinoid syndrome, is much more commonly caused by rosacea, medications, or estrogen/testosterone deficiency.
If a patient presents with flushing plus diarrhea, carcinoid syndrome becomes more likely in differentials. An example of a specific distinguishing feature is transient visual obstructions in patients with idiopathic intracranial hypertension (IIH or pseudotumor cerebri).
Sudden transient visual loss is not a symptom we see often, but headaches and obesity are problems we see every day. A patient with headaches and obesity is very likely to have IIH if they have transient visual obstructions along with headaches and obesity.
3. Intentional physical exams: Do the physical exam focusing on what findings will change your diagnostic probabilities. For example, in this case, if you are considering carcinoid, do a careful abdominal exam, with close attention to the liver, as 75% of patients with carcinoid syndrome have liver metastases.
If you are thinking about IIH, a fundoscopic exam is mandatory, as papilledema is a key feature of this diagnosis.
Read about the rare diagnosis you are considering, this will help with targeting your exam.
4. Remember the unusual presentation of a common disease is more common than the common presentation of a rare disease: Good examples of this are sleep apnea and gastroesophageal reflux disease causing night sweats more commonly than finding lymphomas or active tuberculosis (in the United States) as the cause.3
Pearl: Trigger symptoms help us think of rare diseases, but distinguishing features are most helpful in including or excluding the diagnosis.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Gueret P et al. Drugs. 1990;39 Suppl 2:67-72.
2. Corcuff J et al. Endocr Connect. 2017;6:R87.
3. Smith CS and Paauw DS. J Am Board Fam Pract. 2000;13:424-9.
Sleep apnea has many faces
Fortunately her problem stemmed from sleep apnea, and resolved with continuous positive airway pressure (CPAP) therapy.
Wallace and Bucks performed a meta analysis of 42 studies of memory in patients with sleep apnea and found sleep apnea patients were impaired when compared to healthy controls on verbal episodic memory (immediate recall, delayed recall, learning, and recognition) and visuospatial episodic memory (immediate and delayed recall).1 A meta-analysis by Olaithe and associates found an improvement in executive function in patients with sleep apnea who were treated with CPAP.2 I think this is worth considering especially in your patients who have subjective memory disturbances and do not appear to have a mild cognitive impairment or dementia.
About 15 years ago I saw a 74-year-old man for nocturia. He had seen two urologists and had a transurethral resection of the prostate (TURP) without any real change in his nocturia. I trialed him on all sorts of medications, and he seemed to improve temporarily a little on trazodone (went from seven episodes a night to four).
Eventually, after several years, I sent him for a sleep study. He had severe sleep apnea (Apnea Hypopnea Index, 65; O2 saturations as low as 60%). With treatment, his nocturia resolved. He went from seven episodes to two each night.
Zhou and colleagues performed a meta-analysis of 13 studies looking at the association of sleep apnea with nocturia.3 They found that men with sleep apnea have a high incidence of nocturia.
Miyazato and colleagues looked at the effect of CPAP treatment on nighttime urine production in patients with obstructive sleep apnea.4 In this small study of 40 patients, mean nighttime voiding episodes decreased from 2.1 to 1.2 (P < .01).
I have seen several patients with night sweats who ended up having sleep apnea. These patients have had a resolution of their night sweats with sleep apnea treatment.
Arnardottir and colleagues found that obstructive sleep apnea was associated with frequent nocturnal sweating.5 They found that 31% of men and 33% of women with OSA had nocturnal sweating, compared with about 10% of the general population.
When the OSA patients were treated with positive airway pressure, the prevalence of nocturnal sweating decreased to 11.5%, which is similar to general population numbers. Given how common both sleep apnea and night sweats are, this is an important consideration as you evaluate night sweats.
I have seen many patients who have had atrial fibrillation and sleep apnea. Shapira-Daniels and colleagues did a prospective study of 188 patients with atrial fibrillation without a history of sleep apnea who were referred for ablation.6 All patients had home sleep studies, and testing was consistent with sleep apnea in 82% of patients.
Kanagala and associates found that patients with untreated sleep apnea had a greater chance of recurrent atrial fibrillation after cardioversion.7 Recurrence of atrial fibrillation at 12 months was 82% in untreated OSA patients, higher than the 42% recurrence in the treated OSA group (P = .013) and the 53% recurrence in control patients.
I think sleep apnea evaluation should be strongly considered in patients with atrial fibrillation and should be done before referral for ablations.
Pearl: Consider sleep apnea as a possible cause of or contributing factor to the common primary care problems of cognitive concerns, nocturia, night sweats, and atrial fibrillation.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-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. Wallace A and Bucks RS. Memory and obstructive sleep apnea: a meta-analysis. Sleep. 2013;36(2):203. Epub 2013 Feb 1.
2. Olaithe M and Bucks RS. Executive dysfunction in OSA before and after treatment: a meta-analysis. Sleep. 2013;36(9):1297. Epub 2013 Sep 1.
3. Zhou J et al. Association between obstructive sleep apnea syndrome and nocturia: a meta-analysis. Sleep Breath. 2020 Dec;24(4):1293-8.
4. Miyauchi Y et al. Effect of the continuous positive airway pressure on the nocturnal urine volume or night-time frequency in patients with obstructive sleep apnea syndrome. Urology 2015;85:333.
5. Arnardottir ES et al. Nocturnal sweating–a common symptom of obstructive sleep apnoea: the Icelandic sleep apnoea cohort. BMJ Open. 2013 May 14;3(5):e002795. BMJ Open 2013;3:e002795
6. Shapira-Daniels A et al. Prevalence of undiagnosed sleep apnea in patients with atrial fibrillation and its impact on therapy. JACC Clin Electrophysiol. 2020;6(12):1499. Epub 2020 Aug 12.
7. Kanagala R et al. Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation. 2003;107(20):2589. Epub 2003 May 12.
Fortunately her problem stemmed from sleep apnea, and resolved with continuous positive airway pressure (CPAP) therapy.
Wallace and Bucks performed a meta analysis of 42 studies of memory in patients with sleep apnea and found sleep apnea patients were impaired when compared to healthy controls on verbal episodic memory (immediate recall, delayed recall, learning, and recognition) and visuospatial episodic memory (immediate and delayed recall).1 A meta-analysis by Olaithe and associates found an improvement in executive function in patients with sleep apnea who were treated with CPAP.2 I think this is worth considering especially in your patients who have subjective memory disturbances and do not appear to have a mild cognitive impairment or dementia.
About 15 years ago I saw a 74-year-old man for nocturia. He had seen two urologists and had a transurethral resection of the prostate (TURP) without any real change in his nocturia. I trialed him on all sorts of medications, and he seemed to improve temporarily a little on trazodone (went from seven episodes a night to four).
Eventually, after several years, I sent him for a sleep study. He had severe sleep apnea (Apnea Hypopnea Index, 65; O2 saturations as low as 60%). With treatment, his nocturia resolved. He went from seven episodes to two each night.
Zhou and colleagues performed a meta-analysis of 13 studies looking at the association of sleep apnea with nocturia.3 They found that men with sleep apnea have a high incidence of nocturia.
Miyazato and colleagues looked at the effect of CPAP treatment on nighttime urine production in patients with obstructive sleep apnea.4 In this small study of 40 patients, mean nighttime voiding episodes decreased from 2.1 to 1.2 (P < .01).
I have seen several patients with night sweats who ended up having sleep apnea. These patients have had a resolution of their night sweats with sleep apnea treatment.
Arnardottir and colleagues found that obstructive sleep apnea was associated with frequent nocturnal sweating.5 They found that 31% of men and 33% of women with OSA had nocturnal sweating, compared with about 10% of the general population.
When the OSA patients were treated with positive airway pressure, the prevalence of nocturnal sweating decreased to 11.5%, which is similar to general population numbers. Given how common both sleep apnea and night sweats are, this is an important consideration as you evaluate night sweats.
I have seen many patients who have had atrial fibrillation and sleep apnea. Shapira-Daniels and colleagues did a prospective study of 188 patients with atrial fibrillation without a history of sleep apnea who were referred for ablation.6 All patients had home sleep studies, and testing was consistent with sleep apnea in 82% of patients.
Kanagala and associates found that patients with untreated sleep apnea had a greater chance of recurrent atrial fibrillation after cardioversion.7 Recurrence of atrial fibrillation at 12 months was 82% in untreated OSA patients, higher than the 42% recurrence in the treated OSA group (P = .013) and the 53% recurrence in control patients.
I think sleep apnea evaluation should be strongly considered in patients with atrial fibrillation and should be done before referral for ablations.
Pearl: Consider sleep apnea as a possible cause of or contributing factor to the common primary care problems of cognitive concerns, nocturia, night sweats, and atrial fibrillation.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-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. Wallace A and Bucks RS. Memory and obstructive sleep apnea: a meta-analysis. Sleep. 2013;36(2):203. Epub 2013 Feb 1.
2. Olaithe M and Bucks RS. Executive dysfunction in OSA before and after treatment: a meta-analysis. Sleep. 2013;36(9):1297. Epub 2013 Sep 1.
3. Zhou J et al. Association between obstructive sleep apnea syndrome and nocturia: a meta-analysis. Sleep Breath. 2020 Dec;24(4):1293-8.
4. Miyauchi Y et al. Effect of the continuous positive airway pressure on the nocturnal urine volume or night-time frequency in patients with obstructive sleep apnea syndrome. Urology 2015;85:333.
5. Arnardottir ES et al. Nocturnal sweating–a common symptom of obstructive sleep apnoea: the Icelandic sleep apnoea cohort. BMJ Open. 2013 May 14;3(5):e002795. BMJ Open 2013;3:e002795
6. Shapira-Daniels A et al. Prevalence of undiagnosed sleep apnea in patients with atrial fibrillation and its impact on therapy. JACC Clin Electrophysiol. 2020;6(12):1499. Epub 2020 Aug 12.
7. Kanagala R et al. Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation. 2003;107(20):2589. Epub 2003 May 12.
Fortunately her problem stemmed from sleep apnea, and resolved with continuous positive airway pressure (CPAP) therapy.
Wallace and Bucks performed a meta analysis of 42 studies of memory in patients with sleep apnea and found sleep apnea patients were impaired when compared to healthy controls on verbal episodic memory (immediate recall, delayed recall, learning, and recognition) and visuospatial episodic memory (immediate and delayed recall).1 A meta-analysis by Olaithe and associates found an improvement in executive function in patients with sleep apnea who were treated with CPAP.2 I think this is worth considering especially in your patients who have subjective memory disturbances and do not appear to have a mild cognitive impairment or dementia.
About 15 years ago I saw a 74-year-old man for nocturia. He had seen two urologists and had a transurethral resection of the prostate (TURP) without any real change in his nocturia. I trialed him on all sorts of medications, and he seemed to improve temporarily a little on trazodone (went from seven episodes a night to four).
Eventually, after several years, I sent him for a sleep study. He had severe sleep apnea (Apnea Hypopnea Index, 65; O2 saturations as low as 60%). With treatment, his nocturia resolved. He went from seven episodes to two each night.
Zhou and colleagues performed a meta-analysis of 13 studies looking at the association of sleep apnea with nocturia.3 They found that men with sleep apnea have a high incidence of nocturia.
Miyazato and colleagues looked at the effect of CPAP treatment on nighttime urine production in patients with obstructive sleep apnea.4 In this small study of 40 patients, mean nighttime voiding episodes decreased from 2.1 to 1.2 (P < .01).
I have seen several patients with night sweats who ended up having sleep apnea. These patients have had a resolution of their night sweats with sleep apnea treatment.
Arnardottir and colleagues found that obstructive sleep apnea was associated with frequent nocturnal sweating.5 They found that 31% of men and 33% of women with OSA had nocturnal sweating, compared with about 10% of the general population.
When the OSA patients were treated with positive airway pressure, the prevalence of nocturnal sweating decreased to 11.5%, which is similar to general population numbers. Given how common both sleep apnea and night sweats are, this is an important consideration as you evaluate night sweats.
I have seen many patients who have had atrial fibrillation and sleep apnea. Shapira-Daniels and colleagues did a prospective study of 188 patients with atrial fibrillation without a history of sleep apnea who were referred for ablation.6 All patients had home sleep studies, and testing was consistent with sleep apnea in 82% of patients.
Kanagala and associates found that patients with untreated sleep apnea had a greater chance of recurrent atrial fibrillation after cardioversion.7 Recurrence of atrial fibrillation at 12 months was 82% in untreated OSA patients, higher than the 42% recurrence in the treated OSA group (P = .013) and the 53% recurrence in control patients.
I think sleep apnea evaluation should be strongly considered in patients with atrial fibrillation and should be done before referral for ablations.
Pearl: Consider sleep apnea as a possible cause of or contributing factor to the common primary care problems of cognitive concerns, nocturia, night sweats, and atrial fibrillation.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-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. Wallace A and Bucks RS. Memory and obstructive sleep apnea: a meta-analysis. Sleep. 2013;36(2):203. Epub 2013 Feb 1.
2. Olaithe M and Bucks RS. Executive dysfunction in OSA before and after treatment: a meta-analysis. Sleep. 2013;36(9):1297. Epub 2013 Sep 1.
3. Zhou J et al. Association between obstructive sleep apnea syndrome and nocturia: a meta-analysis. Sleep Breath. 2020 Dec;24(4):1293-8.
4. Miyauchi Y et al. Effect of the continuous positive airway pressure on the nocturnal urine volume or night-time frequency in patients with obstructive sleep apnea syndrome. Urology 2015;85:333.
5. Arnardottir ES et al. Nocturnal sweating–a common symptom of obstructive sleep apnoea: the Icelandic sleep apnoea cohort. BMJ Open. 2013 May 14;3(5):e002795. BMJ Open 2013;3:e002795
6. Shapira-Daniels A et al. Prevalence of undiagnosed sleep apnea in patients with atrial fibrillation and its impact on therapy. JACC Clin Electrophysiol. 2020;6(12):1499. Epub 2020 Aug 12.
7. Kanagala R et al. Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation. 2003;107(20):2589. Epub 2003 May 12.
Case: Patient with statin-associated muscle symptoms
A 66-year-old woman is discharged from the hospital after an MI. Her discharge medications include atorvastatin 40 mg, lisinopril 20 mg, acetylsalicylic acid 81 mg, and clopidogrel 75 mg. At this patient’s follow-up appointment, she mentions that she has muscle pain and stiffness in both legs and her back. Her labs include thyroid-stimulating hormone of 2.0 and vitamin D of 40. She stops the atorvastatin for 2 weeks with resolution of her symptoms.
Which treatment recommendation would you make for this patient?
A. Restart atorvastatin
B. Start rosuvastatin twice a week
C. Start ezetimibe
D. Start a PCSK9 inhibitor
We often see high-risk cardiovascular disease patients who are concerned about muscle side effects brought on by statins. I think we all can agree that this patient needs aggressive medical therapy for prevention of secondary cardiovascular events. I would restart her atorvastatin.
Neilsen and Nordestgaard found that early statin discontinuation rates increased from 6% in 1995 to 18% in 2010.1
Early statin discontinuation correlated with negative statin-related news stories, their paper states. This suggests either an increased awareness of side effects or a possible nocebo effect.
Statin rechallenge results
Joy and colleagues reported the results on eight patients who had developed myalgias within 3 weeks of starting a statin. These patients, who received placebo or statin, completed an N-of-1 trial with three double-blind, crossover comparisons separated by 3-week washout periods.
Patients were evaluated pain on a visual analog scale (VAS). For each N-of-1 trial there was no statistically significant difference in pain or myalgia score between those who took statin and placebo. Five of the eight patients chose to continue on statins at the end of the trial.
Herrett and colleagues performed a more extensive series of N-of-1 trials involving 200 patients who had stopped or were considering stopping statins because of muscle symptoms.3 Participants either received 2 months of atorvastatin 20 mg or placebo for 2-month blocks six times. They rated their muscle symptoms on a VAS at the end of each block. There was no difference in muscle symptom scores between the statin and placebo periods.
Wood and colleagues took it a step further, when they studied an N-of-1 trial that included statin, placebo, and no treatment.4 Each participant received four bottles of atorvastatin 20 mg, four bottles of placebo, and four empty bottles. Each month they used treatment from the bottles based on random sequence and reported daily symptom scores. The mean symptom intensity was 8.0 during no-tablet months, 15.4 during placebo months (P < .001, compared with no-tablet months), and 16.3 during statin months (P < .001, compared with no-tablet months; P = .39, compared with placebo).
Taylor and colleagues studied 120 patients who had prior statin-associated muscle complaints.5 Each patient received either simvastatin 20 mg or placebo for 4 weeks, and then were switched for an additional 4 weeks. A total of 43 patients (36%) had pain on simvastatin but not placebo, 21 (17%) had no pain with either treatment, 21 (17%) reported pain with both treatments, and 35 (29%) had pain with placebo but not simvastatin. These studies support the concept of nocebo effect in patients who have muscle symptoms on statins.
So what should be done? Brennan and Roy did a retrospective study of 118 patients referred to a lipid clinic as being statin intolerant to two or more statins.6 Most of the patients were able to tolerate a statin: 71% tolerated same statin rechallenge, 53% tolerated statin switch, and 57% tolerated a nonstatin therapy.
In the Prosisa study, only 27% of patients who reported statin-associated muscle symptoms had reappearance of muscle symptoms after rechallenge with a statin.7
Research implications
Rechallenge with the same statin seems to be a reasonable first step, followed by switching to a different statin. I also share the concept of nocebo effect with my patients, and tell them I believe they have an excellent chance of tolerating the statin.
Pearl: The majority of patients with muscle symptoms while taking a statin likely have a nocebo effect, and are likely to tolerate rechallenge with the same statin.
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. Nielsen SF and Nordestgaard BG. Eur Heart J. 2016;37:908-16.
2. Joy TR et al. Ann Intern Med. 2014;160:301-10.
3. Herrett E et al. BMJ. 2021 Feb 24;372:n135.
4. Wood FA et al. N Engl J Med 2020;383:2182-4.
5. Taylor BA et al. Atherosclerosis. 2017;256:100-4.
6. Brennen ET and Roy TR. Can J Card. 2017;33(5):666-73.
7. Bonaiti Fet al. Atherosclerosis. 2020;315:E13-4.
A 66-year-old woman is discharged from the hospital after an MI. Her discharge medications include atorvastatin 40 mg, lisinopril 20 mg, acetylsalicylic acid 81 mg, and clopidogrel 75 mg. At this patient’s follow-up appointment, she mentions that she has muscle pain and stiffness in both legs and her back. Her labs include thyroid-stimulating hormone of 2.0 and vitamin D of 40. She stops the atorvastatin for 2 weeks with resolution of her symptoms.
Which treatment recommendation would you make for this patient?
A. Restart atorvastatin
B. Start rosuvastatin twice a week
C. Start ezetimibe
D. Start a PCSK9 inhibitor
We often see high-risk cardiovascular disease patients who are concerned about muscle side effects brought on by statins. I think we all can agree that this patient needs aggressive medical therapy for prevention of secondary cardiovascular events. I would restart her atorvastatin.
Neilsen and Nordestgaard found that early statin discontinuation rates increased from 6% in 1995 to 18% in 2010.1
Early statin discontinuation correlated with negative statin-related news stories, their paper states. This suggests either an increased awareness of side effects or a possible nocebo effect.
Statin rechallenge results
Joy and colleagues reported the results on eight patients who had developed myalgias within 3 weeks of starting a statin. These patients, who received placebo or statin, completed an N-of-1 trial with three double-blind, crossover comparisons separated by 3-week washout periods.
Patients were evaluated pain on a visual analog scale (VAS). For each N-of-1 trial there was no statistically significant difference in pain or myalgia score between those who took statin and placebo. Five of the eight patients chose to continue on statins at the end of the trial.
Herrett and colleagues performed a more extensive series of N-of-1 trials involving 200 patients who had stopped or were considering stopping statins because of muscle symptoms.3 Participants either received 2 months of atorvastatin 20 mg or placebo for 2-month blocks six times. They rated their muscle symptoms on a VAS at the end of each block. There was no difference in muscle symptom scores between the statin and placebo periods.
Wood and colleagues took it a step further, when they studied an N-of-1 trial that included statin, placebo, and no treatment.4 Each participant received four bottles of atorvastatin 20 mg, four bottles of placebo, and four empty bottles. Each month they used treatment from the bottles based on random sequence and reported daily symptom scores. The mean symptom intensity was 8.0 during no-tablet months, 15.4 during placebo months (P < .001, compared with no-tablet months), and 16.3 during statin months (P < .001, compared with no-tablet months; P = .39, compared with placebo).
Taylor and colleagues studied 120 patients who had prior statin-associated muscle complaints.5 Each patient received either simvastatin 20 mg or placebo for 4 weeks, and then were switched for an additional 4 weeks. A total of 43 patients (36%) had pain on simvastatin but not placebo, 21 (17%) had no pain with either treatment, 21 (17%) reported pain with both treatments, and 35 (29%) had pain with placebo but not simvastatin. These studies support the concept of nocebo effect in patients who have muscle symptoms on statins.
So what should be done? Brennan and Roy did a retrospective study of 118 patients referred to a lipid clinic as being statin intolerant to two or more statins.6 Most of the patients were able to tolerate a statin: 71% tolerated same statin rechallenge, 53% tolerated statin switch, and 57% tolerated a nonstatin therapy.
In the Prosisa study, only 27% of patients who reported statin-associated muscle symptoms had reappearance of muscle symptoms after rechallenge with a statin.7
Research implications
Rechallenge with the same statin seems to be a reasonable first step, followed by switching to a different statin. I also share the concept of nocebo effect with my patients, and tell them I believe they have an excellent chance of tolerating the statin.
Pearl: The majority of patients with muscle symptoms while taking a statin likely have a nocebo effect, and are likely to tolerate rechallenge with the same statin.
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. Nielsen SF and Nordestgaard BG. Eur Heart J. 2016;37:908-16.
2. Joy TR et al. Ann Intern Med. 2014;160:301-10.
3. Herrett E et al. BMJ. 2021 Feb 24;372:n135.
4. Wood FA et al. N Engl J Med 2020;383:2182-4.
5. Taylor BA et al. Atherosclerosis. 2017;256:100-4.
6. Brennen ET and Roy TR. Can J Card. 2017;33(5):666-73.
7. Bonaiti Fet al. Atherosclerosis. 2020;315:E13-4.
A 66-year-old woman is discharged from the hospital after an MI. Her discharge medications include atorvastatin 40 mg, lisinopril 20 mg, acetylsalicylic acid 81 mg, and clopidogrel 75 mg. At this patient’s follow-up appointment, she mentions that she has muscle pain and stiffness in both legs and her back. Her labs include thyroid-stimulating hormone of 2.0 and vitamin D of 40. She stops the atorvastatin for 2 weeks with resolution of her symptoms.
Which treatment recommendation would you make for this patient?
A. Restart atorvastatin
B. Start rosuvastatin twice a week
C. Start ezetimibe
D. Start a PCSK9 inhibitor
We often see high-risk cardiovascular disease patients who are concerned about muscle side effects brought on by statins. I think we all can agree that this patient needs aggressive medical therapy for prevention of secondary cardiovascular events. I would restart her atorvastatin.
Neilsen and Nordestgaard found that early statin discontinuation rates increased from 6% in 1995 to 18% in 2010.1
Early statin discontinuation correlated with negative statin-related news stories, their paper states. This suggests either an increased awareness of side effects or a possible nocebo effect.
Statin rechallenge results
Joy and colleagues reported the results on eight patients who had developed myalgias within 3 weeks of starting a statin. These patients, who received placebo or statin, completed an N-of-1 trial with three double-blind, crossover comparisons separated by 3-week washout periods.
Patients were evaluated pain on a visual analog scale (VAS). For each N-of-1 trial there was no statistically significant difference in pain or myalgia score between those who took statin and placebo. Five of the eight patients chose to continue on statins at the end of the trial.
Herrett and colleagues performed a more extensive series of N-of-1 trials involving 200 patients who had stopped or were considering stopping statins because of muscle symptoms.3 Participants either received 2 months of atorvastatin 20 mg or placebo for 2-month blocks six times. They rated their muscle symptoms on a VAS at the end of each block. There was no difference in muscle symptom scores between the statin and placebo periods.
Wood and colleagues took it a step further, when they studied an N-of-1 trial that included statin, placebo, and no treatment.4 Each participant received four bottles of atorvastatin 20 mg, four bottles of placebo, and four empty bottles. Each month they used treatment from the bottles based on random sequence and reported daily symptom scores. The mean symptom intensity was 8.0 during no-tablet months, 15.4 during placebo months (P < .001, compared with no-tablet months), and 16.3 during statin months (P < .001, compared with no-tablet months; P = .39, compared with placebo).
Taylor and colleagues studied 120 patients who had prior statin-associated muscle complaints.5 Each patient received either simvastatin 20 mg or placebo for 4 weeks, and then were switched for an additional 4 weeks. A total of 43 patients (36%) had pain on simvastatin but not placebo, 21 (17%) had no pain with either treatment, 21 (17%) reported pain with both treatments, and 35 (29%) had pain with placebo but not simvastatin. These studies support the concept of nocebo effect in patients who have muscle symptoms on statins.
So what should be done? Brennan and Roy did a retrospective study of 118 patients referred to a lipid clinic as being statin intolerant to two or more statins.6 Most of the patients were able to tolerate a statin: 71% tolerated same statin rechallenge, 53% tolerated statin switch, and 57% tolerated a nonstatin therapy.
In the Prosisa study, only 27% of patients who reported statin-associated muscle symptoms had reappearance of muscle symptoms after rechallenge with a statin.7
Research implications
Rechallenge with the same statin seems to be a reasonable first step, followed by switching to a different statin. I also share the concept of nocebo effect with my patients, and tell them I believe they have an excellent chance of tolerating the statin.
Pearl: The majority of patients with muscle symptoms while taking a statin likely have a nocebo effect, and are likely to tolerate rechallenge with the same statin.
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. Nielsen SF and Nordestgaard BG. Eur Heart J. 2016;37:908-16.
2. Joy TR et al. Ann Intern Med. 2014;160:301-10.
3. Herrett E et al. BMJ. 2021 Feb 24;372:n135.
4. Wood FA et al. N Engl J Med 2020;383:2182-4.
5. Taylor BA et al. Atherosclerosis. 2017;256:100-4.
6. Brennen ET and Roy TR. Can J Card. 2017;33(5):666-73.
7. Bonaiti Fet al. Atherosclerosis. 2020;315:E13-4.
Not your ordinary neuropathy
She has had a diagnosis of type 2 diabetes for the past 4 years. She initially presented with polyuria/polydipsia and a hemoglobin A1c level of 9.5. She has previously not tolerated metformin, and did not want to take any subsequent medications. She was seen 4 months ago and at that time had an A1c level of 12.5. She decided she wanted to really treat her diabetes as well as she could. She started consuming a low carbohydrate diet, restarted metformin and began using a continuous glucose monitor. She also started taking nighttime glargine insulin, and mealtime insulin apart. She reports she lost 20 pounds over the past 4 months, her blood sugars now run between 100-120 fasting, and up to 180 before meals. She has had a severe, sharp pain in both of her feet over the past month that is interfering with sleep and makes walking painful for her. An exam reveals hyperesthesia of both feet, and her A1c level is 7.5. What is the most likely cause of her neuropathic symptoms?
A. Vitamin B12 deficiency
B. Diabetic neuropathy
C. Insulin neuritis
D. Charcot-Marie-Tooth disease
The most likely cause
In this case, certainly considering vitamin B12 deficiency is reasonable. It is highly unlikely though, given the rapidity of onset of symptoms, and that the patient has been on metformin for a very short period of time. Chronic metformin use is associated with low B12 levels, and the American Diabetes Association has advised that regular monitoring of vitamin B12 levels should be done on patients who are on long-term metformin.1
Diabetic neuropathy is also unlikely, given the rapidity of symptoms in this patient. What is most likely in this patient is treatment-induced neuropathy (TIN), first described with the name “insulin neuritis”.
Research on TIN
Gibbons and colleagues evaluated 16 patients with diabetes with recent marked, rapid improvement in glycemic control who developed a sudden, painful neuropathy.2 All developed symptoms within 8 weeks of intensive glucose control, with 69% having autonomic dysfunction as well, and all developing worsening retinopathy.
Gibbons and Freeman did a retrospective study of patients referred to a diabetic neuropathy clinic over a 5-year period to try to understand how prevalent TIN is.3
A total of 954 patients were evaluated for diabetic neuropathy. Treatment induced neuropathy was defined as a painful neuropathy and/or autonomic dysfunction occurring within 8 weeks of intensified treatment and a drop of the A1c level greater than 2 over a 3-month period.
A total of 104 patients (10.9%) met the criteria for treatment induced neuropathy. Patients who had a decrease in A1c had a much greater chance of developing a painful or autonomic neuropathy than patients who had no change in A1c (P < .0001). The same patients had a much higher risk of developing retinopathy (P < .001). The greater the reduction in A1c, the greater the risk. Patients whose A1c decreased by 2%-3% over 3 months had an absolute risk of 20%, whereas those with a A1c decease of greater than 4% had an 80% absolute risk.
Siddique and colleagues reported on three cases with very different clinical presentations of TIN.4 One patient had an acute third nerve palsy, another patient had a lumbosacral radiculoplexus neuropathy, and the third patient presented with a diffuse painful sensory neuropathy and postural hypotension.
Most patients improve over time from their neuropathic symptoms, with better recovery in patients with type 1 diabetes.2
Pearl
Strongly consider treatment induced neuropathy in your patients with diabetes who present with acute painful neuropathy and/or autonomic dysfunction in the setting of rapid improvement of glucose control.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. American Diabetes Association. Diabetes Care. 2019 Jan;42(Suppl 1):S90-102.
2. Gibbons CH and Freeman R. Ann Neurol 2010; 67:534–41.
3. Gibbons CH and Freeman R. Brain. 2015;138:43-52.
4. Siddique N et al. Endocrinol Diabetes Metab Case Rep. 2020 Feb 26;2020:19-0140.
She has had a diagnosis of type 2 diabetes for the past 4 years. She initially presented with polyuria/polydipsia and a hemoglobin A1c level of 9.5. She has previously not tolerated metformin, and did not want to take any subsequent medications. She was seen 4 months ago and at that time had an A1c level of 12.5. She decided she wanted to really treat her diabetes as well as she could. She started consuming a low carbohydrate diet, restarted metformin and began using a continuous glucose monitor. She also started taking nighttime glargine insulin, and mealtime insulin apart. She reports she lost 20 pounds over the past 4 months, her blood sugars now run between 100-120 fasting, and up to 180 before meals. She has had a severe, sharp pain in both of her feet over the past month that is interfering with sleep and makes walking painful for her. An exam reveals hyperesthesia of both feet, and her A1c level is 7.5. What is the most likely cause of her neuropathic symptoms?
A. Vitamin B12 deficiency
B. Diabetic neuropathy
C. Insulin neuritis
D. Charcot-Marie-Tooth disease
The most likely cause
In this case, certainly considering vitamin B12 deficiency is reasonable. It is highly unlikely though, given the rapidity of onset of symptoms, and that the patient has been on metformin for a very short period of time. Chronic metformin use is associated with low B12 levels, and the American Diabetes Association has advised that regular monitoring of vitamin B12 levels should be done on patients who are on long-term metformin.1
Diabetic neuropathy is also unlikely, given the rapidity of symptoms in this patient. What is most likely in this patient is treatment-induced neuropathy (TIN), first described with the name “insulin neuritis”.
Research on TIN
Gibbons and colleagues evaluated 16 patients with diabetes with recent marked, rapid improvement in glycemic control who developed a sudden, painful neuropathy.2 All developed symptoms within 8 weeks of intensive glucose control, with 69% having autonomic dysfunction as well, and all developing worsening retinopathy.
Gibbons and Freeman did a retrospective study of patients referred to a diabetic neuropathy clinic over a 5-year period to try to understand how prevalent TIN is.3
A total of 954 patients were evaluated for diabetic neuropathy. Treatment induced neuropathy was defined as a painful neuropathy and/or autonomic dysfunction occurring within 8 weeks of intensified treatment and a drop of the A1c level greater than 2 over a 3-month period.
A total of 104 patients (10.9%) met the criteria for treatment induced neuropathy. Patients who had a decrease in A1c had a much greater chance of developing a painful or autonomic neuropathy than patients who had no change in A1c (P < .0001). The same patients had a much higher risk of developing retinopathy (P < .001). The greater the reduction in A1c, the greater the risk. Patients whose A1c decreased by 2%-3% over 3 months had an absolute risk of 20%, whereas those with a A1c decease of greater than 4% had an 80% absolute risk.
Siddique and colleagues reported on three cases with very different clinical presentations of TIN.4 One patient had an acute third nerve palsy, another patient had a lumbosacral radiculoplexus neuropathy, and the third patient presented with a diffuse painful sensory neuropathy and postural hypotension.
Most patients improve over time from their neuropathic symptoms, with better recovery in patients with type 1 diabetes.2
Pearl
Strongly consider treatment induced neuropathy in your patients with diabetes who present with acute painful neuropathy and/or autonomic dysfunction in the setting of rapid improvement of glucose control.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. American Diabetes Association. Diabetes Care. 2019 Jan;42(Suppl 1):S90-102.
2. Gibbons CH and Freeman R. Ann Neurol 2010; 67:534–41.
3. Gibbons CH and Freeman R. Brain. 2015;138:43-52.
4. Siddique N et al. Endocrinol Diabetes Metab Case Rep. 2020 Feb 26;2020:19-0140.
She has had a diagnosis of type 2 diabetes for the past 4 years. She initially presented with polyuria/polydipsia and a hemoglobin A1c level of 9.5. She has previously not tolerated metformin, and did not want to take any subsequent medications. She was seen 4 months ago and at that time had an A1c level of 12.5. She decided she wanted to really treat her diabetes as well as she could. She started consuming a low carbohydrate diet, restarted metformin and began using a continuous glucose monitor. She also started taking nighttime glargine insulin, and mealtime insulin apart. She reports she lost 20 pounds over the past 4 months, her blood sugars now run between 100-120 fasting, and up to 180 before meals. She has had a severe, sharp pain in both of her feet over the past month that is interfering with sleep and makes walking painful for her. An exam reveals hyperesthesia of both feet, and her A1c level is 7.5. What is the most likely cause of her neuropathic symptoms?
A. Vitamin B12 deficiency
B. Diabetic neuropathy
C. Insulin neuritis
D. Charcot-Marie-Tooth disease
The most likely cause
In this case, certainly considering vitamin B12 deficiency is reasonable. It is highly unlikely though, given the rapidity of onset of symptoms, and that the patient has been on metformin for a very short period of time. Chronic metformin use is associated with low B12 levels, and the American Diabetes Association has advised that regular monitoring of vitamin B12 levels should be done on patients who are on long-term metformin.1
Diabetic neuropathy is also unlikely, given the rapidity of symptoms in this patient. What is most likely in this patient is treatment-induced neuropathy (TIN), first described with the name “insulin neuritis”.
Research on TIN
Gibbons and colleagues evaluated 16 patients with diabetes with recent marked, rapid improvement in glycemic control who developed a sudden, painful neuropathy.2 All developed symptoms within 8 weeks of intensive glucose control, with 69% having autonomic dysfunction as well, and all developing worsening retinopathy.
Gibbons and Freeman did a retrospective study of patients referred to a diabetic neuropathy clinic over a 5-year period to try to understand how prevalent TIN is.3
A total of 954 patients were evaluated for diabetic neuropathy. Treatment induced neuropathy was defined as a painful neuropathy and/or autonomic dysfunction occurring within 8 weeks of intensified treatment and a drop of the A1c level greater than 2 over a 3-month period.
A total of 104 patients (10.9%) met the criteria for treatment induced neuropathy. Patients who had a decrease in A1c had a much greater chance of developing a painful or autonomic neuropathy than patients who had no change in A1c (P < .0001). The same patients had a much higher risk of developing retinopathy (P < .001). The greater the reduction in A1c, the greater the risk. Patients whose A1c decreased by 2%-3% over 3 months had an absolute risk of 20%, whereas those with a A1c decease of greater than 4% had an 80% absolute risk.
Siddique and colleagues reported on three cases with very different clinical presentations of TIN.4 One patient had an acute third nerve palsy, another patient had a lumbosacral radiculoplexus neuropathy, and the third patient presented with a diffuse painful sensory neuropathy and postural hypotension.
Most patients improve over time from their neuropathic symptoms, with better recovery in patients with type 1 diabetes.2
Pearl
Strongly consider treatment induced neuropathy in your patients with diabetes who present with acute painful neuropathy and/or autonomic dysfunction in the setting of rapid improvement of glucose control.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. American Diabetes Association. Diabetes Care. 2019 Jan;42(Suppl 1):S90-102.
2. Gibbons CH and Freeman R. Ann Neurol 2010; 67:534–41.
3. Gibbons CH and Freeman R. Brain. 2015;138:43-52.
4. Siddique N et al. Endocrinol Diabetes Metab Case Rep. 2020 Feb 26;2020:19-0140.
Fall prevention advice for patients with Parkinson’s
A 75-year-old man with Parkinson’s disease has had three falls over the past 4 weeks. He has been compliant with his Parkinson’s treatment. Which of the following options would most help decrease his fall risk?
A. Vitamin D supplementation
B. Vitamin B12 supplementation
C. Calcium supplementation
D. Tai chi
There has been recent evidence that vitamin D supplementation is not helpful in preventing falls in most community-dwelling older adults. Bolland and colleagues performed a meta-analysis of 81 randomized, controlled trials and found that vitamin D supplementation does not prevent fractures or falls.1 They found no difference or benefit in high-dose versus low-dose vitamin D supplementation.
The U.S. Preventive Services Task Force recommends against vitamin D supplementation for the purpose of preventing falls in community-dwelling adults over the age of 65.2 The same USPSTF report recommends exercise intervention, as having the strongest evidence for fall prevention in community-dwelling adults age 65 or older who are at risk for falls.
The benefits of tai chi
Tai chi with it’s emphasis on balance, strength training as well as stress reduction is an excellent option for older adults.
Lui and colleagues performed a meta-analyses of five randomized, controlled trials (355 patients) of tai chi in patients with Parkinson disease.3 Tai chi significantly decreased fall rates (odds ratio, 0.47; 95% confidence interval, 0.30-0.74; P = .001) and significantly improved balance and functional mobility (P < .001) in people with Parkinson disease, compared with no training.
Tai chi can also help prevent falls in a more general population of elderly patients. Lomas-Vega and colleagues performed a meta-analysis of 10 high-quality studies that met inclusion criteria evaluating tai chi for fall prevention.4 Fall risk was reduced over short-term follow-up (incident rate ratio, 0.57; 95% CI, 0.46-0.70) and a small protective effect was seen over long-term follow-up (IRR, 0.87; 95% CI, 0.77-0.98).
Pearl: Consider tai chi in your elderly patients with fall risk to increase their balance and reduce risks of falls.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Bolland MJ et al. Lancet Diabetes Endocrinol. 2018;6(11):847.
2. U.S. Preventive Services Task Force. JAMA. 2018;319(16):1696.
3. Liu HH et al. Parkinsons Dis. 2019 Feb 21;2019:9626934
4. Lomas-Vega R et al. J Am Geriatr Soc. 2017;65(9):2037.
A 75-year-old man with Parkinson’s disease has had three falls over the past 4 weeks. He has been compliant with his Parkinson’s treatment. Which of the following options would most help decrease his fall risk?
A. Vitamin D supplementation
B. Vitamin B12 supplementation
C. Calcium supplementation
D. Tai chi
There has been recent evidence that vitamin D supplementation is not helpful in preventing falls in most community-dwelling older adults. Bolland and colleagues performed a meta-analysis of 81 randomized, controlled trials and found that vitamin D supplementation does not prevent fractures or falls.1 They found no difference or benefit in high-dose versus low-dose vitamin D supplementation.
The U.S. Preventive Services Task Force recommends against vitamin D supplementation for the purpose of preventing falls in community-dwelling adults over the age of 65.2 The same USPSTF report recommends exercise intervention, as having the strongest evidence for fall prevention in community-dwelling adults age 65 or older who are at risk for falls.
The benefits of tai chi
Tai chi with it’s emphasis on balance, strength training as well as stress reduction is an excellent option for older adults.
Lui and colleagues performed a meta-analyses of five randomized, controlled trials (355 patients) of tai chi in patients with Parkinson disease.3 Tai chi significantly decreased fall rates (odds ratio, 0.47; 95% confidence interval, 0.30-0.74; P = .001) and significantly improved balance and functional mobility (P < .001) in people with Parkinson disease, compared with no training.
Tai chi can also help prevent falls in a more general population of elderly patients. Lomas-Vega and colleagues performed a meta-analysis of 10 high-quality studies that met inclusion criteria evaluating tai chi for fall prevention.4 Fall risk was reduced over short-term follow-up (incident rate ratio, 0.57; 95% CI, 0.46-0.70) and a small protective effect was seen over long-term follow-up (IRR, 0.87; 95% CI, 0.77-0.98).
Pearl: Consider tai chi in your elderly patients with fall risk to increase their balance and reduce risks of falls.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Bolland MJ et al. Lancet Diabetes Endocrinol. 2018;6(11):847.
2. U.S. Preventive Services Task Force. JAMA. 2018;319(16):1696.
3. Liu HH et al. Parkinsons Dis. 2019 Feb 21;2019:9626934
4. Lomas-Vega R et al. J Am Geriatr Soc. 2017;65(9):2037.
A 75-year-old man with Parkinson’s disease has had three falls over the past 4 weeks. He has been compliant with his Parkinson’s treatment. Which of the following options would most help decrease his fall risk?
A. Vitamin D supplementation
B. Vitamin B12 supplementation
C. Calcium supplementation
D. Tai chi
There has been recent evidence that vitamin D supplementation is not helpful in preventing falls in most community-dwelling older adults. Bolland and colleagues performed a meta-analysis of 81 randomized, controlled trials and found that vitamin D supplementation does not prevent fractures or falls.1 They found no difference or benefit in high-dose versus low-dose vitamin D supplementation.
The U.S. Preventive Services Task Force recommends against vitamin D supplementation for the purpose of preventing falls in community-dwelling adults over the age of 65.2 The same USPSTF report recommends exercise intervention, as having the strongest evidence for fall prevention in community-dwelling adults age 65 or older who are at risk for falls.
The benefits of tai chi
Tai chi with it’s emphasis on balance, strength training as well as stress reduction is an excellent option for older adults.
Lui and colleagues performed a meta-analyses of five randomized, controlled trials (355 patients) of tai chi in patients with Parkinson disease.3 Tai chi significantly decreased fall rates (odds ratio, 0.47; 95% confidence interval, 0.30-0.74; P = .001) and significantly improved balance and functional mobility (P < .001) in people with Parkinson disease, compared with no training.
Tai chi can also help prevent falls in a more general population of elderly patients. Lomas-Vega and colleagues performed a meta-analysis of 10 high-quality studies that met inclusion criteria evaluating tai chi for fall prevention.4 Fall risk was reduced over short-term follow-up (incident rate ratio, 0.57; 95% CI, 0.46-0.70) and a small protective effect was seen over long-term follow-up (IRR, 0.87; 95% CI, 0.77-0.98).
Pearl: Consider tai chi in your elderly patients with fall risk to increase their balance and reduce risks of falls.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Bolland MJ et al. Lancet Diabetes Endocrinol. 2018;6(11):847.
2. U.S. Preventive Services Task Force. JAMA. 2018;319(16):1696.
3. Liu HH et al. Parkinsons Dis. 2019 Feb 21;2019:9626934
4. Lomas-Vega R et al. J Am Geriatr Soc. 2017;65(9):2037.
Artifactual hypoglycemia: When there’s a problem in the tube
If you are looking for zebras you might consider adrenal insufficiency, which could cause both hyperkalemia and hypoglycemia, but this would make no sense in someone asymptomatic.
This pattern is one I have seen commonly when I am on call, and I am contacted about abnormal labs. The lab reported no hemolysis seen, but this is the typical pattern seen with hemolytic specimens and/or specimens that have been held a long time before they are analyzed.
Lippi and colleagues reported on the clinically significant increase in potassium in samples that visually appeared not to be hemolyzed.1 Hemolyzed specimens can also drop glucose values, but not as profoundly as raising potassium values. When left unprocessed, glycolysis occurs in the white blood cells of a blood sample and may consume 5%-7% of the sample’s glucose content per hour.2
Khaled and colleagues looked at the drop in glucose levels in samples over time based on what anticoagulants were used.3 They found that, at 3 hours, glucose measurements were decreased by 28.4 mg/dL when sodium citrate is used, 58 mg/dL when EDTA was used, 15.4 mg/dL when fluoride oxalate was used, and 60.2 mg/dL when no anticoagulant is used.
Low blood sugars caused by elevated WBCs in blood samples has been well described.4 It has been described with moderate and very high WBC counts, as well as with the leukocytosis seen with polycythemia vera.5 The term “leukocyte larceny” has been used to describe high WBC counts that can not only utilize glucose, but also oxygen.
Saccheti and colleagues described a patient with a WBC greater than 500,000 who had repeatedly low oxygen levels on blood gases, that did not correlate with the normal oxygen saturations measured by pulse oximetry.6 This same issue has been seen in patients with extreme thrombocytosis.7Pearl: When labs don’t make sense clinically, always look at the possibility that there may be a problem in the tube and not in the person. Especially think of this when blood samples may have been held for a long time before they are run, such as with visiting nurse visits and blood draws at shelters and nursing homes.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Lippi G et al. Clin Chem Lab Med. 2006;44(3):311-6.
2. Mikesh LM and Bruns DE. Clin Chem. 2008 May;54(5):930-2.
3. Khaled S et al. Al-Mukhtar Journal of Sciences. 2018;33(2):100-6.
4. Goodenow TJ and Malarkey WB. JAMA. 1977;237(18):1961-2.
5. R Arem et al. Arch Intern Med. 1982 Nov;142(12):2199-201.
6. Sacchetti A et al. J Emerg Med. 1990;8:567–569.
7. A Mehta et al. Eur Respir J. 2008 Feb;31(2):469-72.
If you are looking for zebras you might consider adrenal insufficiency, which could cause both hyperkalemia and hypoglycemia, but this would make no sense in someone asymptomatic.
This pattern is one I have seen commonly when I am on call, and I am contacted about abnormal labs. The lab reported no hemolysis seen, but this is the typical pattern seen with hemolytic specimens and/or specimens that have been held a long time before they are analyzed.
Lippi and colleagues reported on the clinically significant increase in potassium in samples that visually appeared not to be hemolyzed.1 Hemolyzed specimens can also drop glucose values, but not as profoundly as raising potassium values. When left unprocessed, glycolysis occurs in the white blood cells of a blood sample and may consume 5%-7% of the sample’s glucose content per hour.2
Khaled and colleagues looked at the drop in glucose levels in samples over time based on what anticoagulants were used.3 They found that, at 3 hours, glucose measurements were decreased by 28.4 mg/dL when sodium citrate is used, 58 mg/dL when EDTA was used, 15.4 mg/dL when fluoride oxalate was used, and 60.2 mg/dL when no anticoagulant is used.
Low blood sugars caused by elevated WBCs in blood samples has been well described.4 It has been described with moderate and very high WBC counts, as well as with the leukocytosis seen with polycythemia vera.5 The term “leukocyte larceny” has been used to describe high WBC counts that can not only utilize glucose, but also oxygen.
Saccheti and colleagues described a patient with a WBC greater than 500,000 who had repeatedly low oxygen levels on blood gases, that did not correlate with the normal oxygen saturations measured by pulse oximetry.6 This same issue has been seen in patients with extreme thrombocytosis.7Pearl: When labs don’t make sense clinically, always look at the possibility that there may be a problem in the tube and not in the person. Especially think of this when blood samples may have been held for a long time before they are run, such as with visiting nurse visits and blood draws at shelters and nursing homes.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Lippi G et al. Clin Chem Lab Med. 2006;44(3):311-6.
2. Mikesh LM and Bruns DE. Clin Chem. 2008 May;54(5):930-2.
3. Khaled S et al. Al-Mukhtar Journal of Sciences. 2018;33(2):100-6.
4. Goodenow TJ and Malarkey WB. JAMA. 1977;237(18):1961-2.
5. R Arem et al. Arch Intern Med. 1982 Nov;142(12):2199-201.
6. Sacchetti A et al. J Emerg Med. 1990;8:567–569.
7. A Mehta et al. Eur Respir J. 2008 Feb;31(2):469-72.
If you are looking for zebras you might consider adrenal insufficiency, which could cause both hyperkalemia and hypoglycemia, but this would make no sense in someone asymptomatic.
This pattern is one I have seen commonly when I am on call, and I am contacted about abnormal labs. The lab reported no hemolysis seen, but this is the typical pattern seen with hemolytic specimens and/or specimens that have been held a long time before they are analyzed.
Lippi and colleagues reported on the clinically significant increase in potassium in samples that visually appeared not to be hemolyzed.1 Hemolyzed specimens can also drop glucose values, but not as profoundly as raising potassium values. When left unprocessed, glycolysis occurs in the white blood cells of a blood sample and may consume 5%-7% of the sample’s glucose content per hour.2
Khaled and colleagues looked at the drop in glucose levels in samples over time based on what anticoagulants were used.3 They found that, at 3 hours, glucose measurements were decreased by 28.4 mg/dL when sodium citrate is used, 58 mg/dL when EDTA was used, 15.4 mg/dL when fluoride oxalate was used, and 60.2 mg/dL when no anticoagulant is used.
Low blood sugars caused by elevated WBCs in blood samples has been well described.4 It has been described with moderate and very high WBC counts, as well as with the leukocytosis seen with polycythemia vera.5 The term “leukocyte larceny” has been used to describe high WBC counts that can not only utilize glucose, but also oxygen.
Saccheti and colleagues described a patient with a WBC greater than 500,000 who had repeatedly low oxygen levels on blood gases, that did not correlate with the normal oxygen saturations measured by pulse oximetry.6 This same issue has been seen in patients with extreme thrombocytosis.7Pearl: When labs don’t make sense clinically, always look at the possibility that there may be a problem in the tube and not in the person. Especially think of this when blood samples may have been held for a long time before they are run, such as with visiting nurse visits and blood draws at shelters and nursing homes.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Lippi G et al. Clin Chem Lab Med. 2006;44(3):311-6.
2. Mikesh LM and Bruns DE. Clin Chem. 2008 May;54(5):930-2.
3. Khaled S et al. Al-Mukhtar Journal of Sciences. 2018;33(2):100-6.
4. Goodenow TJ and Malarkey WB. JAMA. 1977;237(18):1961-2.
5. R Arem et al. Arch Intern Med. 1982 Nov;142(12):2199-201.
6. Sacchetti A et al. J Emerg Med. 1990;8:567–569.
7. A Mehta et al. Eur Respir J. 2008 Feb;31(2):469-72.
Chronic abdominal pain: What to do when a patient presents with it
She reports the pain is about a 7 out of 10, located in the right upper quadrant. The pain does not worsen with food and not relieved with bowel movements. She has no nausea or vomiting. She reports that the pain worsens when she is sitting or standing and is relieved by lying down. Her past medical history includes having had a cholecystectomy in 2016, having hypertension, and having type 2 diabetes mellitus.
The patient’s medications include metformin, lisinopril, and empagliflozin. Her blood pressure was 130/70, and her pulse was 80. An abdominal exam of her found tenderness to palpation in the right upper quadrant, and no rebound tenderness. Her labs found a white blood cell count of 5.4, a hematocrit of 44%, an erythrocyte sedimentation rate of 13, a C-reactive protein of 1.0, a bilirubin of .8, an alkaline phosphatase of 100, an aspartate aminotransferase of 30, and an alanine transaminase of 22.
What is the most appropriate next step?
A) Right side up oblique ultrasound.
B) Abdominal CT scan.
C) Upper endoscopy.
D) More detailed physical exam.
The correct answer here is D, a more detailed physical exam is needed. Given the positional nature of this patient’s abdominal pain, an evaluation for an abdominal wall cause is appropriate.
Abdominal wall pain as a cause of chronic abdominal pain is rarely considered, but it really should be. Costanza and colleagues looked at 2,709 patients referred to gastroenterologists for chronic abdominal pain.1 Chronic abdominal wall pain was diagnosed in 137 patients, with the diagnosis unchanged in 97% of these patients after 4 years. Most of the patients were women (four to one), and the diagnosis was almost always unsuspected by the referring physician. Physical exam was helpful in suggesting the diagnosis of abdominal wall pain.
The use of Carnett sign can be helpful. A positive Carnett sign is when abdominal pain increases or remains unchanged with tensing abdomen or when the examiner palpates the tensed abdomen. Thompson and colleagues looked at the outcome of 72 patients with undiagnosed abdominal pain and a positive Carnett sign.2 Despite multiple diagnostic tests and surgeries done on these patients, very few of them had serious underlying pathology.
Thompson and Frances published another study looking at 120 patients presenting to an ED with undiagnosed abdominal pain.3 Twenty-four of the patients had positive abdominal wall tenderness on exam, and of those, only 1 had intra-abdominal pathology.
In another study, 158 patients admitted to the hospital with abdominal pain were evaluated for the presence of abdominal wall pain.4 Fifty-three patients were diagnosed with appendicitis, and 5 had abdominal wall tenderness on exam. Thirty-eight patients had other intra-abdominal pathology, and none of those had abdominal wall tenderness on exam. Of the 67 patients in the study who had nonspecific abdominal pain, 19 had abdominal wall tenderness on exam.
Most physicians do not include evaluation for abdominal wall tenderness as part of their evaluation of patients with abdominal pain. I think looking for this is helpful and, if positive, may lead to a diagnosis, as well as reduce the likelihood of intra-abdominal diagnoses.
What can we do in regard to therapy for patients with an abdominal wall source of pain?
Many patients with abdominal wall pain have anterior cutaneous nerve entrapment syndrome (ACNES). Patient’s with this often have discrete areas of tenderness on exam, often on the lateral edge of the rectus sheath, frequently on the right side of the abdomen. Anesthetic injection at the point of tenderness provides immediate relief for patients with ACNES, and is helpful in confirming the diagnosis.
Boelens and colleagues did injections in 48 patients suspected of having ACNE, randomizing half to receive lidocaine and half to receive saline placebo.5The majority of the patients receiving lidocaine (54%) had a response, compared with 17% of placebo patients (P less than .007).
Greenbaum and colleagues studied 79 patients with chronic abdominal wall pain.6 In this study, 72 of 79 patients had greater than 50% pain relief with anesthetic injection and were followed for a mean of almost 14 months. Only four of these patients ended up having a visceral cause of pain.
Can using injections help pain from ACNES longer term?
Koop and colleagues looked at all published studies in regards to both immediate and longer-term pain relief with injections.7 Both lidocaine injections and injections with lidocaine plus steroids led to long-term pain relief (40%-50% of patients with multiple lidocaine injections and up to 80% with lidocaine plus steroid injections). I think that injections are certainly worth a try in patients with chronic abdominal wall pain.
Pearl
Consider chronic abdominal wall pain in your differential diagnoses for patients with chronic abdominal pain, and use Carnett sign to help with diagnosis.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Costanza CD et al. Clin Gastroenterol Hepatol. 2004 May;2(5):395-9.
2. Thomson WH et al. Br J Surg. 1991 Feb;78(2):223-5.
3. Thomson H, Francis DM. Lancet. 1977 Nov 19;2(8047):1053-4.
4. Gray DW et al. Ann R Coll Surg Engl. 1988 Jul;70(4):233-4.
5. Boelens OB et al. Br J Surg. 2013 Jan;100(2):217-21.
6. Greenbaum DS et al. Dig Dis Sci. 1994 Sep;39(9):1935-41.
7. Koop H et al. Dtsch Arztebl Int. 2016 Jan 29;113(4):51-7.
She reports the pain is about a 7 out of 10, located in the right upper quadrant. The pain does not worsen with food and not relieved with bowel movements. She has no nausea or vomiting. She reports that the pain worsens when she is sitting or standing and is relieved by lying down. Her past medical history includes having had a cholecystectomy in 2016, having hypertension, and having type 2 diabetes mellitus.
The patient’s medications include metformin, lisinopril, and empagliflozin. Her blood pressure was 130/70, and her pulse was 80. An abdominal exam of her found tenderness to palpation in the right upper quadrant, and no rebound tenderness. Her labs found a white blood cell count of 5.4, a hematocrit of 44%, an erythrocyte sedimentation rate of 13, a C-reactive protein of 1.0, a bilirubin of .8, an alkaline phosphatase of 100, an aspartate aminotransferase of 30, and an alanine transaminase of 22.
What is the most appropriate next step?
A) Right side up oblique ultrasound.
B) Abdominal CT scan.
C) Upper endoscopy.
D) More detailed physical exam.
The correct answer here is D, a more detailed physical exam is needed. Given the positional nature of this patient’s abdominal pain, an evaluation for an abdominal wall cause is appropriate.
Abdominal wall pain as a cause of chronic abdominal pain is rarely considered, but it really should be. Costanza and colleagues looked at 2,709 patients referred to gastroenterologists for chronic abdominal pain.1 Chronic abdominal wall pain was diagnosed in 137 patients, with the diagnosis unchanged in 97% of these patients after 4 years. Most of the patients were women (four to one), and the diagnosis was almost always unsuspected by the referring physician. Physical exam was helpful in suggesting the diagnosis of abdominal wall pain.
The use of Carnett sign can be helpful. A positive Carnett sign is when abdominal pain increases or remains unchanged with tensing abdomen or when the examiner palpates the tensed abdomen. Thompson and colleagues looked at the outcome of 72 patients with undiagnosed abdominal pain and a positive Carnett sign.2 Despite multiple diagnostic tests and surgeries done on these patients, very few of them had serious underlying pathology.
Thompson and Frances published another study looking at 120 patients presenting to an ED with undiagnosed abdominal pain.3 Twenty-four of the patients had positive abdominal wall tenderness on exam, and of those, only 1 had intra-abdominal pathology.
In another study, 158 patients admitted to the hospital with abdominal pain were evaluated for the presence of abdominal wall pain.4 Fifty-three patients were diagnosed with appendicitis, and 5 had abdominal wall tenderness on exam. Thirty-eight patients had other intra-abdominal pathology, and none of those had abdominal wall tenderness on exam. Of the 67 patients in the study who had nonspecific abdominal pain, 19 had abdominal wall tenderness on exam.
Most physicians do not include evaluation for abdominal wall tenderness as part of their evaluation of patients with abdominal pain. I think looking for this is helpful and, if positive, may lead to a diagnosis, as well as reduce the likelihood of intra-abdominal diagnoses.
What can we do in regard to therapy for patients with an abdominal wall source of pain?
Many patients with abdominal wall pain have anterior cutaneous nerve entrapment syndrome (ACNES). Patient’s with this often have discrete areas of tenderness on exam, often on the lateral edge of the rectus sheath, frequently on the right side of the abdomen. Anesthetic injection at the point of tenderness provides immediate relief for patients with ACNES, and is helpful in confirming the diagnosis.
Boelens and colleagues did injections in 48 patients suspected of having ACNE, randomizing half to receive lidocaine and half to receive saline placebo.5The majority of the patients receiving lidocaine (54%) had a response, compared with 17% of placebo patients (P less than .007).
Greenbaum and colleagues studied 79 patients with chronic abdominal wall pain.6 In this study, 72 of 79 patients had greater than 50% pain relief with anesthetic injection and were followed for a mean of almost 14 months. Only four of these patients ended up having a visceral cause of pain.
Can using injections help pain from ACNES longer term?
Koop and colleagues looked at all published studies in regards to both immediate and longer-term pain relief with injections.7 Both lidocaine injections and injections with lidocaine plus steroids led to long-term pain relief (40%-50% of patients with multiple lidocaine injections and up to 80% with lidocaine plus steroid injections). I think that injections are certainly worth a try in patients with chronic abdominal wall pain.
Pearl
Consider chronic abdominal wall pain in your differential diagnoses for patients with chronic abdominal pain, and use Carnett sign to help with diagnosis.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Costanza CD et al. Clin Gastroenterol Hepatol. 2004 May;2(5):395-9.
2. Thomson WH et al. Br J Surg. 1991 Feb;78(2):223-5.
3. Thomson H, Francis DM. Lancet. 1977 Nov 19;2(8047):1053-4.
4. Gray DW et al. Ann R Coll Surg Engl. 1988 Jul;70(4):233-4.
5. Boelens OB et al. Br J Surg. 2013 Jan;100(2):217-21.
6. Greenbaum DS et al. Dig Dis Sci. 1994 Sep;39(9):1935-41.
7. Koop H et al. Dtsch Arztebl Int. 2016 Jan 29;113(4):51-7.
She reports the pain is about a 7 out of 10, located in the right upper quadrant. The pain does not worsen with food and not relieved with bowel movements. She has no nausea or vomiting. She reports that the pain worsens when she is sitting or standing and is relieved by lying down. Her past medical history includes having had a cholecystectomy in 2016, having hypertension, and having type 2 diabetes mellitus.
The patient’s medications include metformin, lisinopril, and empagliflozin. Her blood pressure was 130/70, and her pulse was 80. An abdominal exam of her found tenderness to palpation in the right upper quadrant, and no rebound tenderness. Her labs found a white blood cell count of 5.4, a hematocrit of 44%, an erythrocyte sedimentation rate of 13, a C-reactive protein of 1.0, a bilirubin of .8, an alkaline phosphatase of 100, an aspartate aminotransferase of 30, and an alanine transaminase of 22.
What is the most appropriate next step?
A) Right side up oblique ultrasound.
B) Abdominal CT scan.
C) Upper endoscopy.
D) More detailed physical exam.
The correct answer here is D, a more detailed physical exam is needed. Given the positional nature of this patient’s abdominal pain, an evaluation for an abdominal wall cause is appropriate.
Abdominal wall pain as a cause of chronic abdominal pain is rarely considered, but it really should be. Costanza and colleagues looked at 2,709 patients referred to gastroenterologists for chronic abdominal pain.1 Chronic abdominal wall pain was diagnosed in 137 patients, with the diagnosis unchanged in 97% of these patients after 4 years. Most of the patients were women (four to one), and the diagnosis was almost always unsuspected by the referring physician. Physical exam was helpful in suggesting the diagnosis of abdominal wall pain.
The use of Carnett sign can be helpful. A positive Carnett sign is when abdominal pain increases or remains unchanged with tensing abdomen or when the examiner palpates the tensed abdomen. Thompson and colleagues looked at the outcome of 72 patients with undiagnosed abdominal pain and a positive Carnett sign.2 Despite multiple diagnostic tests and surgeries done on these patients, very few of them had serious underlying pathology.
Thompson and Frances published another study looking at 120 patients presenting to an ED with undiagnosed abdominal pain.3 Twenty-four of the patients had positive abdominal wall tenderness on exam, and of those, only 1 had intra-abdominal pathology.
In another study, 158 patients admitted to the hospital with abdominal pain were evaluated for the presence of abdominal wall pain.4 Fifty-three patients were diagnosed with appendicitis, and 5 had abdominal wall tenderness on exam. Thirty-eight patients had other intra-abdominal pathology, and none of those had abdominal wall tenderness on exam. Of the 67 patients in the study who had nonspecific abdominal pain, 19 had abdominal wall tenderness on exam.
Most physicians do not include evaluation for abdominal wall tenderness as part of their evaluation of patients with abdominal pain. I think looking for this is helpful and, if positive, may lead to a diagnosis, as well as reduce the likelihood of intra-abdominal diagnoses.
What can we do in regard to therapy for patients with an abdominal wall source of pain?
Many patients with abdominal wall pain have anterior cutaneous nerve entrapment syndrome (ACNES). Patient’s with this often have discrete areas of tenderness on exam, often on the lateral edge of the rectus sheath, frequently on the right side of the abdomen. Anesthetic injection at the point of tenderness provides immediate relief for patients with ACNES, and is helpful in confirming the diagnosis.
Boelens and colleagues did injections in 48 patients suspected of having ACNE, randomizing half to receive lidocaine and half to receive saline placebo.5The majority of the patients receiving lidocaine (54%) had a response, compared with 17% of placebo patients (P less than .007).
Greenbaum and colleagues studied 79 patients with chronic abdominal wall pain.6 In this study, 72 of 79 patients had greater than 50% pain relief with anesthetic injection and were followed for a mean of almost 14 months. Only four of these patients ended up having a visceral cause of pain.
Can using injections help pain from ACNES longer term?
Koop and colleagues looked at all published studies in regards to both immediate and longer-term pain relief with injections.7 Both lidocaine injections and injections with lidocaine plus steroids led to long-term pain relief (40%-50% of patients with multiple lidocaine injections and up to 80% with lidocaine plus steroid injections). I think that injections are certainly worth a try in patients with chronic abdominal wall pain.
Pearl
Consider chronic abdominal wall pain in your differential diagnoses for patients with chronic abdominal pain, and use Carnett sign to help with diagnosis.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Costanza CD et al. Clin Gastroenterol Hepatol. 2004 May;2(5):395-9.
2. Thomson WH et al. Br J Surg. 1991 Feb;78(2):223-5.
3. Thomson H, Francis DM. Lancet. 1977 Nov 19;2(8047):1053-4.
4. Gray DW et al. Ann R Coll Surg Engl. 1988 Jul;70(4):233-4.
5. Boelens OB et al. Br J Surg. 2013 Jan;100(2):217-21.
6. Greenbaum DS et al. Dig Dis Sci. 1994 Sep;39(9):1935-41.
7. Koop H et al. Dtsch Arztebl Int. 2016 Jan 29;113(4):51-7.